P
|
Drug |
CYP interaction |
Clinical consequences |
paclitaxel
| 2C8 and 3A4 : metabolism (used as a probe for 2C8 activity)
| interaction with eg doxorubicin ?
|
pantoprazole (Proton Pump inhibitor)
| CYP2C19 : substrate (?)
| no significant interaction with
"antipyrine, caffeine, carbamazepine, diazepam, diclofenac,
digoxin, ethanol, glibenclamide, a hormonal contraceptive (combination of levonorgestrel and ethinylestradiol), metoprolol,
nifedipine, phenprocoumon, phenytoin, theophylline and warfarin",
[Int J Clin Pharmacol Ther 1996 Jun;34(6):243-62]
nor with nifedipine
|
paracetamol (= acetaminophen)
| CYP2E1 : METABOLISM
| high activity causes liver toxicity due to formation of
N-acetyl-p-benzoquinone imine (NAPQI). See e.g. [Clin Pharmacol Ther 2000 Mar;67(3):275-82]
|
CYP1A2 (substrate - minor)
| ?
|
paroxetine
| 2C19 : INHIBITS
| ?
|
2D6 : INHIBITS (2 µmol)
| may increase perphenazine, haloperidol, thioridazine and risperidone
levels; clinical interaction with metoprolol reported
|
pefloxacin (See also Quinolones)
| 1A2 : inhibits
| clinically significant [Clin Pharmacol Ther 1999 Mar;65(3):262-74]
eg. theophylline
|
perhexiline (withdrawn d/t nerve toxicity)
| 2D6 : metabolism
| ?
|
perphenazine (Antipsychotic)
| 2D6 : metabolism
| ?
|
2D6 : INHIBITS (IC50 1.5 µM)
| ?
|
pethidine {=meperidine}
| CYP2D6 : metabolism
| ?
|
pentobarbitone (See also Barbiturates)
does NOT induce 2C19
| CYP2E1 : metabolism
| ?
|
phenformin (obsolete drug)
| 2D6
| hypoglycaemia with low 2D6 activity
|
phenobarbitone / phenobarbital
(See also Barbiturates)
| CYP1A2 : INDUCES
| potential for multiple interactions
|
CYP2B6 : INDUCES
|
CYP2C8 : INDUCES
|
CYP2C19 : INDUCES
|
3A4 INDUCES (and 3A5, 3A7)
|
2C9 INDUCES
|
phenytoin
| CYP2C9 : metabolism
| low 2C9 activity causes toxicity ("sulfaphenazole,
phenylbutazone, fluconazole, azapropazone, cotrimoxazole, propoxyphene,
miconazole, amiodarone, disulfiram, metronidazole, and stiripentol");
also CYP2C9*3 genotype
|
CYP2C19 : secondary metabolism
| interactions with "elbamate, omeprazole,
cimetidine, fluoxetine, imipramine, and diazepam" [Epilepsia 1995;36 Suppl 5:S8-13]
|
CYP3A4 : INDUCES
| many potential interactions
|
CYP1A2, 2B6 : INDUCES
| ?
|
pimozide
| CYP3A4 : METABOLISM
| toxicity : fatal arrhythmias with 3A4 inhibition.
|
piroxicam
| CYP2C9 : metabolism
(? and 2C18 )
| ?
|
prednisone
| 2C19 : INDUCES
| ?
|
3A4 : metabolism
| interaction with e.g. diltiazem; fluconazole (Addisonian
crisis reported on stopping fluconazole! [Pediatr Transplant 1999 May;3(2):126-30] );
but 'no interaction with grapefruit juice' [Clin Pharmacol Ther 1995 Mar;57(3):318-24]
|
procainamide
| CYP2D6 : metabolism (to N-hydroxyprocainamide)
| extensive metabolizers get drug induced lupus erythematosus
|
prodipine
| 2D6 : competitive inhibitor
| ?
|
progesterone
| CYP2C19 : metabolism
| ?
|
3A4 : metabolism
|
|
proguanil
| CYP2C19 : low activity
| (? less activation; less effect)
|
promethazine (1st generation antihistamine)
| 2D6 : inhibits (Ki ~ 4-6 µM)
| ?
|
propafenone
| CYP2D6 : metabolism
| low 2D6 activity causes toxicity (congenital, or with e.g.
terbinafine)
|
CYP1A2 : metabolism
| low activity : propafenone metabolites may accumulate!
|
1A2 : inhibits (IC50 20µmol)
| ? clinically significant (disputed, see [Br J Clin Pharmacol 1998 Apr;45(4):361-8] )
|
propofol
| 1A2 : INHIBITS
| potential for 50% inhibition, ? clinical significance
[Xenobiotica 1998 Sep;28(9):845-53]
|
2C9 : INHIBITS
|
2D6 : INHIBITS
|
3A4 : INHIBITS
|
propranolol (Note: ethinyloestradiol +/- norethindrone
has no effect on overall clearance)
| See also: beta-blockers
|
|
CYP1A2 : metabolism
| ?
|
CYP2C19 : metabolism
| ?
|
CYP2E1 : metabolism
| ?
|
2D6 : metabolism
| ?
|
Protease inhibitors (HIV) -
Also see the individual drugs
| CYP3A4 : INHIBIT
| multiple significant interactions with e.g. non-sedating
antihistamines, cisapride, macrolides, ..
|
CYP3A4 : metabolism
| ?
|
1A1 : INDUCE
| ?
|
Proton Pump Inhibitors
(e.g. omeprazole, lansoprazole,
pantoprazole)
| may induce CYP1A2 {??}
| NO interaction with theophylline [Br J Clin Pharmacol 1999 Sep;48(3):438-44 ]
|