Interaction Checker
The content of the interaction checker was last updated in June 2022 and it is the responsibility of the user to assess the clinical relevance of the archived data and the risks and benefits of using such data.
No Interaction Expected
Dasatinib
Acarbose
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. After ingestion of acarbose, the majority of active unchanged drug remains in the lumen of the gastrointestinal tract to exert its pharmacological activity and is metabolised by intestinal enzymes and by microbial flora.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Acenocoumarol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Acenocoumarol is mainly metabolised by CYP2C9 and to a lesser extent by CYP1A2 and CYP2C19. Dasatinib does not inhibit or induce these CYPs. However, dasatinib in combination with acencoumarol increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Acetylsalicylic acid (Aspirin)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. However, dasatinib coadministered with aspirin increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Furthermore, dasatinib use was associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, close monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Agomelatine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as agomelatine is metabolised predominantly via CYP1A2. Dasatinib does not inhibit or induce CYP1A2.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Alendronic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Alendronate is not metabolised and is cleared from the plasma by uptake into bone and elimination via renal excretion. Although no pharmacokinetic interaction is expected, alendronate should be separated from food or other medicinal products and patients must wait at least 30 minutes after taking alendronate before taking any other oral medicinal product.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Alfentanil
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Alfentanil undergoes extensive CYP3A4 metabolism and dasatinib is a weak inhibitor of CYP3A4. As the clinical relevance of this interaction is unknown, monitoring for toxicity may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Alfuzosin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alfuzosin is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase alfuzosin concentrations. Since alfuzosin has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Aliskiren
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aliskiren is minimally metabolised and is mainly excreted unchanged in faeces. P-gp is a major determinant of aliskiren bioavailability. Dasatinib is unlikely to affect aliskiren clearance.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Allopurinol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely as allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Dasatinib not interfere with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Alosetron
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro data indicate that alosetron is metabolised by CYPs 2C9, 3A4 and 1A2. Dasatinib is a weak inhibitor of CYP3A4 and may increase alosetron concentrations. Due to the wide therapeutic index of alosetron, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Alprazolam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alprazolam is mainly metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase alprazolam concentrations. However, since alprazolam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Aluminium hydroxide
Quality of Evidence: Very Low
Summary:
Dasatinib exposure may be altered by coadministration with an antacid. If antacid therapy is needed, the antacid dose should be administered at least 2 hours prior to or 2 hours after the dose of dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ambrisentan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ambrisentan is metabolised by glucuronidation via UGTs 1A3, 1A9 and 2B7, and to a lesser extent by CYP3A4 and CYP2C19. Ambrisentan is also a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase concentrations of ambrisentan. However, since CYP3A4 mediated metabolism is a minor pathway, a clinically significant effect is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Amikacin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as amikacin is eliminated by glomerular filtration. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Amiloride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amiloride is eliminated unchanged in the kidney. In vitro data indicate that amiloride is a substrate of OCT2. Dasatinib is unlikely to affect amiloride renal elimination.
Description:
(See Summary)
Potential Interaction
Dasatinib
Amiodarone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but should be approached with caution. Amiodarone is metabolised by CYP2C8 and CYP3A4. Dasatinib may increase the exposure of amiodarone due to weak CYP3A4 inhibition. Close monitoring for toxicity is recommended when dasatinib is coadministered with substrates of CYP3A4 with a narrow therapeutic index such as amiodarone. Moreover, the major metabolite of amiodarone, desethylamiodarone, is an inhibitor of CYP3A4 (weak), CYP2C9 (moderate), CYP2D6 (moderate), CYP2C19 (weak), CYP1A1 (strong), CYP2B6 (moderate) and P-gp (strong). This does not affect amiodarone. Furthermore, dasatinib should be used with caution when co-administered with a drug with a known risk of Torsade de Pointes such as amoidarone. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Amisulpride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amisulpride is weakly metabolised and is primarily renally eliminated (possibly via OCT). Dasatinib is unlikely to significantly affect amisulpride elimination.
Description:
(See Summary)
Potential Interaction
Dasatinib
Amitriptyline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amitriptyline is metabolised predominantly by CYP2D6 and CYP2C19. Dasatinib does not inhibit or induce these CYPs. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Amlodipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Amlodipine is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase amlodipine concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Amoxicillin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as amoxicillin is mainly excreted in urine by glomerular filtration and tubular secretion. In vitro data indicate that amoxicillin is a substrate of OAT3. Dasatinib is unlikely to interfere with amoxicillin renal elimination.
Description:
(See Summary)
Potential Interaction
Dasatinib
Amphotericin B
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely as amphotericin is not appreciably metabolised and is eliminated to a large extent in the bile. Dasatinib does not interfere with amphotericin B elimination pathway. However, the European SPC for amphotericin B states that concomitant use of amphotericin B and antineoplastic agents can increase the risk of renal toxicity, bronchospasm and hypotension. Furthermore, amphotericin B has a possible risk of QT interval prolongation. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ampicillin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Renal clearance of ampicillin occurs partly by glomerular filtration and partly by tubular secretion. About 20-40% of an oral dose may be excreted unchanged in urine in 6 hours. After parenteral use about 60-80% is excreted in urine within 6 hours. Dasatinib does not interfere with capreomycin renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Anidulafungin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Anidulafungin is not metabolised hepatically but undergoes chemical degradation at physiological temperatures.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Antacids
Quality of Evidence: Very Low
Summary:
Dasatinib exposure may be altered by coadministration with an antacid. If antacid therapy is needed, the antacid dose should be administered at least 2 hours prior to or 2 hours after the dose of dasatinib.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Apixaban
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Apixaban is metabolised by CYP3A4 and to a lesser extent by CYPs 1A2, 2C8, 2C9 and 2C19. Dasatinib is a weak inhibitor of CYP3A4 and may increase apixaban concentrations. The clinical relevance of this interaction is unknown but monitoring may be required. Furthermore, dasatinib in combination with apixaban increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Aprepitant
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but should be approached with caution. Aprepitant is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Dasatinib is a weak inhibitor of CYP3A4 and may increase aprepitant concentrations. Close monitoring for aprepitant toxicity is recommended. Furthermore, during treatment aprepitant is a moderate inhibitor of CYP3A4 and may increase concentrations of dasatinib during the three days of coadministration. Therefore, coadministration is not recommended. If coadministration is unavoidable, consider a 50% dose reduction for dasatinib during the few days of coadministration. Monitor closely for dasatinib toxicity. After treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Concentrations of dasatinib may decrease due to weak induction of CYP3A4, but this is not considered to be clinically relevant.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Aripiprazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aripiprazole is metabolised by CYP3A4 and CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase aripiprazole concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Asenapine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Asenapine is metabolised by glucuronidation (UGT1A4) and oxidative metabolism (CYPs 1A2 (major), 3A4 and 2D6 (minor)). Dasatinib is a weak inhibitor of CYP3A4, however since this is a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Astemizole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Astemizole is metabolised by CYPs 2D6, 2J2 and 3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase astemizole concentrations. The clinical relevance of this interaction is unknown and monitoring may be required as astemizole has a narrow therapeutic index. Caution is needed when dasatinib is co-administered with a drug with a known risk of Torsade de Pointes. In patients, therapeutic doses of dasatinib have been shown to prolong the QTc interval. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Atenolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as atenolol is mainly eliminated unchanged in the kidney, predominantly by glomerular filtration.
Description:
(See Summary)
Potential Interaction
Dasatinib
Atorvastatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Atorvastatin is metabolised by CYP3A4 and is a substrate of P-gp and OATP1B1. Dasatinib is a weak inhibitor of CYP3A4 and may increase atorvastatin concentrations. The clinical relevance of this interaction is unknown. Therefore, it is recommended to replace atorvastatin by another statin, i.e. pravastatin or rosuvastatin, when a statin is indicated.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Azathioprine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Azathioprine is converted to 6-mercaptopurine which is metabolised analogously to natural purines. Dasatinib does not interfere with this metabolic pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
Potential Interaction
Dasatinib
Azithromycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Azithromycin is mainly eliminated via biliary excretion with animal data suggesting this may occur via P-gp and MRP2. Dasatinib does not interact with this pathway. Furthermore, no effect on dasatinib concentrations is expected. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Beclometasone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Beclometasone is a prodrug which is not metabolised by CYP450, but is hydrolysed via esterase enzymes to the highly active metabolite beclometasone-17-monopropionate. Dasatinib does not interact with this pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Bedaquiline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Bedaquiline is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase bedaquiline concentrations. The clinical relevance of this interaction is unknown. However, bedaquiline prolongs the QTc interval and if coadministered with dasatinib an additive or synergistic effect on QT prolongation cannot be excluded. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Bendroflumethiazide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bendroflumethiazide is mainly eliminated by hepatic metabolism (70%) and excreted unchanged in the urine (30%) via OAT1 and OAT3. In vitro data indicate that bendroflumethiazide inhibits these renal transporters but a clinically relevant interaction is unlikely in the range of observed clinical concentrations. In addition, there is no evidence that bendroflumethiazide inhibits or induces CYP450 enzymes and therefore is unlikely to impact dasatinib.
