Aticaprant, also known as CERC-501, binds to the human kappa opioid receptor with high affinity, having a Ki value of 0.807 nM. Its affinity is 30 times greater for the human mu opioid receptor and 190 times greater for the human delta opioid receptor. Aticaprant shows no significant affinity for several non-opioid cell surface G-protein coupled receptor targets, including monoaminergic, muscarinic, cholinergic, and adrenergic receptors, or ion channel/transport protein binding targets or the central benzodiazepine binding site[1].
Aticaprant 动物研究
Animal study
Aticaprant is rapidly absorbed (tmax=1-2 h) with good oral bioavailability (F=25%). Orally administered Aticaprant selectively and effectively occupies central kappa opioid receptors (ED50=0.33 mg/kg). It effectively blocks kappa agonist-mediated analgesia and disruption of pre-pulse inhibition, without affecting mu agonist-mediated effects at doses >30-fold. Aticaprant demonstrates antidepressant-like effects in the forced swim test in mice and enhances the effects of imipramine and citalopram. Aticarant reduces ethanol self-administration in alcohol-preferring rats[1]. Aticaprant can alleviate nicotine withdrawal syndrome and anxiety-related behaviors induced by nicotine cessation[2].
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