Cytochrome P450 : Alphabetical drug list
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1A2 2C9 2C19 2D6 2E1 3A4
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Drug CYP interaction Clinical consequences
toxicity thought to be related to its hydroxylamine metabolite (methaemoglobinaemia, haemolysis, agranulocytosis)
3A4 : substrate (also 2C9) cimetidine may be useful in inhibiting toxic effects! [Gen Pharmacol 1995 Nov;26(7):1461-7]
2E1 : may contribute to metabolism ?
debrisoquine CYP2D6 : metabolism ? (the prototype drug for 2D6 metabolism)
delavirdine (NNRTI) 3A4 : METABOLISM, also inhibits
(metabolism : ? 2D6)
interaction potential
desipramine (See also tricyclics) 2D6 : metabolism
(? with 1A2 [Hayes])
impaired metabolism with 2D6 deficiency
2D6 : ? inhibits ?
dexamethasone CYP3A4 : INDUCES ?
CYP3A4 : metabolism ?
CYP? : increased HETE formation in response to angiotensin-1 receptor stimulation [Biochem Biophys Res Commun 2000 Jun 7; 272(2) : 423-430] ?
dexfenfluramine (appetite suppressant) CYP2D6 : high affinity metabolism poor metabolisers get toxicity (nausea, vomiting)
1A2 : low affinity metabolism ?
dextromethorphan CYP2C9 : metabolism ?
CYP2C19 : metabolism ?
CYP2D6 : metabolism (to DEXTRORPHAN used as a probe for 2D6 activity) ?
CYP3A4 : metabolism ?
dextropropoxyphene CYP2D6 : INHIBITS 'significant interaction with antidepressants' [Acta Psychiatr Scand 1997 Nov;96(5):379-84]
diazepam (See also Benzodiazepines) CYP2C8 : metabolised ?
2C19 : metabolism (N-demethylation) impaired metabolism in Chinese subjects with 2c19 mutations
3A4,3A5 : METABOLISM (3 hydroxylation, N-demethylation) marked prolongation of diazepam half life with grapefruit juice! [ Eur J Drug Metab Pharmacokinet 1998 Jan-Mar;23(1):55-9]; NO clinically significant interaction with itraconazole [Fundam Clin Pharmacol 1996;10(3):314-8]
2B6 : metabolism ?
diclofenac (See also NSAIDs (CYP2C8 > CYP2C19 = CYP2C18 >> CYP2B6 ) [Biochem Pharmacol 1999 Sep 1;58(5):787-96] CYP2C9 : METABOLISM (4-hydroxylation) ? see 3A4 below.
CYP2C9 : inhibition? reduces quinidine N-oxidation by 27% [Br J Clin Pharmacol 1999 Dec;48(6):829-38]
3A4 (5-hydroxylation, product may be hepatotoxic by inhibiting mitochondrial ATP synthesis) low 2C9 + high 3A4 activity could cause hepatotoxicity, with low antioxidant levels
2C8 ? metabolism ?
dihydrocodeine 2D6 : activated to dihydromorphine effects as for codeine although this has been questioned [Br J Clin Pharmacol 1998 Jun;45(6):575-81]
diltiazem (See also Ca channel blockers) CYP3A4 : metabolism ?
3A4 : INHIBITS (IC50 ~ 5 µM ) slowed elimination of eg. midazolam, alfentanil, [Anesthesiology 1996 Dec;85(6):1246-52] and prednisolone (significant); also lovastatin
diphenhydramine (1st generation anti-histamine) 2D6 : inhibits (Ki ~ 11 µM) ?
dirithromycin does NOT inhibit 3A4 [Ann Pharmacother 1997 Mar;31(3):349-56] Nil (in contrast with many other macrolides)
disopyramide 3A4 : METABOLISM toxicity with eg. clarithromycin
disulfiram CYP2E1 : INHIBITS {minimal effect on other isoforms , although rat studies disagree } potential for prevention of xenobiotic toxicity. Enzyme levels return to half normal by day 3, due to 2e1 resynthesis.
{Note: the rare disulfiram hepatotoxicity may be associated with antibodies to CYP! }
docetaxel (see also taxoids) 3A4 : METABOLISM metabolism reduced with 3A4 inhibitors; [Cancer Res 1996 Jan 1;56(1):58-65]
dofetilide 3A4 : metabolism ? potential for interaction
dolasetron (5HT3 antagonist) 3A4 : metabolism ?
2D6 : metabolism {non-significant inhibition of 2D6} ?
donepezil (cholinesterase inhibitor : Alzheimer's) 2D6 and 3A4 : metabolism unclear.
doxorubicin 3A4 : metabolism AND inhibition interactions with eg paclitaxel

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1A2 2C9 2C19 2D6 2E1 3A4

Page author: jo@anaesthetist.com Last update: 2000-6-22