Description:
(See Summary)
Potential Interaction
Dasatinib
Bepridil
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bepridil is metabolised by CYP2D6 (major) and CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but the clinical relevance of this interaction is unknown. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Betamethasone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Betamethasone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase betamethasone concentrations. Since betamethasone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Bezafibrate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as half of bezafibrate dose is eliminated unchanged in the urine.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Bisacodyl
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bisacodyl is converted to an active metabolite by intestinal and bacterial enzymes. Absorption from the gastrointestinal tract is minimal and the small amount absorbed is excreted in urine as the glucuronide.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Bisoprolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Bisoprolol is partly metabolised by CYP3A4 and CYP2D6 and partly eliminated unchanged in the urine. Dasatinib is a weak inhibitor of CYP3A4 and may increase bisoprolol concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Bosentan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Bosentan is a substrate and inducer of CYP3A4 and CYP2C9 and could potentially decrease dasatinib exposure. Dasatinib is a weak inhibitor of CYP3A4 and may increase bosentan concentrations. The clinical relevance of this interaction is unknown. If coadministration is necessary, close monitoring of efficacy is required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Bromazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bromazepam undergoes oxidative biotransformation. Data indicate that CYP3A4 plays a minor role in bromazepam metabolism, but other cytochromes such as CYP2D6 or CYP1A2 may play a role. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Budesonide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Budesonide is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase budesonide concentrations. Since budesonide has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Buprenorphine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Buprenorphine undergoes both N-dealkylation to form the active metabolite norbuprenorphine (via CYP3A4) and glucuronidation (via UGT2B7 and UGT1A1). Dasatinib is a weak CYP3A4 inhibitor and may increase buprenorphine concentrations. As the clinical relevance of this interaction is unknown, monitoring for toxicity may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Bupropion
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bupropion is primarily metabolised by CYP2B6. Dasatinib does not inhibit or induce CYP2B6.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Buspirone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Buspirone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase buspirone concentrations. However, since buspirone does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Calcium
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but a clinically significant interaction is unlikely. Calcium is eliminated through faeces, urine and sweat.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Candesartan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Candesartan is mainly eliminated unchanged via urine and bile.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Capreomycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Capreomycin is predominantly excreted via the kidneys as unchanged drug. Dasatinib does not interfere with capreomycin renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Captopril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Captopril is largely excreted in the urine by OAT1. Dasatinib does not interfere with captopril elimination.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Carbamazepine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but should be avoided. Carbamazepine is primarily metabolised by CYP3A4 and to a lesser extent by CYP2C8. Dasatinib is a weak inhibitor of CYP3A4 (in vivo) and CYP2C8 (in vitro) and may increase carbamazepine exposure. Furthermore, carbamazepine is an inducer of CYPs 2C8 (strong), 2C9 (strong), 3A4 (strong), 1A2 (weak), 2B6 and UGT1A1. Significant decreases in dasatinib plasma exposure may occur due to induction of CYP3A4. Therefore, coadministration should be avoided. Decreased dasatinib exposure can lead to decreased efficacy. Selection of an alternative concomitant medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is clinically necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Furthermore, close monitoring for carbamazepine toxicity is recommended. Consider monitoring of dasatinib and carbamazepine plasma concentrations, if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Carvedilol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carvedilol undergoes glucuronidation via UGTs 1A1, 2B4 and 2B7, and metabolism via CYP2D6 and to a lesser extent CYPs 2C9 and 1A2. Dasatinib does not induce or inhibits these UGTs or CYPs.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Caspofungin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Caspofungin undergoes spontaneous chemical degradation and metabolism via a non CYP-mediated pathway. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cefalexin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefalexin is predominantly renally eliminated unchanged by glomerular filtration and tubular secretion via OAT1 and MATE1. Dasatinib does not interfere with cefalexin renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cefazolin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefazolin is predominantly excreted unchanged in urine, mainly by glomerular filtration with some renal tubular secretion via OAT3. Dasatinib does not interfere with cefazolin renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cefixime
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as cefixime is renally excreted predominantly by glomerular filtration. Dasatinib does not interfere with cefixime renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cefotaxime
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefotaxime is partially metabolised by non-specific esterases. Most of a dose of cefotaxime is excreted in the urine - about 60% as unchanged drug and a further 24% as desacetyl-cefotaxime, an active metabolite. Dasatinib does not interfere with cefotaxime renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ceftazidime
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as ceftazidime is excreted predominantly by renal glomerular filtration. Dasatinib does not interfere with ceftazidime renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ceftriaxone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ceftriaxone is eliminated mainly as unchanged drug; approximately 60% of the dose being excreted in the urine predominantly by glomerular filtration and the remainder via the biliary and intestinal tracts. Dasatinib does not interfere with ceftriaxone renal elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Celecoxib
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Celecoxib is primarily metabolised by CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cetirizine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cetirizine is only metabolised to a limited extent and is eliminated unchanged in the urine through both glomerular filtration and tubular secretion. Dasatinib is unlikely to interact with the renal elimination of cetirizine.
Description:
(See Summary)
Potential Interaction
Dasatinib
Chloramphenicol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Chloramphenicol is predominately eliminated by the kidneys as an inactive metabolite. A small portion is hepatically metabolised via glucuronidation. Dasatinib does not interact with these pathways. However, in vitro studies have shown that chloramphenicol inhibits CYP3A4. Coadministration may potentially increase levels of dasatinib via this mechanism, increasing the risk of adverse events. As the clinical significance of this interaction is unknown, close monitoring is recommended. Ocular use: Chloramphenicol is systemically absorbed when used topically in the eye, therefore the concentrations used are unlikely to cause a clinically relevant interaction.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Chlordiazepoxide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Chlordiazepoxide is extensively metabolised by CYP3A4, but does not inhibit or induce cytochromes. Dasatinib is a weak inhibitor of CYP3A4 and may increase chlordiazepoxide exposure. Monitoring for chlordiazepoxide toxicity is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Chlorphenamine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorphenamine is predominantly metabolised in the liver via CYP2D6. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
Potential Interaction
Dasatinib
Chlorpromazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Chlorpromazine is metabolised mainly by CYP2D6, but also by CYP1A2. Dasatinib does not inhibit or induce CYP2D6 or CYP1A2. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Chlortalidone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlortalidone is mainly excreted unchanged in the urine and faeces.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ciclosporin (Cyclosporine)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Ciclosporin is a substrate of CYP3A4 and P-gp, and inhibits CYP3A4 and OATP1B1, potentially increasing dasatinib concentrations. Dasatinib is a weak inhibitor of CYP3A4 and may increase ciclosporin concentrations. The clinical relevance of this interaction is unknown. No a priori dosage adjustment is commended for dasatinib, but close monitoring of toxicity is recommended. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cilazapril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cilazapril is mainly eliminated unchanged by the kidneys.
Description:
(See Summary)
Potential Interaction
Dasatinib
Cimetidine
Quality of Evidence: Very Low
Summary:
Coadministration is not recommended. Dasatinib exposure may decrease due to gastric pH elevation by cimetidine. Consider the use of antacids in place of H2 antagonist or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ciprofloxacin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Ciprofloxacin is primarily eliminated unchanged in the kidneys by glomerular filtration and tubular secretion via OAT3. Ciprofloxacin is also metabolised and partially cleared through the bile and intestines. Dasatinib does not interfere with the elimination of ciprofloxacin. However, ciprofloxacin is a weak to moderate inhibitor of CYP3A4 and strong inhibitor of CYP1A2. Concentrations of dasatinib may increase due to inhibition of CYP3A4. Selection of an alternate concomitant medicinal product, with no or minimal potential to inhibit CYP3A4 should be considered. If coadministration is unavoidable, monitor closely for dasatinib toxicity and a dose reduction should be considered. Consider monitoring of dasatinib plasma concentrations, if available. In addition, ciprofloxacin may prolong the QT interval. In patients, therapeutic doses of dasatinib have been shown to prolong the QTc interval. In a thorough QT study in healthy volunteers dasatinib did not show relevant QT prolongation (on average 3-5 msec and upperbound of 95% CI <8 ms). However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Cisapride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and should be avoided. Cisapride is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase cisapride concentrations. However, the clinical relevance of this interaction is unknown. Note: Dasatinib should be used with caution when co-administered with a drug with a known risk of Torsade de Pointes.
Description:
(See Summary)
Potential Interaction
Dasatinib
Citalopram
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Citalopram is metabolised by CYPs 2C19 (38%), 2D6 (31%) and 3A4 (31%). Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Clarithromycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Clarithromycin may increase dasatinib concentrations due to inhibition of CYP3A4. Inhibitors of CYP3A4 should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to inhibit CYP3A4 should be considered. If coadministration is clinically necessary, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Monitoring of dasatinib toxicity and plasma concentration is recommended, if available. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Clavulanic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clavulanic acid is extensively metabolised (likely non CYP mediated pathway) and excreted in the urine by glomerular filtration. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Clemastine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clemastine is predominantly metabolised in the liver via CYP2D6. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Clindamycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Clindamycin is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase clindamycin concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Clobetasol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with the topical use of clobetasol.
Description:
(See Summary)
Potential Interaction
Dasatinib
Clofazimine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clofazimine is largely excreted unchanged in the faeces, both as unabsorbed drug and via biliary excretion. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Clofibrate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clofibrate is hydrolysed to an active metabolite, clofibric acid. Excretion of clofibric acid glucuronide is possibly performed via OAT1. Dasatinib does not interfere with clofibrate elimination.
