Common side effects are diarrhea and abdominal pain.

Clopidogrel or its metabolites are not inducers or mechanism-based inhibitors of the quantitatively major CYP isoenzymes in the liver (i.e. CYP 3A4/5, CYP 2C9 and CYP 1A2). Clopidogrel is a mechanism-based inhibitor of CYP 2B6 and a metabolite of clopidogrel is a mechanism-based inhibitor of CYP 2C8.The amount of CYP 2C8 and 2B6 in the liver is relatively low and the de novo synthesis of these enzymes secondary to the mechanism-based inhibition is therefore limited and will not lead to a significant upregulation in the heme biosynthesis via ALAS-1.

Alpha amino acid ester

Clopidogrel is a platelet aggregation inhibitor indicated for the prevention of atherothrombotic events (myocardial infarction, stroke and vascular death) in patients with atherosclerosis documented by recent stroke, recent myocardial infarction, or established peripheral arterial disease. Clopidogrel has a half-life of 6 hours.

Clopidogrel is a prodrug and the active metabolite is formed primarily by CYP2C19 with contributions from several other CYP enzymes, including CYP1A2, CYP2B6, CYP2C9 and CYP3A4 (Jiang 2015). Clopidogrel is first metabolised to a 2-oxo-clopidogrel intermediate metabolite. Subsequent metabolism of the 2-oxo-clopidogrel intermediate metabolite results in formation of the active metabolite, a thiol derivative of clopidogrel (SPC). Clopidogrel is found to be a mechanism-based inhibitor of CYP 2B6 (strong) and of CYP 2C19 (weak) (Richter 2004). The inhibition of CYP 2B6 have shown to cause clinically relevant drug-drug interactions with CYP 2B6 substrates (Turpeinen 2005). The glucuronide metabolite clopidogrel acyl-β-D-glucuronide is a mechanism-based inhibitor of CYP 2C8 (Tornio 2014). CYP2C8 accounts for 5% ( Pelkonen 2008) or 7% (Aquilante 2013) of the total CYP content in the liver, while the content of CYP 2B6 is reported to vary from 2% to 10% (Wang 2008) and below 5% (Pelkonen 2008).

Uneventful use reported in 9 patients with acute porphyria.