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PDE5 Inhibitors

Sildenafil, tadalafil, vardenafil and avanafil are approved for erectile dysfunction (ED); tadalafil also treats the signs and symptoms of BPH. All four are prescription-only in the US; generic sildenafil, tadalafil and vardenafil are available. Pulmonary-hypertension products and regimens have different indications and dosing and should not be added to an ED prescription.[1][2][3][4]

PDE5 inhibition slows breakdown of cyclic GMP generated through nitric oxide signaling, promoting cavernosal smooth-muscle relaxation. Sexual stimulation is still required.[1][2] PDE5 is also expressed in the prostate, bladder, ureter and vasculature, which is the rationale for the lower urinary tract and other non-erectile uses below.[21]

For alternative treatments see Intracavernosal injection agents and Intraurethral alprostadil. Treatment decisions and cardiovascular assessment are also discussed under Erectile dysfunction.

US doses and practical differences​

The table describes standard adult ED dosing before adjustments for interactions or organ impairment.[1][2][3][4]

AgentUsual starting regimenAdjustment and timingPractical distinction
Sildenafil50 mg as needed25–100 mg; approximately one hour before sex, permissible window 30 minutes to four hours beforehand; no more than once dailyA high-fat meal delays absorption and lowers peak level; the label permits dosing with or without food. Choose lower initial doses in the situations below[1]
Tadalafil, as needed10 mgDecrease to 5 mg or increase to 20 mg; no more than once dailyEffect may persist up to 36 hours; food does not meaningfully alter dosing[2]
Tadalafil, daily ED2.5 mg at roughly the same time each dayIncrease to 5 mg if appropriateDaily BPH or ED/BPH regimen is ordinarily 5 mg, subject to renal and interaction limits[2]
Vardenafil, film-coated tablet10 mgAdjust to 5–20 mg; about 60 minutes before sex; no more than once dailyA high-fat meal lowers peak level; the label permits dosing with or without food. QT precautions; lower doses are needed with selected interactions. Orally disintegrating products have their own label and are not automatically interchangeable[3]
Avanafil100 mg as needed100 or 200 mg as early as about 15 minutes before sex; 50 mg approximately 30 minutes beforehand; no more than once dailyA high-fat meal delays peak absorption (mean time to peak concentration 1.12–1.25 hours later at 200 mg), although the US label permits dosing with or without food; strong CYP3A4 inhibitors preclude use and moderate CYP3A4 inhibitors limit the dose to 50 mg per 24 hours[4]

No drug is universally the most effective or best tolerated. Cross-trial rankings depend on dose, population, endpoint and indirect comparisons. EAU 2026 recommends PDE5 inhibitors as first-line ED therapy and finds no demonstrated difference in efficacy among the four (level of evidence 1a); two meta-analyses it cites favor sildenafil 50 mg for efficacy and tadalafil 10 mg for tolerability when starting.[5] A later dose-specific network meta-analysis of 83 on-demand trials (6,029 men) ranked sildenafil 50–100 mg highest for achieving IIEF-EF >26, but cross-drug comparisons were mostly indirect.[50] Choose according to timing preference, previous response, cost or access and adverse effects, then reassess.[5]

Before calling treatment unsuccessful​

AUA 2018 recommends informing men with ED about oral PDE5 inhibitors as a treatment option, including benefits and risks , giving instructions that maximize benefit and titrating the dose to optimal efficacy .[6]

EAU 2026 likewise advises fully informing patients how the drugs work and how to take them, because incorrect use or inadequate information is the main cause of non-response .[5] Confirm correct drug, dose, timing, sexual stimulation and repeated opportunities to use it. A high-fat meal can delay absorption of sildenafil, vardenafil and avanafil; tadalafil absorption is not meaningfully affected. The avanafil label permits dosing with food despite delayed peak absorption because overall exposure changes little.[4] AUA 2018 notes that incorrect use, chiefly missing sexual stimulation or a large meal, accounts for most reported non-response, and that re-education restores response in a substantial minority. Discuss anxiety, relationship factors, underlying vascular or neurological disease and medication contributors. Titrate within the product's limits; changing agents or daily versus as-needed tadalafil may be reasonable, but a fixed number of maximal-dose attempts with every agent is not an AUA requirement before offering another treatment.[5][6]