Description:
(See Summary)
Potential Interaction
Dasatinib
Clomipramine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clomipramine is metabolised by CYPs 3A4, 1A2 and 2C19 to desmethylclomipramine, an active metabolite which has a higher activity than the parent drug. In addition, clomipramine and desmethylclomipramine are metabolised by CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase clomipramine concentrations, but the clinical relevance of this interaction is unknown. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Clonidine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Approximately 70% of administered clonidine is excreted in the urine, mainly in the form of the unchanged parent drug (40-60% of the dose). Clonidine is a weak inhibitor of OCT2 and is unlikely to interact with dasatinib elimination. In addition, dasatinib does not interfere with clonidine elimination.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Clopidogrel
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clopidogrel is a prodrug and is converted to its active metabolite via CYPs 3A4, 2B6, 2C19 and 1A2. Dasatinib is a weak inhibitor of CYP3A4 but the clinical relevance of this interaction is unknown. Furthermore, dasatinib in combination with clopidogrel increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. In addition, dasatinib use was associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Clorazepate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clorazepate is rapidly converted to nordiazepam which is then metabolised to oxazepam by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase nordiazepam concentrations. However, since nordiazepam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cloxacillin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Cloxacillin is metabolised to a limited extent, and the unchanged drug and metabolites are excreted in the urine by glomerular filtration and renal tubular secretion. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Clozapine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clozapine is metabolised mainly by CYP1A2 and CYP3A4, and to a lesser extent by CYP2C19 and CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase concentrations of clozapine. Close monitoring for clozapine toxicity is recommended when dasatinib is coadministered with clozapine. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended. Furthermore, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Codeine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Codeine is converted via CYP2D6 to morphine, an active metabolite with analgesic and opioid properties. Morphine is further metabolised by conjugation with glucuronic acid to morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active). Morphine is also a substrate of P-gp. Furthermore, codeine is converted via CYP3A4 to norcodeine, an inactive metabolite. Dasatinib is a weak inhibitor of CYP3A4, but since CYP3A4 mediated metabolism is a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Colchicine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Colchicine is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase colchicine concentrations. As the clinical relevance of this interaction is unknown, monitoring for colchicine toxicity may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Cycloserine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cycloserine is predominantly renally excreted via glomerular filtration. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Dabigatran
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dabigatran is transported via P-gp and is renally excreted. Dasatinib does not inhibit or induce P-gp. However, dasatinib in combination with dabigatran increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Dalteparin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dalteparin is excreted largely unchanged via the kidneys. Dasatinib does not interfere with the renal excretion of dalteparin. However, dasatinib in combination with dalteparin increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Dapsone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metabolism of dapsone is mainly by N-acetylation with a component of N-hydroxylation, and is via multiple CYP P450 enzymes. Dasatinib is a weak inhibitor of CYP3A4. As multiple pathways are involved in the metabolism of dapsone, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Desipramine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely as desipramine is metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Desogestrel
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase desogestrel concentrations. However, since desogestrel does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Dexamethasone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Dexamethasone has been described as a weak inducer of CYP3A4 and could possibly decrease dasatinib plasma concentrations. However, the clinical relevance of CYP3A4 induction by dexamethasone has not been established yet. Monitoring may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Dextropropoxyphene
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Dextropropoxyphene is mainly metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase dextropropoxyphene concentrations. As the clinical relevance of this interaction is unknown, monitoring for toxicity may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Diamorphine (diacetylmorphine)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diamorphine is rapidly metabolised by sequential deacetylation to morphine which is then mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Dasatinib does not inhibit or induce UGTs.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Diazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diazepam is metabolised to nordiazepam (by CYP3A4 and CYP2C19) and to temazepam (mainly by CYP3A4). Dasatinib is a weak inhibitor of CYP3A4 and may increase diazepam concentrations. However, since diazepam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Diclofenac
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diclofenac is partly glucuronidated by UGT2B7 and partly oxidised by CYP2C9. Dasatinib does not inhibit or induce CYP2C9 or UGT2B7.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Digoxin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Digoxin is eliminated renally via the renal transporters OATP4C1 and P-gp. Dasatinib does not interfere with digoxin elimination.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Dihydrocodeine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dihydrocodeine undergoes predominantly direct glucuronidation, with CYP3A4 mediated metabolism accounting for only 5-10% of the overall metabolism. Dasatinib is a weak inhibitor of CYP3A4, but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Diltiazem
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Diltiazem is metabolised by CYP3A4 and CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase diltiazem concentrations. The clinical relevance of this interaction is unknown. Diltiazem is a moderate inhibitor of CYP3A4 and therefore could potentially increase dasatinib exposure. Inhibitors of CYP3A4 should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to inhibit CYP3A4 should be considered. If coadministration is unavoidable, monitor closely for dasatinib toxicity and dose reduction should be considered. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
Potential Interaction
Dasatinib
Diphenhydramine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Diphenhydramine is mainly metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Dipyridamole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dipyridamole is glucuronidated by many UGTs, specifically those of the UGT1A subfamily. Dasatinib does not inhibit or induce UGTs. However, dasatinib in combination with dipyridamole increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Disopyramide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Disopyramide is metabolised by CYP3A4 (25%) and 50% of the drug is eliminated unchanged in urine. Dasatinib is a weak inhibitor of CYP3A4 and may increase disopyramide concentrations. Since CYP3A4 mediated metabolism is only a minor pathway, a pharmacokinetic interaction is unlikely. In healthy volunteers dasatinib did not show relevant QT prolongation (on average 3-5 msec and upperbound of 95% CI <8 ms). However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Dolasetron
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dolasetron is converted by carbonyl reductase to its active metabolite, hydrodolasetron, which is mainly glucuronidated (60%) and metabolised by CYP2D6 (10-20%) and CYP3A4 (<1%). Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. Note: Dolasetron may prolong the QT interval and dasatinib has been shown to prolong the QT interval. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Domperidone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Domperidone is mainly metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase domperidone concentrations. The clinical relevance of this interaction is unknown. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Dopamine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dopamine is metabolised in the liver, kidneys, and plasma by monoamine oxidase (MAO) and catechol-O-methyltransferase to inactive compounds. About 25% of a dose of dopamine is metabolised to norepinephrine within the adrenergic nerve terminals. There is little potential for dopamine to affect disposition of dasatinib, or to be affected if co-administered with dasatinib.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Doxazosin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Doxazosin is metabolised mainly by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase doxazosin concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Doxepin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxepin is metabolised to nordoxepin (a metabolite with comparable pharmacological activity as the parent compound) mainly by CYP2C19. In addition, doxepin and nordoxepin are metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2C19 or CYP2D6.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Doxycycline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxycycline is excreted in the urine and faeces as unchanged active substance. Between 40-60% of an administered dose can be accounted for in urine. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Dronabinol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dronabinol is mainly metabolised by CYP2C9 and to a lesser extent by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Drospirenone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Drospirenone is metabolised to a minor extent via CYP3A4. Dasatinib is a weak inhibitor of CYP3A4. However, since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Dulaglutide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as dulaglutide is degraded by endogenous endopeptidases. Dulaglutide delays gastric emptying and could possibly decrease the absorption rate of concomitantly administered oral drugs. Since dasatinib efficacy is more likely to be correlated to trough plasma concentrations instead of maximum plasma concentrations of dasatinib, the clinical relevance of delayed absorption is considered to be limited.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Duloxetine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Duloxetine is metabolised by CYP2D6 and CYP1A2. Dasatinib does not inhibit or induce CYP2D6 or CYP1A2.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Dutasteride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dutasteride is mainly metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase dutasteride concentrations. Since dutasteride has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Dydrogesterone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dydrogesterone is metabolised to dihydrodydrogesterone (possibly via CYP3A4). Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Edoxaban
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Edoxaban is transported via P-gp. Dasatinib is unlikely to interfere with this pathway. However, dasatinib in combination with edoxaban increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Eltrombopag
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Eltrombopag is metabolised by cleavage conjugation (via UGT1A1, UGT1A3) and oxidation (via CYP1A2 and CYP2C8). Dasatinib does not interact with this pathway. However, dasatinib in combination with eltrombopag increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Enalapril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Enalapril is hydrolysed to enalaprilat which is eliminated renally (possibly via OATs). Dasatinib is unlikely to interfere with this pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Enoxaparin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Enoxaparin does not undergo cytochrome metabolism but is desulphated and depolymerised in the liver, and is predominantly renally excreted. Dasatinib does not interact with this metabolic pathway. However, dasatinib in combination with enoxaparin increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Eprosartan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as eprosartan is largely excreted in bile and urine as unchanged drug.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ertapenem
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ertapenem is mainly eliminated through the kidneys by glomerular filtration with tubular secretion playing a minor component. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Erythromycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Erythromycin may increase dasatinib concentrations due to inhibition of CYP3A4. Inhibitors of CYP3A4 should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to inhibit CYP3A4 should be considered. If coadministration is clinically necessary, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Monitoring of dasatinib toxicity and plasma concentration is recommended, if available. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Escitalopram
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Escitalopram is metabolised by CYPs 2C19 (37%), 2D6 (28%) and 3A4 (35%) to form N-desmethylescitalopram. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Esomeprazole
Quality of Evidence: Very Low
Summary:
Coadministration is not recommended. Esomeprazole is metabolised by CYP2C19 and CYP3A4. Esomeprazole inhibits CYP2C19 and dasatinib is a weak inhibitor of CYP3A4. Due to the wide therapeutic index of esomeprazole, this interaction is unlikely to be clinically relevant. However, in healthy volunteers (n=14), dasatinib (100 mg) coadministration with omeprazole (40 mg for 4 days) reduced the AUC and Cmax of dasatinib by 43% and 42%, respectively. Dasatinib exposure may decrease due to gastric pH elevation by esomeprazole. Consider the use of antacids in place of H2 antagonists or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Estazolam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Estazolam is metabolised to its major metabolite 4-hydroxyestazolam via CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase estazolam concentrations. However, since estazolam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Estradiol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Estradiol is metabolised by CYP3A4, CYP1A2 and is glucuronidated. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ethambutol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethambutol is partly metabolised by alcohol dehydrogenase (20%) and partly eliminated unchanged in the faeces (20%) and urine (50%). Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ethinylestradiol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethinylestradiol undergoes oxidation (CYP3A4>CYP2C9), sulfation and glucuronidation (UGT1A1). Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ethionamide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethionamide is extensively metabolised in the liver; animal studies suggest involvement of flavin-containing monooxygenases. Dasatinib does not interfere with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Etonogestrel
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etonogestrel is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase etonogestrel concentrations. However, since etonogestrel does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Everolimus (Immunosuppressant)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Everolimus is mainly metabolised by CYP3A4 and is a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase everolimus concentrations. As the clinical relevance of this interaction is unknown, monitoring for everolimus toxicity may be required. Due to the risk of additive haematological toxicity, haematological parameters should also be monitored if coadministered.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Exenatide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as exenatide is cleared mainly by glomerular filtration. Exenatide delays gastric emptying and could possibly decrease the absorption rate of concomitantly administered oral drugs. Since dasatinib efficacy is more likely to be correlated to trough plasma concentrations instead of maximum plasma concentrations of dasatinib, the clinical relevance of delayed absorption is considered to be limited.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ezetimibe
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ezetimibe is glucuronidated by UGTs 1A1 and 1A3 and to a lesser extent by UGTs 2B15 and 2B7. Dasatinib does not inhibit or induce UGTs.
