Nuvenzepine is an antagonist of mAChR. It has the potential for gastrospasm treatment.

Nuvenzepine demonstrates nearly equal potency to pirenzepine in competitively inhibiting bethanechol-induced gallbladder contractions and exhibits a four-fold greater potency in preventing vagal-stimulated tracheal constrictions. Additionally, it has a four-fold higher affinity than pirenzepine in competitively antagonizing acetylcholine-induced contractions in both isolated ileal musculature and longitudinal ileum dispersed cells [1].

Nuvenzepine, distinct from pirenzepine, actively moderates colonic motility and, when administered intraduodenally in anaesthetized cats, exhibits a prolonged, dose-dependent suppression of neostigmine-induced intestinal movement. This compound significantly reduces gastric acid secretion and intestinal hypermotility in rats while manifesting minimal atropine-like side effects. It is characterized by slow oral absorption, with an absolute bioavailability of 30 to 40%, slow elimination, negligible accumulation in the body, and minimal metabolism. Notably, Nuvenzepine's efficacy in inhibiting ileal motor activity is tenfold that of pirenzepine and demonstrates a 25-30 times higher potency in suppressing pentagastrin-stimulated gastric acid secretion in conscious cats, indicating its significant therapeutic potential.