Eli Lilly Nederland B.V.

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Tadalafilinhibits phosphodiesterase type 5 (PDE-5) in smooth muscle of pulmonary vasculature where PDE-5 is responsible for the degradation of cyclic guanosine monophosphate (cGMP). Increased cGMP concentration results in pulmonary vasculature relaxation; vasodilation in the pulmonary bed and the systemic circulation (to a lesser degree) may occur. Tadalafil enhances the effect of NO by inhibiting phosphodiesterase type 5 (PDE-5), which is responsible for degradation of cGMP in the corpus cavernosum; when sexual stimulation causes local release of NO, inhibition of PDE-5 by tadalafil causes increased levels of cGMP in the corpus cavernosum, resulting in smooth muscle relaxation and inflow of blood to the corpus cavernosum.Does not directly cause penile erections, but
affects the response to sexual stimulation.

Absolute bioavailability has not been determined; rate and extent of absorption are not influenced by food.

Hepatic, via CYP3A4 to metabolites (inactive).

Time to Peak
Plasma: ~2 hours (range: 30 minutes to 6 hours).

Half-Life Elimination
15 to 17.5 hours; Pulmonary hypertension (not receiving bosentan): 35 hours.

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