Description:
(See Summary)
Potential Interaction
Dasatinib
Famotidine
Quality of Evidence: Low
Summary:
Coadministration is not recommended. In healthy volunteers (n=24), dasatinib (50 mg twice daily) coadministered with famotidine (40 mg 2 hours after initial dasatinib dose) decreased the AUC and Cmax of dasatinib by 63% and 61%, respectively. Dasatinib exposure may decrease due to gastric pH elevation by famotidine. Consider the use of antacids in place of H2 antagonists or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Felodipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Felodipine is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase felodipine concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Fenofibrate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fenofibrate is hydrolysed to an active metabolite, fenofibric acid. In vitro data suggest that fenofibric acid inhibits OAT3. Dasatinib does not interact with this pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Fentanyl
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Fentanyl undergoes extensive metabolism by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase fentanyl concentrations. As the clinical relevance of this interaction is unknown, monitoring for toxicity may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Fexofenadine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fexofenadine undergoes negligible metabolism and is mainly eliminated unchanged in faeces.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Finasteride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Finasteride is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase finasteride concentrations. Since finasteride has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Fish oils
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Flecainide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Flecainide is metabolised mainly via CYP2D6, with a proportion (approximately 30%) of the parent drug also renally eliminated unchanged. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Flucloxacillin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Flucloxacillin is mainly renally eliminated partly by glomerular filtration and partly by active secretion via OAT1. Dasatinib does not interact with this metabolic pathway. However, flucloxacillin was shown to induce CYP3A4 and could potentially decrease dasatinib exposure. Close monitoring is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Fluconazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and is not recommended as dasatinib concentrations may increase due to inhibition of CYP3A4 by fluconazole. Concurrent use of CYP3A4 inhibitors should be avoided. If coadministration is unavoidable, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Monitoring of dasatinib plasma concentrations should be considered, if available. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Flucytosine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Flucytosine is metabolised to 5-fluorouracil (5-FU). 5-FU is further metabolised by dihydropyrimidine dehydrogenase (DPD) to an inactive metabolite. Dasatinib does not interfere with this elimination pathway. However, 5-FU binds to the enzyme thymidylate synthase resulting in DNA damage. This mechanism occurs in all fast dividing cells including bone marrow cells, resulting in haematological toxicity. Dasatinib also induces haematological toxicity which could be enhanced by the use of flucytosine. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Fludrocortisone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fludrocortisone is metabolised in the liver to inactive metabolites, possibly via CYP3A. Dasatinib is a weak inhibitor of CYP3A4 and may increase fludrocortisone concentrations. Since fludrocortisone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Flunitrazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flunitrazepam is metabolised mainly via CYP3A4 and CYP2C19. Dasatinib is a weak inhibitor of CYP3A4 and may increase flunitrazepam concentrations. However, since flunitrazepam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Fluoxetine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluoxetine is metabolised by CYPs 2D6 and 2C9 and to a lesser extent by CYPs 2C19 and 3A4 to form norfluoxetine. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely
Description:
(See Summary)
Potential Interaction
Dasatinib
Fluphenazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Fluphenazine is metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Flurazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of flurazepam is most likely CYP-mediated. Dasatinib is a weak inhibitor of CYP3A4 and may increase flurazepam concentrations. However, since flurazepam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Fluticasone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluticasone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase fluticasone concentrations. Since fluticasone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Fluvastatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as fluvastatin is mainly metabolised by CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Fluvoxamine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Fluvoxamine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Dasatinib does not inhibit or induce CYP2D6 or CYP1A2. However, fluvoxamine inhibits CYPs 1A2, 2C19, 3A4, 2C9 and so dasatinib concentrations may be slightly increased if co-administered with fluvoxamine. As the clinical relevance of these interactions are unknown, monitoring may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Fondaparinux
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance pharmacokinetic interaction is unlikely. Fondaparinux does not undergo cytochrome metabolism but is predominantly renally excreted. Dasatinib does not interact with this metabolic pathway. However, dasatinib in combination with fondaparinux increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Formoterol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Formoterol is eliminated primarily by direct glucuronidation, with O-demethylation (by CYPs 2D6, 2C19, 2C9, and 2A6) followed by further glucuronidation being another pathway. As multiple CYP450 and UGT enzymes catalyse the transformation the potential for a pharmacokinetic interaction is low.
Description:
(See Summary)
Potential Interaction
Dasatinib
Fosaprepitant
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but should be approached with caution. Fosaprepitant is rapidly, almost completely, converted to the active metabolite aprepitant. Dasatinib does not interact with this metabolic pathway. Aprepitant is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Dasatinib is a weak inhibitor of CYP3A4 and may increase aprepitant concentrations. Close monitoring for aprepitant toxicity is recommended. Furthermore, during treatment aprepitant is a moderate inhibitor of CYP3A4 and may increase concentrations of dasatinib during the three days of coadministration. Therefore, coadministration is not recommended. If coadministration is unavoidable, consider a 50% dose reduction for dasatinib during the few days of coadministration. Monitor closely for dasatinib toxicity. After treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Concentrations of dasatinib may decrease due to weak induction of CYP3A4, but this is not considered to be clinically relevant.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Fosphenytoin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but should be avoided. Fosphenytoin is rapidly converted to the active metabolite phenytoin. Phenytoin is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C19. Dasatinib does not interact with this pathway. However, phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Concentrations of dasatinib may decrease due to strong induction of CYP3A4. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Furosemide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Furosemide is glucuronidated mainly in the kidney (UGT1A9) and to a lesser extent in the liver (UGT1A1). A large proportion of furosemide is also eliminated unchanged renally (via OATs). Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Gabapentin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as gabapentin is cleared mainly by glomerular filtration. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Gemfibrozil
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gemfibrozil is metabolised by UGT2B7. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Gentamicin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gentamicin is eliminated unchanged predominantly via glomerular filtration. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Gestodene
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gestodene is metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2C19. Dasatinib is a weak inhibitor of CYP3A4 and may increase gestodene concentrations. Since gestodene does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Glibenclamide (Glyburide)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Glibenclamide is mainly metabolised by CYP3A4 and to a lesser extent by CYP2C9. Dasatinib is a weak inhibitor of CYP3A4 and may increase glibenclamide concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Gliclazide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gliclazide is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C19. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Glimepiride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glimepiride is mainly metabolised by CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Glipizide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glipizide is mainly metabolised by CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
Potential Interaction
Dasatinib
Granisetron
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Granisetron is metabolised by CYP3A4 and is a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase granisetron concentrations. The clinical relevance of this interaction is unknown. Furthermore, granisetron may prolong the QT interval. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Grapefruit juice
Quality of Evidence: Very Low
Summary:
Coadministration should be avoided. Grapefruit juice is a known inhibitor of CYP3A4, potentially increasing dasatinib concentrations. However, the magnitude of this potential interaction is difficult to predict as the effect of grapefruit juice is concentration-, dose- and preparation-dependent and varies widely across brands.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Green tea
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Griseofulvin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Less than 1% of a griseofulvin dose is excreted unchanged via the kidneys. Dasatinib does not interfere with griseofulvin elimination pathway. However, griseofulvin is a liver microsomal enzyme inducer and may lower plasma levels, and therefore reduce the efficacy, of concomitantly administered medicinal products metabolised by CYP3A4, such as dasatinib.
Description:
(See Summary)
Potential Interaction
Dasatinib
Haloperidol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Haloperidol has a complex metabolism as it undergoes glucuronidation (UGT2B7>1A4, 1A9), carbonyl reduction as well as oxidative metabolism (CYP3A4 and CYP2D6). Dasatinib is a weak inhibitor of CYP3A4 and may increase haloperidol concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Heparin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on the metabolism and clearance a pharmacokinetic interaction is unlikely. Heparin is thought to be eliminated via the reticuloendothelial system. Dasatinib does not interact with this metabolic pathway. However, dasatinib in combination with heparin increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Hydralazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydralazine is metabolised via primary oxidative metabolism and acetylation. Although in vitro studies have suggested that hydralazine is a mixed enzyme inhibitor, which may weakly inhibit CYP3A4 and CYP2D6, it is not expected that this will lead to a clinical relevant interaction with dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Hydrochlorothiazide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrochlorothiazide is not metabolised and is cleared by the kidneys via OAT1. In vitro data indicate that hydrochlorothiazide is unlikely to inhibit OAT1 in the range of clinically relevant drug. Significant interactions are not expected with dasatinib.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Hydrocodone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Hydrocodone is metabolised by CYP2D6 to hydromorphone and by CYP3A4 to norhydrocodone, both of which have analgesic effects. Dasatinib is a weak inhibitor of CYP3A4 and may increase hydrocodone concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Hydrocortisone (oral)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrocortisone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase hydrocortisone concentrations. Since hydrocortisone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Hydrocortisone (topical)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with the topical use of hydrocortisone.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Hydromorphone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydromorphone is eliminated via glucuronidation, mainly by UGT2B7. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Hydroxyurea (Hydroxycarbamide)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydroxyurea is not a substrate of CYP enzymes or P-gp. However, coadministration may increase risk of gastrointestinal toxicity, haematological toxicity or mucositis. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
Potential Interaction
Dasatinib
Hydroxyzine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydroxyzine is partly metabolised by alcohol dehydrogenase and partly by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase hydroxyzine concentrations. Since hydroxyzine does not have a narrow therapeutic index, a clinically relevant interaction is unlikely. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ibandronic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ibandronic acid is not metabolised and is cleared from the plasma by uptake into bone and elimination via renal excretion. Although no pharmacokinetic interaction is expected, ibandronic acid should be taken after an overnight fast (at least 6 hours) and before the first food or drink of the day. Medicinal products and supplements should be similarly avoided prior to taking ibandronic acid. Fasting should be continued for at least 30 minutes after taking ibandronic acid.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Ibuprofen
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ibuprofen is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C8 and direct glucuronidation. Dasatinib does not interact with this metabolic pathway. However, dasatinib coadministered with ibuprofen increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Furthermore, dasatinib use was associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Iloperidone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Iloperidone is metabolised by CYP3A4 and CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase iloperidone concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Imipenem/Cilastatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Imipenem and cilastatin are eliminated by glomerular filtration and to a lesser extent, active tubular secretion. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Imipramine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Imipramine is metabolised by CYPs 3A4, 2C19 and 1A2 to desipramine. Imipramine and desipramine are both metabolised by CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is one of multiple pathways a clinically relevant interaction is unlikely. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Indapamide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Indapamide is extensively metabolised by CYP P450. Dasatinib is a weak inhibitor of CYP3A4. The clinical relevance of this interaction is unknown. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Insulin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Interferon alpha
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. However, coadministration may increase risk of neutropenia, fatigue, and thrombocytopenia. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Interleukin 2 (Aldesleukin)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Interleukin-2 is mainly eliminated by glomerular filtration. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ipratropium bromide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. A small proportion of an inhaled ipratropium dose is systemically absorbed (6.9%). Metabolism is via ester hydrolysis and conjugation. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Irbesartan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Irbesartan is metabolised by glucuronidation and oxidation (mainly CYP2C9). Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Iron supplements
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Isoniazid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Isoniazid is acetylated in the liver to form acetylisoniazid which is then hydrolysed to isonicotinic acid and acetylhydrazine. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Isosorbide dinitrate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. In vitro studies suggest that CYP3A4 has a role in nitric oxide formation from isosorbide dinitrate. Dasatinib is a weak inhibitor of CYP3A4 and may increase isosorbide dinitrate concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Itraconazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and is not recommended as dasatinib concentrations may increase due to inhibition of CYP3A4 by itraconazole. Concurrent use of CYP3A4 inhibitors should be avoided. If coadministration is unavoidable, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Additionally, close monitoring for dasatinib toxicity is recommended. Consider monitoring of dasatinib plasma concentrations, if available. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ivabradine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ivabradine is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase ivabradine concentrations. The clinical relevance of this interaction is unknown. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. According to the product labels the use of ivabradine in patients treated with QT prolonging medicinal products should be avoided. If the combination appears necessary, close ECG monitoring is required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Kanamycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as kanamycin is eliminated unchanged predominantly via glomerular filtration. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ketoconazole
Quality of Evidence: Low
Summary:
Coadministration is not recommended. Coadministration of dasatinib (20 mg once daily) and ketoconazole (200 mg twice daily) increased total dasatinib Cmax and AUC by 4- and 5-fold, respectively, due to inhibition of CYP3A4. Concurrent use of CYP3A4 inhibitors should be avoided. If coadministration is clinically necessary, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Close monitoring of dasatinib plasma concentrations should be considered, if available. Additional monitoring for dasatinib toxicity is also recommended. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Labetalol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Labetalol is mainly glucuronidated (via UGT1A1 and UGT2B7). Dasatinib does not interact with this pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Lacidipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Lacidipine is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase lacidipine concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Lactulose
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metabolism of lactulose to lactic acid occurs via gastro-intestinal microbial flora only.
