Small molecule
PubChem CID 110635
Tadalafil
Cialis
- Mechanism of action
- Phosphodiesterase-5 (PDE5) inhibitor
- In plain language
- Relaxes smooth muscle in specific tissues by blocking the enzyme that normally shuts off a blood-vessel-relaxing signal, boosting blood flow to the penis during arousal and easing pressure from an enlarged prostate.
- How it works
- Tadalafil (Cialis) is a selective inhibitor of phosphodiesterase type 5 (PDE5). Per the FDA label, penile erection during sexual stimulation results from nitric oxide release from nerve terminals and endothelial cells, which stimulates cGMP synthesis in smooth muscle, causing relaxation and increased blood flow into the corpus cavernosum; tadalafil's inhibition of PDE5 slows the breakdown of this cGMP, enhancing the effect. Because sexual stimulation is required to trigger local nitric oxide release, PDE5 inhibition by tadalafil has no effect in its absence. The same PDE5-mediated effect on cGMP is also observed in the smooth muscle of the prostate, bladder, and their vascular supply, which underlies its use in benign prostatic hyperplasia, though the label notes the exact mechanism for reducing BPH symptoms has not been established.
- Therapeutic applications
- Tadalafil is FDA-indicated, as Cialis, for the treatment of erectile dysfunction (ED), the signs and symptoms of benign prostatic hyperplasia (BPH), and the combination of ED and BPH. When used with finasteride to initiate BPH treatment, use is recommended for up to 26 weeks, as the incremental benefit of tadalafil beyond that point is unknown. A separate tadalafil product, Adcirca, is indicated to improve exercise ability in pulmonary arterial hypertension.
- Class
- Small molecule
- Therapeutic area
- Vascular
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