AUA 2018 recommends measuring morning total testosterone in men with ED .[6] AUA 2018 advises telling men with ED and confirmed testosterone deficiency that a PDE5 inhibitor may work better combined with testosterone therapy (moderate recommendation, Grade C; five small, mostly low-quality trials with one to 3.5 months of follow-up; pooled IIEF-EF difference 2.69 points versus PDE5 inhibitor alone in the four trials that made that comparison).[6] The AUA 2018 ED guideline discussion states that testosterone is not effective ED monotherapy, whereas EAU 2026 strongly recommends testosterone therapy first line for hypogonadal men with mild ED and weakly recommends combining it with a PDE5 inhibitor for more severe ED.[6][54] See Testosterone replacement.[5][6]

Etiology changes the baseline response rate before non-response is attributed to incorrect use. These studies measured different populations and outcomes. In a 12-week randomized trial of 303 men 12–48 months after bilateral nerve-sparing prostatectomy, a mean 41% of intercourse attempts succeeded among tadalafil recipients.[42] In a nonrandomized cohort of 110 men with ED after prostate radiation, IIEF-defined sildenafil response was 76% after brachytherapy and 68% after external-beam radiation within 12 months, declining to 44% and 38% at 25–36 months, respectively.[43] In a 12-week randomized diabetes trial without an autonomic-neuropathy entry criterion, 71/117 (61%) sildenafil-treated men versus 25/114 (22%) placebo-treated men reported at least one successful intercourse attempt.[44] Upstream injury to the cavernous nerves or autonomic pathway impairs the NO/cGMP mechanism PDE5 inhibitors depend on, which is part of the rationale for a lower threshold to escalate to intracavernosal injection or a vacuum device in these populations rather than repeated dose titration alone.[40][41][42][43][44]

A small non-randomized series reported off-label supratherapeutic dosing (sildenafil up to 200 mg on demand, above the FDA-approved 100 mg maximum) as salvage for prior 100 mg non-responders, with 13 of 54 men (24%) responding. Side effects were reported by 34 of 54 men (63%) at their maximal tested dose (150 or 200 mg), and 4 of the 13 responders (31%) discontinued because of them. This is not a routine escalation step; it requires explicit off-label counseling and documentation.[46]

Safety checks that change prescribing​

Nitrates and guanylate-cyclase stimulators

Do not combine PDE5 inhibitors with organic nitrates or nitrites, including recreational “poppers,” the nitric-oxide donor nicorandil, or guanylate-cyclase stimulators such as riociguat.[5] The interaction can cause severe hypotension. If chest pain occurs after a PDE5 inhibitor, seek emergency care and disclose the agent and last dose; do not self-administer a nitrate.[1][2][3][4]

Timing does not turn this into a routine combination. Princeton IV advises avoiding nitrates for at least 24 hours after sildenafil, vardenafil or avanafil, and 48 hours after tadalafil. The US sildenafil and vardenafil labels do not establish a universally safe nitrate interval. Tadalafil and avanafil labels allow consideration in a life-threatening situation only after at least 48 and 12 hours, respectively, with close medical supervision and hemodynamic monitoring.[1][2][3][4][7] The avanafil label's emergency provision differs from the more conservative Princeton consensus interval.[1][2][3][4][7] Observational data support caution: in a Swedish register of men with stable coronary disease on nitrates (55,777 nitrate users, 5,710 also filling a PDE5 inhibitor), combined use was associated with higher all-cause mortality (HR 1.39, 95% CI 1.28–1.51) and myocardial infarction (HR 1.72, 95% CI 1.55–1.90).[34]