Description:
(See Summary)
Potential Interaction
Dasatinib
Lansoprazole
Quality of Evidence: Very Low
Summary:
Coadministration is not recommended. Lansoprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. However, when coadministered with omeprazole, the AUC and Cmax of dasatinib was decreased by 43% and 42%, respectively. Therefore, dasatinib exposure may decrease due to gastric pH elevation by lansoprazole. Consider the use of antacids in place of H2 antagonists or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Lercanidipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Lercanidipine is mainly metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase lercanidipine concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Levocetirizine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as less than 14% of a dose of levocetirizine is metabolised. Levocetirizine is mainly eliminated unchanged in urine through both glomerular filtration and tubular secretion.
Description:
(See Summary)
Potential Interaction
Dasatinib
Levofloxacin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Levofloxacin is renally eliminated mainly by glomerular filtration and active secretion (possibly OCT2). Dasatinib does not interact with this metabolic pathway. In healthy volunteers, dasatinib did not show relevant QT prolongation (on average 3-5 msec and upperbound of 95% CI <8 ms). However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Levomepromazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Levomepromazine is metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Levonorgestrel
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Levonorgestrel is metabolised by CYP3A4 and is glucuronidated to a minor extent. Dasatinib is a weak inhibitor of CYP3A4 and may increase levonorgestrel concentrations. Since levonorgestrel does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Levonorgestrel (Emergency Contraception)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Levonorgestrel is metabolised by CYP3A4 and is glucuronidated to a minor extent. Dasatinib is a weak inhibitor of CYP3A4 and may increase levonorgestrel concentrations. Since levonorgestrel does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Levothyroxine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Levothyroxine is metabolised by deiodination (by enzymes of deiodinase family) and glucuronidation. Dasatinib does not interact with levothyroxine metabolism.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Lidocaine (Lignocaine)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. CYP1A2 is the predominant enzyme involved in lidocaine metabolism in the range of therapeutic concentrations with a minor contribution from CYP3A4. Dasatinib does not inhibit or induce CYP1A2.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Linagliptin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Linagliptin is mainly eliminated as parent compound in faeces, with metabolism by CYP3A4 representing a minor elimination pathway. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. Linagliptin is also a substrate of P-gp and an inhibitor of CYP3A4. Dasatinib concentrations may increase due to inhibition of CYP3A4. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Linezolid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Linezolid undergoes non-CYP mediated metabolism.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Liraglutide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as liraglutide is degraded by endogenous endopeptidases.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Lisinopril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lisinopril is eliminated unchanged renally via glomerular filtration.
Description:
(See Summary)
Potential Interaction
Dasatinib
Lithium
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Lithium is mainly eliminated unchanged by the kidneys. Lithium is freely filtered at a rate that is dependent upon the glomerular filtration rate therefore no pharmacokinetic interaction is expected. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Live vaccines
Quality of Evidence: Very Low
Summary:
Coadministration of live vaccines (such as BCG vaccine; measles, mumps and rubella vaccines; varicella vaccines; typhoid vaccines; rotavirus vaccines; yellow fever vaccines; oral polio vaccine) has not been studied. In patients, who are receiving cytotoxics or other immunosuppressant drugs, use of live vaccines for immunisation is contraindicated. If coadministration is judged clinically necessary, use with extreme caution since generalized infections can occur.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Loperamide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Loperamide is mainly metabolised by CYP3A4 and CYP2C8. Dasatinib is a weak inhibitor of CYP3A4 and may increase loperamide concentrations. Due to the wide therapeutic index of loperamide, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Loratadine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Loratadine is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase loratadine concentrations. This is unlikely to be clinically relevant as loratadine has a wide therapeutic index.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Lorazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lorazepam is eliminated by non-CYP-mediated pathways and no effect on plasma concentrations is expected when coadministered with dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Lormetazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lormetazepam is mainly glucuronidated. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Losartan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Losartan is converted to its active metabolite mainly by CYP2C9 and to a lesser extent CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Lovastatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Lovastatin is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase lovastatin concentrations. The clinical relevance of this interaction is unknown. Therefore, it is recommended to replace lovastatin by another statin, i.e. pravastatin or rosuvastatin, when a statin is indicated.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Macitentan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Macitentan is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 2C19, 2C9 and 2C8. Dasatinib is a weak inhibitor of CYP3A4 and may increase macitentan concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Magnesium
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Magnesium is eliminated in the kidney, mainly by glomerular filtration.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Maprotiline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Maprotiline is mainly metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Medroxyprogesterone (depot)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Medroxyprogesterone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase medroxyprogesterone concentrations. Since medroxyprogesterone does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Medroxyprogesterone (non-depot)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Medroxyprogesterone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase medroxyprogesterone concentrations. However, since medroxyprogesterone does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Mefenamic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mefenamic acid is metabolised by CYP2C9 and glucuronidated by UGT2B7 and UGT1A9. Dasatinib does not inhibit or induce these CYPs or UGTs.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Megestrol acetate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Megestrol acetate is mainly eliminated in the urine.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Meropenem
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Meropenem is primarily eliminated by the kidney with in vitro data suggesting it is a substrate of the renal transporters OAT3>OAT1. Dasatinib does not interfere with this elimination pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Mesalazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mesalazine is metabolised to N-acetyl-mesalazine by N-acetyltransferase. Dasatinib does not interact with this pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Metamizole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and should be approached with caution. Metamizole may decrease dasatinib concentrations due to induction of CYP3A4. A decrease in dasatinib exposure can lead to decreased efficacy. Selection of an alternative concomitant medication with no or minimal enzyme induction potential is recommended. As the clinical relevance of this interaction is unknown, close monitoring and dose adjustment may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Metformin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metformin is mainly eliminated unchanged in the urine (via OCT2). Dasatinib does not interact with these metabolic and elimination pathways.
Description:
(See Summary)
Potential Interaction
Dasatinib
Methadone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Methadone is demethylated by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase methadone concentrations. Dasatinib should be used with caution when coadministered with a drug with a known risk of Torsade de Pointes. In healthy volunteers, dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Methyldopa
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methyldopa is excreted in urine largely by glomerular filtration, primarily unchanged and as the mono-O-sulfate conjugate. It is unlikely to affect the disposition of dasatinib, or to be altered by coadministration with dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Methylphenidate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methylphenidate is not metabolised by cytochrome P450s to a clinically relevant extent and does not inhibit or induce cytochrome P450s.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Methylprednisolone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methylprednisolone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase methylprednisolone concentrations. Since methylprednisolone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Metoclopramide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metoclopramide is partially metabolised by the CYP450 system (mainly CYP2D6). Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Metolazone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as metolazone is largely excreted unchanged in urine.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Metoprolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metoprolol is mainly metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
Potential Interaction
Dasatinib
Metronidazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Elevated plasma concentrations have been reported for some CYP3A substrates (e.g. tacrolimus, ciclosporin) with metronidazole. However, metronidazole did not increase concentrations of several CYP3A probe drugs (e.g. midazolam, alprazolam). Since the mechanism of the interaction with CYP3A has not yet been identified, an interaction with dasatinib cannot be excluded and close monitoring is recommended. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Mexiletine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mexiletine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Dasatinib does not inhibit or induce CYP2D6 or CYP1A2.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Mianserin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Mianserin is metabolised by CYPs 2D6 and 1A2, and to a lesser extent by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4. Although the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Miconazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Miconazole inhibits CYP2C9 and CYP3A4 and could potentially increase dasatinib concentrations. Concurrent use of CYP3A4 inhibitors should be avoided. If coadministration is clinically necessary, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Monitoring of dasatinib plasma concentrations should be considered, if available. Additional monitoring for dasatinib toxicity is also recommended. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended. Note, no a priori dosage adjustment is recommended for dasatinib with dermal administration of miconazole, since systemic exposure of miconazole is limited when used topically.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Midazolam (oral)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Midazolam is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase midazolam concentrations. Since midazolam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Midazolam (parenteral)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Midazolam is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase midazolam concentrations. Since midazolam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Milnacipran
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Milnacipran is mainly eliminated unchanged (50%), and as glucuronides (30%) and oxidative metabolites (20%). Dasatinib is unlikely to interfere with these pathways.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Mirtazapine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Mirtazapine is metabolised to 8-hydroxymirtazapine by CYP2D6 and CYP1A2, and to N-desmethylmirtazapine mainly by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Mometasone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mometasone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase mometasone concentrations. Since mometasone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Montelukast
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Montelukast is mainly metabolised by CYP2C8 and to a lesser extent by CYPs 3A4 and 2C9. Dasatinib is a weak inhibitor of CYP3A4. However, since CYP3A4 plays a minor role in the metabolism of montelukast, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Morphine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Morphine is mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Dasatinib does not inhibit or induce UGTs.
Description:
(See Summary)
Potential Interaction
Dasatinib
Moxifloxacin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Moxifloxacin is predominantly glucuronidated by UGT1A1. Dasatinib does not interfere with this elimination pathway. Furthermore, in healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Mycophenolate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Mycophenolate is mainly glucuronidated by UGT1A9 and UGT2B7. Dasatinib does not interact with this metabolic pathway. In addition, inhibition of OAT1/OAT3 renal transporters by mycophenolic acid (active metabolite) is unlikely to interfere with dasatinib elimination. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Nadroparin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Nadroparin is renally excreted by a nonsaturable mechanism. Dasatinib does not interact with this elimination pathway. However, coadministration may increase the risk of bleeding due to the thrombocytopenic effect of dasatinib. As the clinical relevance of this interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Nandrolone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nandrolone is metabolised in the liver by alpha-reductase. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Naproxen
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Naproxen is mainly glucuronidated by UGT2B7 (major) and demethylated to desmethylnaproxen by CYP2C9 (major) and CYP1A2. Dasatinib does not inhibit or induce these CYPs or UGTs.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Nateglinide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nateglinide is mainly metabolised by CYP2C9 (70%) and to a lesser extent by CYP3A4 (30%). Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Nebivolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nebivolol metabolism involves CYP2D6. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
Potential Interaction
Dasatinib
Nefazodone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Nefazodone is metabolised mainly by CYP3A4 and is also an inhibitor of CYP3A4. Nefazodone may increase dasatinib concentrations due to inhibition of CYP3A4. Concurrent use of CYP3A4 inhibitors should be avoided. If coadministration is necessary, close monitoring for toxicity and dose reduction of dasatinib should be considered. Consider monitoring of dasatinib plasma concentrations if available. Dasatinib is a weak inhibitor of CYP3A4 and may increase nefazodone concentrations, but the clinical relevance of this interaction is unknown.
