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

Nuvenzepine is almost equipotent to pirenzepine in competitively preventing bethanechol-induced gall-bladder contractions and it shows a four-fold higher potency than pirenzepine in blocking vagal-stimulated tracheal constrictions. Nuvenzepine displays a four-fold higher affinity than pirenzepine in competitively antagonizing acetylcholine-induced contractions on isolated ileal musculature and on longitudinal ileum dispersed cells [1].

Nuvenzepine is also active, unlike pirenzepine, on colonic stimulated motility. In anaesthetized cats, intraduodenally administration of Nuvenzepine shows a long-lasting and dose-dependent inhibition of neostigmine-induced intestinal motility. Nuvenzepine has been found to be very active in inhibiting gastric acid secretion and intestinal hypermotility in rats, with very slight atropine-like side effects. The oral absorption rate is relatively slow, that the absolute bioavailability is 30 to 40%, that the elimination rate is slow and there is no accumulation in the body, and that there is very little metabolism. Nuvenzepine displays a potency 10 times greater than that of pirenzepine on ileal motor activity. Nuvenzepine inhibits pentagastrin-stimulated gastric acid secretion resulting 25-30 times more potent than pirenzepine in conscious cats [2][3].