Sildenafil

Potent selective PDE5 inhibitor with a shorter duration of action than tadalafil. Enhances nitric oxide-mediated vasodilation by preventing cGMP breakdown. Originally developed for angina, repurposed for erectile dysfunction. Also FDA-approved for pulmonary arterial hypertension at higher doses.

Half-life

4 hours

Bioavailability

41% (oral, reduced by high-fat meals)

Route

oral

Evidence tier

T1 — Multiple RCTs

Optimization pillars

recovery

References

2 peer-reviewed

Dose ranges

Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.

conservative

20–25 mg PRN

Low-dose vascular support or PAH

moderate

25–50 mg PRN

Standard erectile function

aggressive

50–100 mg PRN

Max single dose

Monitoring

lipid-panel
hs-crp

Contraindications

nitrate-therapy
severe-hepatic-impairment
hypotension
recent-stroke-or-mi
retinitis-pigmentosa

References

PMID:9691472Sildenafil: an orally active type 5 cyclic GMP-specific phosphodiesterase inhibitor for the treatment of penile erectile dysfunction — Int J Impot Res, 1996
PMID:16360569Sildenafil citrate therapy for pulmonary arterial hypertension — N Engl J Med, 2005

Notes

Sildenafil is the molecule that launched a billion-dollar category and changed how medicine thinks about repurposing. Developed for angina. Failed that indication. Accidentally discovered its most famous effect in Phase I trials. The 4-hour half-life makes it an event-driven compound, not a daily-driver like tadalafil. For systemic vascular optimization, the pharmacokinetics favor tadalafil. For acute application with rapid clearance, sildenafil is the tool. Know which problem you are solving before you choose your PDE5 inhibitor.

This is not medical advice

Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.

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