Active Pharmaceutical Ingredients

Chemical structure:

IUPAC name:

(+)-(S)-methyl 2-(2-chlorophenyl)-2-(6,7-dihydrothieno[3,2-c]pyridin-5(4H)-yl)acetate

CAS number:

113665-84-2

Therapy area:

Anti-coagulant

References:

IP/USP/Ph.Eur

Status:

Commercial sale

Mechanism of action

Clopidogrel is activated by the enzymes CYP2C19, CYP1A2, and CYP2B6 in two phases, followed by CYP2C19, CYP2C9, CYP2B6, and CYP3A. The P2Y12 subtype of the ADP receptor, which is crucial for the activation of platelets and eventual cross-linking by the protein fibrin, is thus selectively and irreversibly inhibited by the active metabolite. When a quick effect is required, a loading dosage of either 600 or 300 mg of oral clopidogrel is delivered since platelet inhibition can be seen two hours after a single dose, but the drug's
beginning of action is sluggish.

Chemical structure:

IUPAC name:

5-Chloro-6′-methyl-3-[4-(methylsulfonyl)phenyl]-2,3′-bipyridine

CAS number:

202409-33-4

Therapy area:

NSAID

References:

IH/IP

Status:

Commercial sale

Mechanism of action

Etoricoxib, like every other “coxib,” preferentially inhibits isoform 2 of the cyclooxygenase enzyme (COX-2). It selects COX-2 inhibition over COX-1 by a factor of around 106. As a result, less prostaglandins (PGs) are produced from arachidonic acid. Among the several roles played by PGs, their contribution to the chain of events leading to inflammation should be emphasised. Comparing selective COX-2 inhibitors to conventional non-steroidal anti-inflammatory medications, the latter exhibit decreased COX-1 activity (NSAID). Many sizable clinical trials with various coxibs have shown that this decreased activity is the reason for the decreased gastrointestinal adverse effects.