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

Alvameline is metabolized by human liver microsomes to Lu 31-126 mainly by CYP2D6. To Lu 29-297 and Lu 25-077 mainly by CYP1A2, CYP2A6, CYP2C19, and CYP3A4. To Lu 32-181 by CYP1A2 and possibly by CYP2C19. One metabolite, Lu 32-181, could be reduced back to alvameline, a reaction not inhibited by the applied cytochrome P-450 inhibitors[1].

Alvameline has been shown to improve cognitive function following traumatic brain injury in rats. Alvameline produces a concentration-dependent rightward shift of the concentration-response curves for carbachol in both human and pig detrusor, the pKb values being 6.2 and 5.8. Alvameline competitively and effectively antagonizes carbachol-induced contractions and contractions induced by electrical field stimulation in human detrusor muscle. Alvameline treated rats causes a 13% and 5% decrease in the medial septal nucleus, a 48 and 23% decrease in the vertical limb nucleus of the diagonal band, and a 51 and 28% decrease in the nucleus basalis magnocellularis, respectively[3]. Contractions induced by electrical field stimulation in human detrusor are almost completely inhibited by 100 μM alvameline. In contrast, electrical field stimulation-induced contractions in pig detrusor are less sensitive to alvameline, resulting in a final inhibition of 32% with the highest concentration used (100 μM)[2].