Tadalafil (IC-351) is a carboline-based compound with vasodilatory activity. Tadalafil selectively inhibits the cyclic guanosine monophosphate (cGMP)-specific type 5 phosphodiesterase- (PDE-5)-mediated degradation of cGMP, which is found in the smooth muscle of the corpus cavernosa and corpus spongiosum of the penis. Inhibition of cGMP degradation by tadalafil results in prolonged muscle relaxation, vasodilation, and blood engorgement of the corpus cavernosa, and, so, prolonged penile erection.

Tadalafil (at doses of 2 or 10 mg/kg) significantly promotes neural function recovery and increases both cerebral vascular density and the percentage of BrdU-positive endothelial cells. In rats undergoing sham surgery, Tadalafil (at a dose of 2 mg/kg) almost completely restored penile tissue oxygenation and countered the increase induced by nerve transection, while substantially enhancing the muscle/fiber ratio in certain penile tissue sections. When administered to the rat brain, Tadalafil selectively elevated cGMP levels rather than cyclic adenosine monophosphate. Furthermore, Tadalafil reduced the number of apoptotic cells in rats and increased the phosphorylation of kinase Akt and extracellular signal-regulated kinases 1/2 (two survival-related kinases).

When acting on human hepatocytes, Tadalafil (1 mM) notably increases the expression of CYP3A proteins. Tadalafil can bind to type 5 phosphodiesterase (PDE5) with a dissociation constant (KD) of 2.4 nM, and this binding is stimulated by cyclic guanosine monophosphate (cGMP).