Description:
(See Summary)
Potential Interaction
Dasatinib
Nicardipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Nicardipine is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 2D6 and 2C8. Dasatinib is a weak inhibitor of CYP3A4 and may increase nicardipine concentrations. The clinical relevance of this interaction is unknown. Nicardipine inhibits CYP3A4 and could potentially increase dasatinib concentrations. No a priori dosage adjustment is recommended for dasatinib. Close monitoring of dasatinib tolerability and blood pressure is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Nicotinamide (Niacinamide)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nicotinamide is converted to N-methylnicotinamide by nicotinamide methyltransferase which in turn is metabolised by xanthine oxidase and aldehyde oxidase. Dasatinib does not interact with this metabolic pathway. In addition, nicotinic acid and its metabolites do not inhibit CYP-mediated reactions in vitro and therefore are unlikely to impact dasatinib exposure.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Nifedipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Nifedipine is metabolised mainly by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase nifedipine concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Nimesulide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nimesulide is extensively metabolised in the liver following multiple pathways including CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Nisoldipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Nisoldipine is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase nisoldipine concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Nitrendipine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Nitrendipine is extensively metabolised mainly by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase nitrendipine concentrations. As the clinical relevance of this interaction is unknown, monitoring of blood pressure may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Nitrofurantoin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nitrofurantoin is partly metabolised in the liver via glucuronidation and N-acetylation and partly eliminated in urine as unchanged drug (30-40%). Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Norelgestromin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norelgestromin is metabolised to norgestrel (possibly by CYP3A4). Dasatinib is a weak inhibitor of CYP3A4 and may increase norelgestromin concentrations. Since norelgestromin does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Norethisterone (Norethindrone)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norethisterone is extensively biotransformed, first by reduction and then by sulfate and glucuronide conjugation. Dasatinib does not interact with these metabolic pathways.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Norgestimate
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norgestimate is rapidly deacetylated to the active metabolite which is further metabolised via CYP450. Dasatinib is a weak inhibitor of CYP3A4 but since norgestimate does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Norgestrel
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norgestrel is a racemic mixture with levonorgestrel being biologically active. Levonorgestrel is mainly metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase norgestrel concentrations. Since levonorgestrel does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Nortriptyline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Nortriptyline is metabolised mainly by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Nystatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Systemic absorption of nystatin from oral or topical dosage forms is not significant, therefore no interactions are expected.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ofloxacin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ofloxacin is renally eliminated unchanged by glomerular filtration and active tubular secretion via both cationic and anionic transport systems. Dasatinib is unlikely to interfere with this pathway. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Olanzapine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Olanzapine is metabolised mainly by CYP1A2, but also by glucuronidation (UGT1A4). Dasatinib does not inhibit or induce CYP1A2 and UGT1A4.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Olmesartan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Olmesartan medoxomil is de-esterified to the active metabolite olmesartan which is eliminated in the faeces and urine.
Description:
(See Summary)
Potential Interaction
Dasatinib
Omeprazole
Quality of Evidence: Low
Summary:
Coadministration is not recommended. Omeprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYP3A4. Omeprazole induces CYP1A2 and inhibits CYP2C19 whereas dasatinib is a weak inhibitor of CYP3A4 and may increase omeprazole concentrations. Due to the wide therapeutic index of omeprazole, a clinically relevant interaction is unlikely. However, in healthy volunteers (n=14), dasatinib (100 mg) coadministration with omeprazole (40 mg for 4 days) reduced the AUC and Cmax of dasatinib by 43% and 42%, respectively. Dasatinib exposure may decrease due to gastric pH elevation by omeprazole. Consider the use of antacids in place of H2 antagonists or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ondansetron
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Ondansetron is metabolised mainly by CYP1A2 and CYP3A4 and to a lesser extent by CYP2D6. Ondansetron is a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase ondansetron concentrations. The clinical relevance of this interaction is unknown. Furthermore, ondansetron may prolong the QT interval dose dependently. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Oxazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxazepam is mainly glucuronidated. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Oxcarbazepine
Quality of Evidence: Very Low
Summary:
Coadministration should be avoided as significant decreases in dasatinib plasma exposure may occur due to induction of CYP3A4. Decreased dasatinib exposure can lead to decreased efficacy. Selection of an alternative concomitant medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is clinically necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Oxprenolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxprenolol is largely metabolised via glucuronidation and dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Oxycodone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Oxycodone is metabolised principally to noroxycodone via CYP3A and oxymorphone via CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase oxycodone concentrations. As the clinical relevance of this interaction is unknown, monitoring for toxicity may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Paliperidone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Paliperidone is primarily eliminated renally (possibly via OCT) with minimal metabolism occurring via CYP2D6 and CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since this is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Palonosetron
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Palonosetron is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP1A2. Palonosetron is a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase palonosetron concentrations. Due to the wide therapeutic index of palonosetron, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pamidronic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as pamidronic acid is not metabolised and is cleared as unchanged drug via urine.
Description:
(See Summary)
Potential Interaction
Dasatinib
Pantoprazole
Quality of Evidence: Very Low
Summary:
Coadministration is not recommended. Pantoprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYPs 3A4, 2D6 and 2C9. Dasatinib is a weak inhibitor of CYP3A4 and may increase pantoprazole concentrations. Due to the wide therapeutic index of pantoprazole, a clinically relevant interaction is unlikely. However, when coadministered with omeprazole, the AUC and Cmax of dasatinib was decreased by 43% and 42%, respectively. Therefore, dasatinib exposure may decrease due to gastric pH elevation by pantoprazole. Consider the use of antacids in place of H2 antagonists or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Para-aminosalicylic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Para-aminosalicylic acid and its acetylated metabolite are mainly excreted in urine by glomerular filtration and tubular secretion. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Paracetamol (Acetaminophen)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Paracetamol is mainly metabolised by glucuronidation (via UGTs 1A9 (major), 1A6, 1A1 and 2B15), sulfation, and to a lesser extent, by oxidation (CYPs 2E1 (major), 1A2, 3A4 and 2D6). Dasatinib does not inhibit or induce UGT1A9 and CYP2E1.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Paroxetine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Paroxetine is mainly metabolised by CYP2D6 and CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase paroxetine concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Peginterferon alfa-2a
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. However, coadministration may increase risk of neutropenia, fatigue, and thrombocytopenia. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Penicillins
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Penicillins are mainly eliminated in urine (20% by glomerular filtration and 80% by tubular secretion via OAT). Dasatinib does not interfere with elimination of penicillins.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Perazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Perazine is demethylated via CYP3A4 and to a lesser extent by CYP2C9, and oxidised via FMO3. Dasatinib is a weak inhibitor of CYP3A4 and may increase perazine concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Periciazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of periciazine has not been well characterised but is likely to involve CYP2D6. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Perindopril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Perindopril is hydrolysed to the active metabolite perindoprilat probably via CYP3A4 and is metabolised to other inactive metabolites. Elimination occurs predominantly via urine. Dasatinib is a weak inhibitor of CYP3A4 and may decrease biotransformation to the active substance. As the clinical relevance of this interaction is unknown, monitoring for blood pressure may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Perphenazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Perphenazine is metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pethidine (Meperidine)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pethidine is metabolised mainly by CYP2B6 and to a lesser extent by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Phenelzine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Phenelzine is primarily metabolised by oxidation via monoamine oxidase and to a lesser extent acetylation. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Phenobarbital (Phenobarbitone)
Quality of Evidence: Very Low
Summary:
Coadministration should be avoided as significant decreases in dasatinib plasma exposure may occur due to induction of CYP3A4. Decreased dasatinib exposure can lead to decreased efficacy. Selection of an alternative concomitant medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is clinically necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
Potential Interaction
Dasatinib
Phenprocoumon
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but should be approached with caution. Phenprocoumon is metabolised by CYP2C9 and CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase phenprocoumon concentrations. Close monitoring of INR/PT is recommended. Note: Dasatinib in combination with phenprocoumon increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Phenytoin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but should be avoided. Phenytoin is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C19. Dasatinib does not inhibit or induce CYP2C9 or CYP2C19. However, phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Concentrations of dasatinib may decrease due to strong induction of CYP3A4. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Phytomenadione (Vitamin K)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. An in vitro study found that the only CYP450 enzyme involved in phytomenadione metabolism was CYP4F2. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Pimozide
Quality of Evidence: Low
Summary:
Coadministration has not been studied and is contraindicated. Pimozide is mainly metabolised by CYP3A4 and to a lesser extent by CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase pimozide concentrations. Dasatinib should be used with caution as pimozide has a narrow therapeutic index. Furthermore, the product labels for pimozide contraindicate its use in the presence of other drugs that prolong the QT interval, such as dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pindolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pindolol is partly metabolised to hydroxymetabolites (possibly via CYP2D6) and partly eliminated unchanged in the urine. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pioglitazone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Pioglitazone is metabolised mainly by CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Dasatinib is a weak inhibitor of CYP3A4. As multiple pathways are involved in pioglitazone metabolism, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Pipotiazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. The metabolism of pipotiazine has not been well described but may involve CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Piroxicam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Piroxicam is primarily metabolised by CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pitavastatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pitavastatin is metabolised by UGTs 1A3 and 2B7 with minimal metabolism by CYPs 2C9 and 2C8. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Posaconazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and is not recommended as dasatinib concentrations may increase due to inhibition of CYP3A4 by posaconazole. Concurrent use of CYP3A4 inhibitors should be avoided. If coadministration is clinically necessary, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Monitoring of dasatinib plasma concentrations should be considered, if available. Additional monitoring for dasatinib toxicity is also recommended. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Potassium
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on limited data available an interaction appears unlikely. Potassium is eliminated renally.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Prasugrel
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Prasugrel is a prodrug and is converted to its active metabolite mainly by CYP3A4 and CYP2B6. Dasatinib is a weak inhibitor of CYP3A4. As the clinical relevance of this interaction is unknown, monitoring may be required. Furthermore, dasatinib in combination with prasugrel increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pravastatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pravastatin is minimally metabolised via CYP enzymes and is a substrate of OATP1B1. Dasatinib does not inhibit or induce OATP1B1.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Prazosin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prazosin is extensively metabolised, primarily by demethylation and conjugation. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Prednisolone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prednisolone undergoes hepatic metabolism via CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase prednisolone concentrations. Since prednisolone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Prednisone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prednisone is converted to the active metabolite prednisolone by 11-B-hydroxydehydrogenase. Prednisolone is then metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase prednisolone concentrations. Since prednisolone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pregabalin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as pregabalin is cleared mainly by glomerular filtration. Dasatinib does not interact with this pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Prochlorperazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Prochlorperazine is metabolised by CYP2D6 and CYP2C19. Dasatinib does not inhibit or induce these CYPs. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Promethazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Promethazine is metabolised by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Propafenone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Propafenone is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2 and CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Propranolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Propranolol is metabolised by 3 routes (aromatic hydroxylation by CYP2D6, N-dealkylation followed by side chain hydroxylation via CYPs 1A2, 2C19, 2D6, and direct glucuronidation). Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Prucalopride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prucalopride is minimally metabolised and mainly eliminated renally, partly by active secretion by renal transporters. No clinically relevant interactions were observed when prucalopride was coadministered with inhibitors of renal P-gp, OAT and OCT transporters.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pyrazinamide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pyrazinamide is mainly metabolised by xanthine oxidase. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Pyridoxine (Vitamin B6)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Quetiapine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Quetiapine is primarily metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase quetiapine concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Quinapril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Quinapril is de-esterified to the active metabolite quinaprilat which is eliminated primarily by renal excretion via OAT3. Dasatinib does not impact this renal transporter.
