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Prescription medication — not a dietary supplement
Avanafil (Stendra)is a prescription (or investigational) drug, not a supplement. It is included here for reference because people research and discuss it (often used off-label) — not as a recommendation. Take it only under a qualified clinician's supervision and only as prescribed; do not source it from grey-market vendors, where identity, purity, and dosing are unverified. The evidence below reflects its clinical trials.
What the evidence says
Most Avanafil (Stendra) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality meta-analyses and randomised trials published 2012–2017.
Based on 6 studies · 1 meta-analysis · 2 RCTs
Confidence
ModerateBy outcome
Avanafil (Stendra) has an evidence score of 3.6/10 — moderate evidence based on 6 indexed studies, including 2 meta-analyses. The newest oral PDE5 inhibitor (Stendra; Spedra in the EU) for erectile dysfunction, FDA-approved in 2012. Same class and mechanism as sildenafil and tadalafil (PDE5 inhibition → ↑cGMP → nitric-oxide vasodilation), but engineered for fast onset (~15-30 minutes) and high PDE5 selectivity, which may mean fewer visual side effects. Robust phase-3 RCT evidence for ED, including diabetic ED and post-prostatectomy. A prescription drug, not a supplement. Representative study: PMID 24589460.
The commonly studied dose of Avanafil (Stendra) is Approved on-demand ED dosing is 50-200 mg taken roughly 15-30 minutes before activity (100 mg typical start; range 50-200 mg). It can be taken with or without food. Any use is clinician-directed; this is not a supplement regimen.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Nicotinamide Riboside
Mostly mechanism / observationalA vitamin B3 precursor that reliably raises cellular NAD+ levels and is well tolerated — but human trials have so far shown mostly null or mixed results on the functional outcomes (muscle, metabolism, blood pressure, cognition) that elevation is meant to drive.
MitoQ
Mostly mechanism / observationalLast reviewed June 2026 · evidence from 6 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Avanafil (PDE5 inhibitor)
The newest oral PDE5 inhibitor (Stendra; Spedra in the EU) for erectile dysfunction, FDA-approved in 2012. Same class and mechanism as sildenafil and tadalafil (PDE5 inhibition → ↑cGMP → nitric-oxide vasodilation), but engineered for fast onset (~15-30 minutes) and high PDE5 selectivity, which may mean fewer visual side effects. Robust phase-3 RCT evidence for ED, including diabetic ED and post-prostatectomy. A prescription drug, not a supplement.
Avanafil has a strong, well-replicated phase-3 RCT and meta-analytic base for erectile dysfunction, including diabetic ED, plus systematic-review support for the PDE5-inhibitor class after radical prostatectomy and a clear pharmacological rationale for its fast onset and high PDE5 selectivity. The score sits in the moderate tier because this is a prescription drug with a single narrow approved indication and a serious nitrate contraindication — it is an informational entry, not a supplement recommendation.
Avanafil is an oral phosphodiesterase-5 (PDE5) inhibitor — the newest of its class, marketed as Stendra in the US and Spedra in Europe and FDA-approved in 2012 for erectile dysfunction.
Like sildenafil and tadalafil it blocks PDE5, raising cyclic GMP and prolonging nitric-oxide-mediated smooth-muscle relaxation and vasodilation in the penile (and broader) vasculature.
What distinguishes avanafil is its pharmacology: it was designed for rapid absorption and fast onset — often working in roughly 15-30 minutes — and for high selectivity for PDE5 over related phosphodiesterases.
In particular it has markedly less cross-reactivity with PDE6 (concentrated in the retina) than sildenafil, which is the rationale for potentially fewer visual disturbances, and reduced PDE1 activity, relevant to flushing and tachycardia. It is short-acting, suiting on-demand use.
The efficacy evidence is strong: the phase-3 REVIVE trial and a parallel REVIVE-Diabetes trial were double-blind, placebo-controlled randomized studies showing clinically meaningful improvement on the International Index of Erectile Function and on per-attempt success rates across a broad ED population including men with diabetes, and a 52-week open-label extension supported sustained efficacy and tolerability.
A systematic review and meta-analysis confirmed efficacy and a favorable tolerability profile relative to placebo, and systematic-review evidence for the PDE5-inhibitor class supports erectile-function recovery after nerve-sparing radical prostatectomy.
The common adverse effects are the familiar vasodilatory ones — headache, flushing, and nasal congestion — and they are generally mild and dose-related.