IssuePrescribing implication
Cardiovascular fitnessDefer ED drug treatment when sexual activity is medically inadvisable. Unstable angina, recent cardiovascular events, marked hypotension or uncontrolled hypertension require appropriate assessment; exact excluded populations differ by label
Alpha-blockers and other antihypertensivesAdditive hypotension is possible. For ED combination treatment, establish stability on the alpha-blocker and start the PDE5 inhibitor at its lowest recommended dose; volume depletion increases risk
Vardenafil and QTAvoid with congenital QT prolongation or class IA/III antiarrhythmics; review other QT-prolonging medication
Prior NAIONUS labels call for caution and an individualized benefit–risk assessment. Ophthalmology input may be appropriate
Retinitis pigmentosaSildenafil label advises caution because data are lacking; tadalafil, vardenafil and avanafil labels do not recommend use in inherited degenerative retinal disease.
Sudden visual or hearing lossStop the drug and obtain urgent assessment
Prolonged erectionAn erection persisting four hours requires urgent care, regardless of whether it is painful
Common adverse effectsHeadache, flushing, dyspepsia and congestion; sildenafil can cause transient color-vision changes, and tadalafil can cause back pain/myalgia
AlcoholSubstantial intake can worsen orthostasis and sexual performance

These are selected label precautions, not a substitute for the complete product-specific contraindications and interactions.[1][2][3][4]

Background on the ocular, auditory and skin safety signals. A case-crossover study of PDE5 inhibitor exposure before acute NAION found an approximately twofold increased risk within five half-lives of use (43 definite cases with PDE5 inhibitor exposure in the preceding 30 days, OR 2.15, 95% CI 1.06–4.34)[36]. A population-based cohort study of sudden sensorineural hearing loss similarly found a small increased risk with current PDE5 inhibitor use (adjusted hazard ratio 1.25, 95% CI 1.01–1.55), rising with recent rather than current use; evidence is insufficient to determine whether this represents permanent loss risk, and men reporting hearing change should stop the drug and be evaluated.[36][37][38][39] Retrospective series and a meta-analysis of five observational studies found PDE5 inhibitor use associated with a slightly increased odds of melanoma (OR 1.12, 95% CI 1.03–1.21) and basal cell carcinoma, but risk was elevated with a single filled prescription and not with repeat fills.[36][37][38][39]

Spinal cord injury, autonomic dysfunction and neurologic disease​

PDE5 inhibitors and intracavernosal alprostadil are the effective treatments for erectile dysfunction in neurologic disease.[35] AUA 2018 advises using PDE5 inhibitors with caution, at least initially at lower doses, in men with mild-to-moderate hepatic or renal impairment or spinal cord injury because of possible delayed metabolism, and generally not in severe renal or liver disease.[6] In autonomic dysfunction (for example high spinal cord lesions or multiple system atrophy), start low and check blood pressure, as additive hypotension is the main concern.

Renal, hepatic and interaction adjustments​

AgentSelected high-yield US label limits
SildenafilConsider 25 mg initially with age over 65, hepatic impairment, CrCl below 30 mL/min or strong CYP3A4 inhibition. With ritonavir, maximum 25 mg in 48 hours. With stable alpha-blocker therapy, start 25 mg[1]
Tadalafil, as neededCrCl 30–50: start 5 mg, maximum 10 mg in 48 hours. CrCl below 30 or dialysis: maximum 5 mg in 72 hours. Potent CYP3A4 inhibitor: maximum 10 mg in 72 hours[2]
Tadalafil, dailyNot recommended with CrCl below 30 or dialysis. For BPH/ED-BPH with CrCl 30–50, start 2.5 mg, consider 5 mg according to response. Potent CYP3A4 inhibitor: maximum 2.5 mg daily, which does not provide the standard BPH dose[2]
Tadalafil and liver diseaseAs-needed dosing in Child-Pugh A/B should not exceed 10 mg; daily use requires caution because evidence is limited. Not recommended in Child-Pugh C[2]
Vardenafil tabletsConsider 5 mg initially at age 65 or older. Child-Pugh B: start 5 mg, maximum 10 mg; do not use with Child-Pugh C or dialysis. Ritonavir/cobicistat: maximum 2.5 mg in 72 hours; other inhibitor-specific dose limits also apply[3]
AvanafilDo not use with strong CYP3A4 inhibitors; with moderate inhibitors, maximum 50 mg in 24 hours. Start 50 mg with stable alpha-blocker treatment. Do not use in severe renal disease/dialysis or severe hepatic impairment[4]