Description:
(See Summary)
Potential Interaction
Dasatinib
Quinidine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Quinidine is a substrate of CYP3A4 and an inhibitor of CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase quinidine concentrations. The clinical relevance of this interaction is unknown but the combination should be used with caution since quinidine has a narrow therapeutic index. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Rabeprazole
Quality of Evidence: Very Low
Summary:
Coadministration is not recommended. Rabeprazole is mainly metabolised via non-enzymatic reduction and in lesser extent by CYP2C19 and CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase rabeprazole concentrations. Due to the wide therapeutic index of rabeprazole, a clinically relevant interaction is unlikely. However, when coadministered with omeprazole, the AUC and Cmax of dasatinib was decreased by 43% and 42%, respectively. Therefore, dasatinib exposure may decrease due to gastric pH elevation by rabeprazole. Consider the use of antacids in place of H2 antagonists or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Ramipril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Ramipril is hydrolysed to the active metabolite ramiprilat probably via CYP3A4, and is metabolised to the diketopiperazine ester, diketopiperazine acid and the glucuronides of ramipril and ramiprilat. Dasatinib is a weak inhibitor of CYP3A4 and may decrease biotransformation to the active substance. As the clinical relevance of this interaction is unknown, monitoring for blood pressure may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ranitidine
Quality of Evidence: Low
Summary:
Coadministration is not recommended. When coadministered with omeprazole, the AUC and Cmax of dasatinib was decreased by 43% and 42%, respectively. Therefore, dasatinib exposure may decrease due to gastric pH elevation by ranitidine. Consider the use of antacids in place of H2 antagonists or proton pump inhibitors in patients treated with dasatinib. If coadministration is clinically necessary, dasatinib should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of the H2-antagonist or proton pump inhibitor. Monitoring of dasatinib plasma concentrations should be considered if available.
Description:
(See Summary)
Potential Interaction
Dasatinib
Ranolazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Ranolazine is primarily metabolised by CYP3A4 and to a lesser extent by CYP2D6. Ranolazine is also a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase ranolazine concentrations. Furthermore, ranolazine is a weak inhibitor of P-gp, CYP3A4 and CYP2D6. Concentrations of dasatinib may increase due to inhibition of CYP3A4. No a priori dosage adjustment for dasatinib and ranolazine is recommended. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Reboxetine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Reboxetine is metabolised by CYP3A4. Data indicate that reboxetine is a weak inhibitor of CYP3A4 in vitro but there was no inhibitory effect in vivo. Dasatinib is a weak inhibitor of CYP3A4 and may increase reboxetine concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Repaglinide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Repaglinide is metabolised by CYP2C8 and CYP3A4 with clinical data indicating it is a substrate of the hepatic transporter OATP1B1. Dasatinib is a weak inhibitor of CYP3A4 and may increase repaglinide concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Retinol (Vitamin A)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Vitamin A esters are hydrolysed by pancreatic enzymes to retinol, which is then absorbed and re-esterified. Some retinol is stored in the liver. Retinol not stored in the liver undergoes glucuronide conjugation and subsequent oxidation to retinal and retinoic acid. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Riboflavin (Vitamin B2)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Rifabutin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and should be avoided as significant decreases in dasatinib plasma concentrations may occur due to induction of CYP3A4. A decrease in dasatinib exposure can lead to decreased efficacy. Selection of an alternative concomitant medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is clinically necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Rifampicin
Quality of Evidence: Low
Summary:
Coadministration should be avoided as significant decreases in dasatinib plasma concentrations may occur due to induction of CYP3A4. Coadministration of dasatinib and rifampicin (600 mg daily for 8 days) decreased the Cmax and AUC of dasatinib by 81% and 82%, respectively. A decrease in dasatinib exposure can lead to decreased efficacy. Selection of an alternative concomitant medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is clinically necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Rifapentine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and should be avoided as significant decreases in dasatinib plasma concentrations may occur due to induction of CYP3A4. A decrease in dasatinib exposure can lead to decreased efficacy. Selection of an alternative concomitant medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is clinically necessary, a 3-fold dosage increase of dasatinib should be considered in combination with careful monitoring of clinical response. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Rifaximin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rifaximin is mainly excreted in the faeces, almost entirely as unchanged drug. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Risperidone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Risperidone is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Risperidone is a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase risperidone concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Rivaroxaban
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Rivaroxaban is partly metabolised in the liver (by CYP3A4, CYP2J2 and hydrolytic enzymes) and partly eliminated unchanged in urine (by P-gp and BCRP). Dasatinib is a weak inhibitor of CYP3A4 and may increase rivaroxaban concentrations. Furthermore, dasatinib in combination with rivaroxaban increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of these interactions is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Rosiglitazone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosiglitazone is metabolised mainly by CYP2C8 and to a lesser extent CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Rosuvastatin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosuvastatin is largely excreted unchanged in faeces via OATP1B1. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Salbutamol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Salbutamol is metabolised to the inactive salbutamol-4’-O-sulphate. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Salmeterol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Salmeterol is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4. However, the systemic absorption of salmeterol after bronchial administration is low. Therefore, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Saxagliptin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Saxagliptin is mainly metabolised by CYP3A4 and is a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase saxagliptin concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Senna
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Senna glycosides are hydrolysed by colonic bacteria in the intestinal tract and the active anthraquinones liberated into the colon. Excretion occurs in urine, faeces, and also in other secretions. No clinically significant drug interactions are known.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Sertindole
Quality of Evidence: Low
Summary:
Coadministration has not been studied and is contraindicated. Based on metabolism and clearance a pharmacokinetic interaction is unlikely as sertindole is metabolised by CYP2D6 and CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase sertindole concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required. However, the product labels for sertindole contraindicate its use in the presence of other drugs that prolong the QT interval, such as dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Sertraline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sertraline is metabolised mainly by CYP2B6 and to a lesser extent by CYPs 2C9, 2C19, 2D6 and 3A4. Dasatinib is a weak inhibitor of CYP3A4, however since CYP3A4 mediated metabolism is a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Sildenafil (Pulmonary Arterial Hypertension)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Sildenafil is metabolised mainly by CYP3A4 and to a lesser extent by CYP2C9. Dasatinib is a weak inhibitor of CYP3A4 and may increase sildenafil concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Simvastatin
Quality of Evidence: Low
Summary:
Simvastatin is metabolised by CYP3A4 and the metabolite is a substrate of OATP1B1. Dasatinib is a weak inhibitor of CYP3A4. In healthy individuals (n=54), coadministration of dasatinib (single dose 100 mg) and simvastatin increased the AUC and Cmax of dasatinib by 20% and 37%, respectively. It cannot be excluded that the effect is larger after multiple doses of dasatinib. Therefore, it is recommended to replace simvastatin by another statin, i.e. pravastatin or rosuvastatin, when a statin is indicated.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Sirolimus
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Sirolimus is metabolised by CYP3A4 and is a substrate of P-gp. Dasatinib is a weak inhibitor of CYP3A4 and may increase sirolimus concentrations. The clinical relevance of this interaction is unknown. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Sitagliptin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Sitagliptin is primarily eliminated in the urine as unchanged drug (active secretion by OAT3, OATP4C1 and P-gp) and metabolism by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Sodium nitroprusside
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sodium nitroprusside is rapidly metabolised, likely by interaction with sulfhydryl groups in the erythrocytes and tissues. Cyanogen (cyanide radical) is produced which is converted to thiocyanate in the liver by the enzyme thiosulfate sulfurtransferase. There is little potential for sodium nitroprusside to affect the disposition of dasatinib, or to be affected if coadministered with dasatinib.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Sotalol
Quality of Evidence: Low
Summary:
Coadministration has not been studied and is not recommended. Based on metabolism and clearance a pharmacokinetic interaction is unlikely as sotalol is excreted unchanged via renal elimination. However, coadministration is not recommended due to the potential of life threatening arrhythmias such as torsade de pointes and sudden death. The product labels for sotalol advises extreme caution if given with other drugs that prolong the QT interval, such as dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Spectinomycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Spectinomycin is predominantly eliminated unchanged in the kidneys via glomerular filtration. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Spironolactone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Spironolactone is partly metabolised by the flavin containing monooxygenases. Dasatinib does not affect this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Stanozolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Stanozolol undergoes hepatic metabolism. Dasatinib is a weak inhibitor of CYP3A4 and may increase stanozolol concentrations. Since stanozolol has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
St John's Wort
Quality of Evidence: Low
Summary:
Coadministration has not been studied and should be avoided. St John’s wort may cause significant and unpredictable decreases in the plasma concentrations of dasatinib due to induction of CYP3A4.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Streptokinase
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. However, dasatinib in combination with streptokinase increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of this pharmacodynamic interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Streptomycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as streptomycin is eliminated by glomerular filtration. Dasatinib does not interact with this elimination pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Sulfadiazine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro studies suggest a role of CYP2C9 in sulfadiazine metabolism. Dasatinib does not interfere with sulfadiazine metabolism.