The critical safety boundary is identical to the rest of the class: avanafil is absolutely contraindicated with nitrates in any form, because the combination can cause severe, potentially fatal hypotension.
It requires caution with alpha-blockers and other antihypertensives and with strong CYP3A4 inhibitors (which raise its levels), and it carries the rare class risks of priapism, non-arteritic anterior ischemic optic neuropathy (NAION), and sudden hearing loss.
The score reflects strong, well-replicated efficacy for erectile dysfunction set against the fact that this is a prescription drug with a narrow approved indication and a serious nitrate contraindication — an informational entry, not a recommendation.
Avanafil blocks PDE5, raising cyclic GMP and prolonging nitric-oxide-mediated vasodilation — the basis for its erectile effect.
Engineered for rapid absorption (onset ~15-30 min) and high selectivity for PDE5 over PDE6 (retinal) and PDE1, the rationale for fewer visual side effects and a fast time-to-effect.
Enhanced NO/cGMP signaling improves penile blood flow and supports endothelial smooth-muscle relaxation.
How Avanafil (Stendra) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
Approved on-demand ED dosing is 50-200 mg taken roughly 15-30 minutes before activity (100 mg typical start; range 50-200 mg). It can be taken with or without food. Any use is clinician-directed; this is not a supplement regimen.
Can be taken without food
| Form | Type |
|---|---|
| 💊Oral tablet (avanafil) | Recommended |
| 💊Sildenafil (short-acting PDE5 inhibitor) | Alternative |
| 💊Tadalafil (long-acting PDE5 inhibitor) | Alternative |
Avanafil's fast onset and high selectivity suit on-demand use; tadalafil suits steady daily dosing.
Compare Avanafil (Stendra) vs Sildenafil (Viagra) →Minimum: 1 weeks
Optimal: 12 weeks
Cycling: Not required
Note: Short-acting and on-demand — taken ~15-30 minutes before activity; absorption is largely food-independent. Never combine with nitrates.
Dose-response data unavailable. The current published research for Avanafil (Stendra) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
Phase-3 RCT and meta-analytic evidence for clinically meaningful improvement in erectile function versus placebo, including in men with diabetes.
Rapidly absorbed — often effective within ~15-30 minutes, faster than older PDE5 inhibitors; short-acting and suited to on-demand use.
High PDE5 selectivity with low PDE6 (retinal) cross-reactivity is the rationale for fewer visual disturbances than sildenafil.
Common vasodilatory effects — headache, flushing, and nasal congestion; usually mild and dose-related; rare NAION and sudden hearing loss.
Combined with nitrates it causes severe, potentially fatal hypotension; caution with alpha-blockers and strong CYP3A4 inhibitors.
Absolute contraindication — dangerous hypotension.
Avoid until cleared by a clinician.
Use low starting doses and monitor blood pressure.
Discuss the rare risk of optic-nerve injury with a clinician before use.
Combined PDE5 inhibitor + nitrate causes severe, potentially fatal hypotension — an absolute contraindication.
Additive blood-pressure lowering — use caution and lower starting doses.
Tip: Vasodilatory; usually mild and transient.
Tip: Class/dose-related; typically self-limited.
Tip: Seek urgent care; avoid nitrates; an erection lasting >4 hours is a medical emergency.
Timing is flexible for Avanafil (Stendra) — consistent daily use matters more than the time of day. Rapidly absorbed with a fast onset (~15-30 minutes), so it is taken on-demand shortly before activity.
Avanafil (Stendra) is generally safe at recommended doses, with a few precautions worth noting. The most commonly reported side effects are headache / flushing, nasal congestion, priapism / NAION (sudden vision loss) / sudden hearing loss / symptomatic hypotension. Use caution if any of these apply to you: Concurrent nitrates (any form); Recent cardiovascular event / unstable angina; Severe hypotension.
A mitochondria-targeted antioxidant — CoQ10 conjugated to a triphenylphosphonium (TPP+) cation so it accumulates several-hundred-fold inside mitochondria. Sold OTC as a supplement. Its best human signal is improved endothelial/vascular function in older adults (one small RCT); several trials are null (Parkinson's, exercise adaptation), and almost all outcomes are surrogate/biomarker, not hard clinical endpoints.
Raise avanafil levels (e.g. ritonavir, ketoconazole, clarithromycin); dose reduction or avoidance advised.