Check all concurrent restrictions; a permissible dose under one condition does not override another contraindication.[1][2][3][4]

Ritonavir-boosted protease inhibitors used for HIV (for example darunavir or atazanavir with ritonavir) are the ritonavir/strong-CYP3A4-inhibitor exposure the sildenafil, tadalafil and vardenafil dose caps above are built around. In the vardenafil label's interaction study using ritonavir 600 mg twice daily, vardenafil exposure rose 49-fold and its half-life increased to 26 hours. Select the PDE5 inhibitor using the product-specific interaction limits above.[3]

Routine stacking of PDE5 inhibitors is not supported by US labeling. Specialist off-label combinations described in guidelines require explicit planning and monitoring; patients should not add sildenafil to daily tadalafil on their own.[1][2][5]

Over-the-counter and herbal "ED supplements." Products marketed for erectile performance (DHEA, L-arginine/L-citrulline, yohimbine, avena sativa, tribulus terrestris and various ginsengs) have variable, generally limited efficacy evidence.[5] U.S. dietary supplements do not receive FDA premarket approval for safety or effectiveness.[52] In one selected sample of 91 purported herbal or natural sexual-performance products sold or seized in the United States, 74 contained undeclared sildenafil, tadalafil or PDE5-inhibitor analogues.[45] Heavy metals were identified in a separate study of herbal sex-enhancement products purchased in Port Harcourt, Nigeria.[53] A man taking nitrates who unknowingly consumes an adulterated supplement is exposed to the same hypotension risk as a deliberate combination. In a systematic review of placebo-controlled ED drug trials, 27–35% of placebo recipients reported improved erections; perceived improvement can occur without active treatment.[51]

LUTS/BPH: benefit and combination treatment​

AUA 2026 recommends offering tadalafil 5 mg daily for LUTS/BPH with or without ED .[8] Symptom improvement is modest on average. In the 2018 Cochrane review, the placebo-adjusted IPSS difference was 1.89 points lower (95% CI 1.50–2.27 lower; 4,293 participants; low-certainty evidence, six to 12 weeks). The approximately five- or six-point improvements were within-group changes.[8][9]

The mechanisms proposed for the lower urinary tract are better tissue oxygenation, prostatic and bladder-neck smooth-muscle relaxation, reduced stromal proliferation, reduced bladder afferent activity and less prostatic inflammation.[21] Tadalafil improves erectile function while treating LUTS/BPH; alpha-blockers generally do not impair erectile function, although tamsulosin and silodosin can cause ejaculatory dysfunction.[21][55] Pooled placebo-controlled data show little change in Qmax.[21]

Tadalafil is a symptom treatment; it has not established the prostate-shrinking or long-term retention or surgery-prevention effects of 5-alpha-reductase inhibitors.[8][9]

CombinationEvidence and label distinction
Tadalafil + uroselective alpha-blockerAUA 2026 permits this conditionally (Grade C)[8], with generally small additional symptom benefits and monitoring for hypotension. The US CIALIS label still does not recommend the combination for BPH.[2]
Alpha-blocker + PDE5 inhibitor (mixed agents; meta-analysis)A meta-analysis of 11 randomized trials (855 men) across PDE5 inhibitors found greater improvement with an alpha-blocker plus a PDE5 inhibitor than with an alpha-blocker alone: IPSS mean difference 1.66 points, Qmax 0.94 mL/s and IIEF 4.73 points. Trials were small and heterogeneous in agent, dose and duration[22]
Tadalafil + 5-ARIAUA 2026 permits this conditionally for LUTS/BPH with estimated prostate volume over 30 cc and/or PSA over 1.5 ng/mL.[8] A 2026 trial randomized 667 men with prostate volume at least 30 mL to dutasteride 0.5 mg plus tadalafil 5 mg daily or either monotherapy. In the 619-man efficacy set (449 with recorded week-48 IPSS), modeled estimates for the combination showed 5.09 and 5.29 points greater adjusted IPSS improvement than dutasteride and tadalafil, respectively, at 48 weeks; Qmax and PVR did not differ significantly. In the 655-man safety set, treatment-emergent adverse events occurred in 72/219, 46/217 and 58/219, respectively. Retention and surgery prevention were not tested.[49] The CIALIS label describes initiation with finasteride for up to 26 weeks; incremental benefit with finasteride beyond that period remains unknown.[2]