Description:
(See Summary)
Potential Interaction
Dasatinib
Sulpiride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Sulpiride is mainly excreted in urine and faeces as unchanged drug. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Interaction
Dasatinib
Tacrolimus
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Dasatinib is metabolised mainly by CYP3A4. Tacrolimus inhibits CYP3A4 and OATP1B1 in vitro but produced modest inhibition of CYP3A4 and OATP1B1 in the range of clinical concentrations. Tacrolimus could potentially increase dasatinib concentrations although only to a modest extent. No a priori dosage adjustment of dasatinib is recommended. In addition, dasatinib is a weak inhibitor of CYP3A4 and may slightly increase tacrolimus concentrations. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended. Furthermore, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Tadalafil (Pulmonary Arterial Hypertension)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Tadalafil is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase tadalafil concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Tamsulosin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tamsulosin is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase tamsulosin concentrations. Since tamsulosin has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Tazobactam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tazobactam is excreted as unchanged drug (approximately 80%) and inactive metabolite (approximately 20%) in the urine. Dasatinib does not interact with this elimination pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Telithromycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Telithromycin may increase dasatinib concentrations due to inhibition of CYP3A4. Inhibitors of CYP3A4 should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to inhibit CYP3A4 should be considered. If coadministration is clinically necessary, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Monitoring of dasatinib toxicity and plasma concentration is recommended, if available. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Telmisartan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Telmisartan is mainly glucuronidated by UGT1A3. Dasatinib not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Temazepam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Temazepam is mainly glucuronidated. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Terbinafine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Terbinafine is metabolised by CYPs 1A2, 2C9, 3A4 and to a lesser extent by 2C8 and 2C19. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only one of multiple pathways, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Testosterone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Testosterone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase testosterone concentrations. Since testosterone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Tetracycline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tetracycline is eliminated unchanged primarily by glomerular filtration.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Theophylline
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Theophylline is mainly metabolised by CYP1A2. Dasatinib does not inhibit or induce CYP1A2.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Thiamine (Vitamin B1)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Thioridazine
Quality of Evidence: Low
Summary:
Coadministration has not been studied and is contraindicated. Based on metabolism and clearance a pharmacokinetic interaction is unlikely. Thioridazine is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. However, the product labels for thioridazine contraindicate its use in the presence of other drugs that prolong the QT interval, such as dasatinib.
Description:
(See Summary)
Potential Interaction
Dasatinib
Tiapride
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely as tiapride is excreted largely unchanged in urine. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Ticagrelor
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Ticagrelor undergoes extensive CYP3A4 metabolism and is a mild inhibitor of CYP3A4. Dasatinib concentrations may be slightly increased if co-administered with ticagrelor. Dasatinib is also a weak inhibitor of CYP3A4 and may increase ticagrelor concentrations. Coadministration of dasatinib and ticagrelor increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of these interactions is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Timolol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Timolol is predominantly metabolised in the liver by CYP2D6. Dasatinib does not inhibit or induce CYP2D6. Furthermore, the systemic absorption of timolol after ocular administration is low.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Tinzaparin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Tinzaparin is renally excreted as unchanged or almost unchanged drug. Dasatinib does not interact with this elimination pathway. However, coadministration may increase the risk of bleeding due to the thrombocytopenic effect of dasatinib. As the clinical relevance of this interaction is unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Tolbutamide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tolbutamide is mainly metabolised by CYP2C9 and to a lesser extent by CYPs 2C8 and 2C19. Dasatinib does not inhibit or induce these CYPs.
Description:
(See Summary)
Potential Interaction
Dasatinib
Tolterodine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Tolterodine is primarily metabolised by CYP2D6 with CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase tolterodine concentrations. The clinical relevance of this interaction is unknown. However, multiple oral therapeutic (4 mg) and supratherapeutic (8 mg) doses of tolterodine have been shown to prolong the QTc interval. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Torasemide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Torasemide is metabolised mainly by CYP2C9. Dasatinib does not inhibit or induce CYP2C9.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Tramadol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Tramadol is metabolised by CYPs 3A4, 2B6, and 2D6. Dasatinib is a weak inhibitor of CYP3A4, but since CYP3A4 mediated metabolism is only one of multiple pathways, a clinically relevant interaction is unlikely. However, monitoring for toxicity may be required
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Trandolapril
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Trandolapril is hydrolysed to trandolaprilat probably via CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may decrease biotransformation to the active substance. As the clinical relevance of this interaction is unknown, monitoring for blood pressure may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Tranexamic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as tranexamic acid is mainly cleared by glomerular filtration.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Tranylcypromine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tranylcypromine is hydroxylated and acetylated. Dasatinib does not interact with this metabolic pathway.
Description:
(See Summary)
Potential Interaction
Dasatinib
Trazodone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Trazodone is primarily metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase trazodone concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Triamcinolone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Triamcinolone is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase triamcinolone concentrations. Since triamcinolone has a wide therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Triazolam
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Triazolam is metabolised by CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase triazolam concentrations. Since triazolam does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Trimethoprim/Sulfamethoxazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Trimethoprim is primarily eliminated by the kidneys through glomerular filtration and tubular secretion. In vitro data suggest that trimethoprim inhibits the renal transporters OCT2 and MATE1. No pharmacokinetic interaction is expected with dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Trimipramine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Trimipramine is metabolised mainly by CYP2D6. Dasatinib does not inhibit or induce CYP2D6.
Description:
(See Summary)
Potential Interaction
Dasatinib
Tropisetron
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Tropisetron is metabolised mainly by CYP2D6 and is a substrate of P-gp. Dasatinib does not inhibit or induce CYP2D6. However, tropisetron may prolong the QT interval. In healthy volunteers dasatinib did not show relevant QT prolongation. Grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Ulipristal
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ulipristal is mainly metabolised by CYP3A4 and to a lesser extent CYP1A2 and CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase ulipristal concentrations. Since ulipristal does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Valproic acid (Valproate)
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Valproic acid is primarily metabolised by glucuronidation (50%) and mitochondrial beta-oxidation (30-40%). To a lesser extent (10%) valproic acid is metabolised by CYP2C9 and CYP2C19. Valproic acid is also an inhibitor of CYP2C9. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Valsartan
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Valsartan is eliminated unchanged mostly through biliary excretion. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Vancomycin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as vancomycin is excreted unchanged via glomerular filtration.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Venlafaxine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Venlafaxine is mainly metabolised by CYP2D6 and to a lesser extent by CYPs 3A4, 2C19 and 2C9. Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. Monitoring may be required.
Description:
(See Summary)
Potential Interaction
Dasatinib
Verapamil
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Verapamil is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 1A2, 2C8, 2C9 and 2C18. Dasatinib is a weak inhibitor of CYP3A4 and may increase verapamil concentrations. The clinical relevance of this interaction is unknown. Verapamil is a moderate inhibitor of CYP3A4 and therefore could potentially increase dasatinib exposure. Concurrent use of CYP3A4 inhibitors should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to inhibit CYP3A4 should be considered. If coadministration is unavoidable, monitor closely for dasatinib toxicity and dose reduction should be considered. Consider monitoring of dasatinib plasma concentrations, if available.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Vildagliptin
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically relevant interaction is unlikely. Vildagliptin is inactivated via non CYP mediated hydrolysis. Additionally, vildagliptin is a substrate of P-gp. Dasatinib does not interact with this pathway.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Vitamin E
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.
Description:
(See Summary)
Potential Interaction
Dasatinib
Voriconazole
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied and is not recommended as dasatinib concentrations may increase due to inhibition of CYP3A4 by voriconazole. Concurrent use of CYP3A4 inhibitors should be avoided. If coadministration is clinically necessary, a dose decrease should be considered. A dose decrease to 20 mg daily is recommended in patients who received a daily dose of 100 mg. A dose decrease to 40 mg daily is recommended in patients who received a daily dose of 140 mg. Monitoring of dasatinib plasma concentrations should be considered, if available. Additional monitoring for dasatinib toxicity is also recommended. In healthy volunteers dasatinib did not show relevant QT prolongation. However, grade 3 QT interval prolongation was reported in 1% of patients treated with dasatinib. Therefore, dasatinib should be administered with caution to patients who have or may develop prolongation of QTc. Hypokalaemia or hypomagnesaemia should be corrected prior to dasatinib administration. If coadministration is necessary, close monitoring including ECG assessment is recommended.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Warfarin
Quality of Evidence: Moderate
Summary:
Coadministration has not been studied. Warfarin is a mixture of enantiomers which are metabolised by different cytochromes. R-warfarin is primarily metabolised by CYP1A2 and CYP3A4. S-warfarin (more potent) is metabolised by CYP2C9. Dasatinib is a weak inhibitor of CYP3A4 but the clinical relevance of this interaction is unknown. Furthermore, dasatinib in combination with warfarin increases the risk of bleeding due to the thrombocytopenic effect of dasatinib. Dasatinib use was also associated with decreased platelet aggregation in 70% of patients with CML. As the clinical relevance of these interactions are unknown, monitoring for bleeding may be required.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Xipamide
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Approximately 90% of xipamide is excreted in the urine, mainly as unchanged drug (~50%) and glucuronides (30%).
Description:
(See Summary)
No Interaction Expected
Dasatinib
Zaleplon
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zaleplon is mainly metabolised by aldehyde oxidase and to a lesser extent CYP3A4. Dasatinib is a weak inhibitor of CYP3A4 and may increase zaleplon concentrations. Since zaleplon does not have a narrow therapeutic index, a clinically relevant interaction is unknown.
Description:
(See Summary)
Do Not Coadminister
Dasatinib
Ziprasidone
Quality of Evidence: Low
Summary:
Coadministration has not been studied and is contraindicated. Based on metabolism and clearance a pharmacokinetic interaction is unlikely. Approximately two thirds of ziprasidone metabolic clearance is by reduction, with less than one third by CYP enzymes (mainly CYP3A4). Dasatinib is a weak inhibitor of CYP3A4 but since CYP3A4 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. However, the product labels for ziprasidone contraindicate its use in the presence of other drugs that prolong the QT interval, such as dasatinib.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Zoledronic acid
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as zoledronic acid is not metabolised and is cleared as unchanged drug via urine.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Zolpidem
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zolpidem is metabolised mainly by CYP3A4 and to a lesser extent by CYP2C9 and CYP1A2. Dasatinib is a weak inhibitor of CYP3A4 and may increase zolpidem concentrations. Since zolpidem does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
No Interaction Expected
Dasatinib
Zopiclone
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zopiclone is metabolised mainly by CYP3A4 and to a lesser extent by CYP2C8. Dasatinib is a weak inhibitor of CYP3A4 and may increase zopiclone concentrations. Since zopiclone does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Zotepine
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Zotepine is mainly metabolised by CYP3A4 and to a lesser extent CYP1A2 and CYP2D6. Dasatinib is a weak inhibitor of CYP3A4 and may increase Zotepine concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
Potential Weak Interaction
Dasatinib
Zuclopenthixol
Quality of Evidence: Very Low
Summary:
Coadministration has not been studied. Zuclopenthixol is metabolised by sulphoxidation, N-dealkylation (via CYP2D6 and CYP3A4) and glucuronidation. Dasatinib is a weak inhibitor of CYP3A4 and may increase zuclopenthixol concentrations. As the clinical relevance of this interaction is unknown, monitoring may be required.
Description:
(See Summary)
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