Alvameline (Lu25-109) is a partial M1 agonist and an M2/M3 antagonist.

Alvameline undergoes metabolism in human liver microsomes, predominantly transforming into Lu 31-126 via CYP2D6. It also metabolizes into Lu 29-297 and Lu 25-077 primarily through CYP1A2, CYP2A6, CYP2C19, and CYP3A4, and into Lu 32-181 via CYP1A2 and possibly CYP2C19. Notably, the metabolite Lu 32-181 can be converted back into alvameline, a process unaffected by the presence of cytochrome P-450 inhibitors[1].

Alvameline has demonstrated efficacy in enhancing cognitive functions in rats after traumatic brain injury and exhibits concentration-dependent antagonism of carbachol-induced contractions in human and pig detrusor muscles, with pKb values of 6.2 in humans and 5.8 in pigs. Specifically, it competitively inhibits carbachol and electrically induced contractions in human detrusor muscle, while also causing significant decreases in the medial septal nucleus, vertical limb nucleus of the diagonal band, and nucleus basalis magnocellularis in treated rats by up to 13%, 48%, and 51%, respectively. Additionally, alvameline nearly completely blocks electrically stimulated contractions in human detrusor at 100 μM concentration but is less effective in pig detrusor, achieving a maximum inhibition of 32% at the same concentration.