The label's instruction to stop an alpha-blocker at least a day before starting daily CIALIS for BPH describes switching away from the alpha-blocker. It is not a one-day pause that makes subsequent combination dosing label-concordant.[2][8]

See Alpha-blockers and 5-alpha-reductase inhibitors for agent selection and progression prevention.

After radical prostatectomy: treatment versus rehabilitation​

Offer treatment for postoperative ED and support resumption of sexual activity. AUA 2018 advises telling men that early PDE5 inhibitor use after radical prostatectomy or radiotherapy may not improve spontaneous, unassisted erectile function .[6] An erection improved while taking medication is different from recovery of unassisted function after medication stops.[5][6][10]

  • REACTT: 423 men with normal preoperative function undergoing bilateral nerve-sparing prostatectomy were randomized to tadalafil 5 mg daily, 20 mg on demand or placebo for nine months. After six weeks off treatment, IIEF-EF at least 22 occurred in 20.9%, 16.9% and 19.1%, respectively; neither tadalafil comparison was significant. Daily tadalafil improved drug-assisted outcomes and reduced measured length loss by a mean 4.1 mm versus placebo during treatment, but did not improve the primary unassisted-function endpoint.[11]
  • Jo 2018: 120 men with preoperative IIEF-5 of at least 17 were randomized after nerve-sparing robotic prostatectomy to sildenafil 100 mg twice weekly for three months starting at catheter removal, or the same regimen starting three months after surgery. Full recovery (IIEF-5 of at least 17) at 12 months was 41.4% versus 17.7% (HR 2.94, p = 0.034).[23] It is a single-center trial with a twice-weekly rather than nightly regimen.[23]
  • Cochrane 2018: eight randomized trials with 1,699 participants provided mostly very-low-certainty evidence. Scheduled PDE5 therapy did not establish better recovery than on-demand treatment.[10]
  • 2021 network meta-analysis: a positive signal for regular sildenafil 100 mg came from comparisons across 22 studies/2,711 patients, with wide uncertainty and incomplete adverse-event reporting.[12]

Choose daily or on-demand treatment according to the patient's goals, response and tolerability. Escalation to vacuum support, urethral therapy or injections can assist sexual activity; the best regimen for restoring unassisted function remains uncertain.[5][10]

Recurrent ischemic priapism: preventive use remains uncertain​

AUA/SMSNA 2022 advises informing patients that optimal strategies to prevent recurrent ischemic priapism are unknown .[47] It lists sildenafil and tadalafil among reported preventive treatments, with conflicting efficacy.[47] A PDE5 inhibitor may be considered off label under specialist supervision, started when the penis is flaccid, for selected recurrent ischemic priapism. EAU 2026 rates the evidence for preventive PDE5 inhibitors in stuttering priapism as level 3, recommends starting them only while the penis is flaccid , and notes a delay of about one week before effect.[13] It is not treatment for an acute ischemic episode, and tadalafil 5 mg each morning is not an established universal default.[13]

Regimented daily PDE5 inhibitor use is thought to recondition downregulated PDE5 regulation in the penis. Two observational reports support the approach. In Burnett's 2006 case series of seven men (four sickle cell, three idiopathic), treatment alleviated or resolved recurrences in six of seven, with erectile function preserved.[25] In Hou and Burnett's 2021 retrospective review, 24 evaluable patients (median 3 months of treatment) had a 4.4-fold fall in emergency-department visits per month, and 22 of 24 reported improvement; the 17 patients who relapsed after stopping had longer and more frequent episodes.[24] AUA/SMSNA discusses these reports as suggesting fewer or shorter episodes, while retaining uncertainty about prevention.[47] Because these designs are uncontrolled, the randomized data below temper them.

