Abstract
Flunarizine is a selective calcium entry blocker used for prophylaxis of severe refractory migraine and symptomatic treatment of vestibular vertigo. In human subcellular fractions, aryl hydroxylation was a major metabolic pathway. In primary cell cultures of human hepatocytes, N‐dealkylation at the 1‐ and 4‐piperazine nitrogen yielded 2 and 6, respectively. Glucuronide conjugate of 2 was also observed. CYP2D6 was involved in the arylhydroxylation of the cinnamyl moiety of flunarizine in human liver microsomes, and CYP2C9 together with 1A1, 1A2, and/or 2A6 mediated the N‐desalkylation at the 1‐ and 4‐positions of the piperazine ring of flunarizine.
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