The early sildenafil randomized trial enrolled only 13 patients with sickle cell disease and did not show a significant blinded primary benefit.[14] More recently, the 2025 PIN phase 2 feasibility trial randomized 64 men with sickle cell anemia to hydroxyurea plus tadalafil or hydroxyurea plus placebo. Over a median ten months, it demonstrated feasibility but no significant additional reduction in priapism with tadalafil. Both PIN trial arms improved from pretreatment levels.[15]

See Priapism management for acute treatment and individualized recurrence prevention.

Other urologic uses​

SettingAppropriate interpretation
Peyronie's diseaseTreat accompanying ED when appropriate. See Peyronie's agents
Premature ejaculationOff-label in the US. EAU 2026 recommends treating ED, other sexual dysfunction or genitourinary infection first , and using PDE5 inhibitors alone or combined with other therapies in men with premature ejaculation without ED ; combined PDE5 inhibitor and SSRI outperforms SSRI alone (level 1a).[17] Regulatory approval of dapoxetine or topical spray elsewhere is not FDA approval
Ureteral stone passagePDE5-containing combinations have trial signals, but the EAU strongly recommends offering an alpha-blocker as one MET option for selected conservatively managed distal stones 5–10 mm.[18]
Female sexual dysfunctionNot a US-approved indication for these ED products. Investigational and selected off-label data are insufficient for routine treatment of female interest/arousal problems
Renal protectionNot an approved or established clinical indication; preclinical ischemia models do not justify prophylactic prescribing

These distinctions are supported by the relevant labels, current EAU sections and selected primary evidence.[1][2][16][17][18]

Peyronie's disease evidence. PDE5 inhibitors have antifibrotic effects on myofibroblasts. In laboratory and rat models, vardenafil and tamoxifen together inhibited myofibroblast transformation more than either drug alone.[26] In a retrospective review of men with isolated ultrasound septal scars (no deformity), 35 received tadalafil 2.5 mg daily for six months; scar resolution occurred in 69% versus 10% of controls and IIEF-5 rose from 11 to 18.[27] These are hypothesis-generating findings. In a retrospective cohort of men with acute Peyronie's disease and ED, curvature progressed by 12 weeks in 25.9% of 108 taking tadalafil 5 mg daily versus 39.7% of 83 untreated controls.[16] In another retrospective active-phase cohort, 99/101 treated men took daily sildenafil and 2/101 took tadalafil; versus 32 untreated men, adjusted curvature change did not differ significantly at final follow-up (mean 11.3 and 13.6 months, respectively; −4.7°, 95% CI −10 to 0.6; p = 0.08), while mean pain duration was 9.1 versus 12.2 months (p = 0.04).[56]

AUA/SMSNA 2020 recommends treating comorbid ED in men with PE according to the AUA ED guideline .[48] Its first-line PE pharmacotherapies are daily SSRIs, on-demand clomipramine or dapoxetine where available, and topical penile anesthetics .[48] PDE5 inhibitors are not in that first-line list. AUA/SMSNA Statement 12 advises treatment of coexisting erectile dysfunction in men with PE .[48] A 2017 systematic review of randomized trials found longer intravaginal ejaculatory latency time with PDE5 inhibitors than placebo and with a PDE5 inhibitor plus an SSRI than an SSRI alone.[57] EAU 2026 separately recommends PDE5 inhibitors alone or in combination for PE without ED .[17]

Premature ejaculation evidence. A 2017 meta-analysis of 23 studies (6,145 men) found PDE5 inhibitors more effective than placebo or SSRIs for ejaculatory latency, and combined PDE5 inhibitor plus SSRI better than either alone, with more side effects when combined with an SSRI.[28] A Bayesian network meta-analysis found sildenafil superior to sertraline for latency (mean difference 1.63 minutes, 95% CrI 0.10–2.79) and more adverse events than placebo.[29]

Ureteral stone evidence. A 2024 pooled analysis of 14 studies found tadalafil associated with a higher expulsion rate and shorter expulsion time than tamsulosin for distal stones under 10 mm, but the 5 mg and 10 mg subgroups did not individually beat tamsulosin.[30] Network meta-analyses (50 and 78 randomized trials) rank silodosin plus tadalafil best for expulsion time, and tamsulosin plus tadalafil best for pain episodes; expulsion-rate ranking was led by naftopidil plus corticosteroid.[31][32] For conservatively managed distal stones 5–10 mm, EAU 2026 strongly recommends an alpha-blocker as a medical-expulsive-therapy option.[18] Adding tadalafil has combination-study support but remains off label; review interactions and hypotension risk when ED is also being treated.[18][31][32][2]

Female sexual dysfunction evidence. A meta-analysis of 14 placebo-controlled trials found improvement on some sexual-function measures but inconsistent results and more headache, flushing and visual change.[33]

Kidney transplantation​

ED treatment after transplantation requires renal-function, blood-pressure and interaction review. A ten-patient sildenafil study found increased sildenafil exposure and marked blood-pressure reductions compared with historical healthy controls. A subsequent nine-patient study of sildenafil 25 mg daily for nine days did not materially change tacrolimus exposure, but again lowered blood pressure.[20] Neither study establishes a blanket contraindication to daily tadalafil in every tacrolimus recipient. Choose agent and dose with the transplant team according to the actual regimen and organ function.[19][20]

See Also​

References​

1. Pfizer. VIAGRA US prescribing information. DailyMed.

2. Eli Lilly. CIALIS US prescribing information. DailyMed.

3. Vardenafil hydrochloride film-coated tablets: US prescribing information. DailyMed.

4. STENDRA US prescribing information. DailyMed.

5. EAU. Guidelines on Sexual and Reproductive Health, Limited Update March 2026, section 5.6 (treatment of erectile dysfunction) and 5.6.12 (recommendations). Guideline.

6. Burnett AL, et al. Erectile Dysfunction: AUA Guideline. J Urol. 2018. doi:10.1016/j.juro.2018.05.004.

7. Kloner RA, et al. Princeton IV consensus guidelines: PDE5 inhibitors and cardiac health. J Sex Med. 2024;21:90–116. doi:10.1093/jsxmed/qdad163.

8. Goueli R, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline (2026) Part II: Medical Management. J Urol. 2026;216:152–160. doi:10.1097/JU.0000000000005098.

9. Pattanaik S, et al. Phosphodiesterase inhibitors for lower urinary tract symptoms consistent with benign prostatic hyperplasia. Cochrane Database Syst Rev. 2018;CD010060. doi:10.1002/14651858.CD010060.pub2.

10. Philippou YA, et al. Penile rehabilitation for postprostatectomy erectile dysfunction. Cochrane Database Syst Rev. 2018;CD012414. doi:10.1002/14651858.CD012414.pub2.

11. Montorsi F, et al. Effects of tadalafil treatment on erectile function recovery following bilateral nerve-sparing radical prostatectomy: a randomised placebo-controlled study (REACTT). Eur Urol. 2014;65:587–596. doi:10.1016/j.eururo.2013.09.051.

12. Sari Motlagh R, et al. Penile Rehabilitation Strategy after Nerve Sparing Radical Prostatectomy: A Systematic Review and Network Meta-Analysis of Randomized Trials. J Urol. 2021;205:1018–1030. doi:10.1097/JU.0000000000001584.

13. EAU. Guidelines on Sexual and Reproductive Health, Limited Update March 2026, section 10.2.1 (stuttering priapism). Guideline.

14. Burnett AL, et al. Randomized controlled trial of sildenafil for preventing recurrent ischemic priapism in sickle cell disease. Am J Med. 2014;127:664–668. doi:10.1016/j.amjmed.2014.03.019.

15. Idris IM, et al. A controlled trial for preventing priapism in sickle cell anemia: hydroxyurea plus placebo vs hydroxyurea plus tadalafil. Blood. 2025;145:3101–3112. doi:10.1182/blood.2024027898.

16. Spirito L, et al. Daily low-dose tadalafil may reduce the penile curvature progression rate in patients with acute Peyronie's disease: a retrospective comparative analysis. Int J Impot Res. 2024;36:129–134. doi:10.1038/s41443-022-00651-8.

17. EAU. Guidelines on Sexual and Reproductive Health, Limited Update March 2026, section 6.2.7 (premature ejaculation). Guideline.

18. EAU. Urolithiasis: Guidelines. 2026. Guideline.

19. Christ B, et al. Interactions of sildenafil and tacrolimus in men with erectile dysfunction after kidney transplantation. Urology. 2001;58:589–593. doi:10.1016/S0090-4295(01)01306-1.

20. Christ B, et al. Investigation on interaction between tacrolimus and sildenafil in kidney-transplanted patients with erectile dysfunction. Int J Clin Pharmacol Ther. 2004;42:149–156. doi:10.5414/CPP42149.

21. Gacci M, Andersson KE, Chapple C, et al. Latest Evidence on the Use of Phosphodiesterase Type 5 Inhibitors for the Treatment of Lower Urinary Tract Symptoms Secondary to Benign Prostatic Hyperplasia. Eur Urol. 2016;70(1):124-133. doi:10.1016/j.eururo.2015.12.048

22. Zhang J, Li X, Yang B, et al. Alpha-blockers with or without phosphodiesterase type 5 inhibitor for treatment of lower urinary tract symptoms secondary to benign prostatic hyperplasia: a systematic review and meta-analysis. World J Urol. 2019;37(1):143-153. doi:10.1007/s00345-018-2370-z

23. Jo JK, Jeong SJ, Oh JJ, et al. Effect of Starting Penile Rehabilitation with Sildenafil Immediately after Robot-Assisted Laparoscopic Radical Prostatectomy on Erectile Function Recovery: A Prospective Randomized Trial. J Urol. 2018;199(6):1600-1606. doi:10.1016/j.juro.2017.12.060

24. Hou LT, Burnett AL. Regimented Phosphodiesterase Type 5 Inhibitor Use Reduces Emergency Department Visits for Recurrent Ischemic Priapism. J Urol. 2021;205(2):545-553. doi:10.1097/JU.0000000000001365

25. Burnett AL, Bivalacqua TJ, Champion HC, et al. Feasibility of the use of phosphodiesterase type 5 inhibitors in a pharmacologic prevention program for recurrent priapism. J Sex Med. 2006;3(6):1077-1084. doi:10.1111/j.1743-6109.2006.00333.x

26. Ilg MM, Mateus M, Stebbeds WJ, et al. Antifibrotic Synergy Between Phosphodiesterase Type 5 Inhibitors and Selective Oestrogen Receptor Modulators in Peyronie's Disease Models. Eur Urol. 2019;75(2):329-340. doi:10.1016/j.eururo.2018.10.014

27. Chung E, Deyoung L, Brock GB. The role of PDE5 inhibitors in penile septal scar remodeling: assessment of clinical and radiological outcomes. J Sex Med. 2011;8(5):1472-1477. doi:10.1111/j.1743-6109.2011.02217.x

28. Sun Y, Yang L, Bao Y, et al. Efficacy of PDE5Is and SSRIs in men with premature ejaculation: a new systematic review and five meta-analyses. World J Urol. 2017;35(12):1817-1831. doi:10.1007/s00345-017-2086-5

29. Jin K, Deng L, Qiu S, et al. Comparative efficacy and safety of phosphodiesterase-5 inhibitors with selective serotonin reuptake inhibitors in men with premature ejaculation: A systematic review and Bayesian network meta-analysis. Medicine (Baltimore). 2018;97(49):e13342. doi:10.1097/MD.0000000000013342

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