Tadalafil: A PDE5 Inhibitor for Erectile Dysfunction, BPH, and Pulmonary Arterial Hypertension

This article is for informational purposes only and does not constitute medical advice. Superpower Health facilitates access to compounded tadalafil through licensed providers and compounding pharmacy partners. Always consult a qualified healthcare provider before starting any prescription medication.

Most people know tadalafil as a weekend pill. That framing misses most of what this molecule actually does. Tadalafil is the only phosphodiesterase type 5 inhibitor [approved for daily continuous use](https://pubmed.ncbi.nlm.nih.gov/16780568/), and its mechanism operates well beyond the physiology of erections — reaching into vascular endothelial function, lower urinary tract dynamics, and pulmonary circulation. For a drug with this breadth of clinical application, the on-demand framing tells a very partial story.

Tadalafil (brand name Cialis) is available through Superpower's licensed provider network as a compounded troche, a sublingual or buccal formulation that dissolves in the mouth. Here is how tadalafil works at the molecular level, what the clinical evidence shows across its approved indications, and which biomarkers providers typically assess before prescribing it.

Key Takeaways

• Regulatory Status: FDA-approved as Cialis for erectile dysfunction (2003), benign prostatic hyperplasia (2011), and pulmonary arterial hypertension as Adcirca (2009). Compounded tadalafil is available through licensed providers.
• Research Stage: Approved and marketed; compounded troche formulations available through Superpower's provider network
• Availability: Prescription only; available through Superpower's licensed provider network as a compounded troche
• Prescribing information: View full prescribing information (DailyMed)
• How it works: Inhibits PDE5 enzyme, preventing cGMP breakdown and sustaining smooth muscle relaxation via nitric oxide signaling.
• What the research shows: Trials demonstrate improvements in erectile function, BPH symptoms, and exercise capacity in pulmonary arterial hypertension with daily dosing.

What Is Tadalafil?

Tadalafil belongs to the phosphodiesterase type 5 (PDE5) inhibitor class, which also includes sildenafil (Viagra) and vardenafil (Levitra). Its distinguishing pharmacokinetic feature is a [17.5-hour elimination half-life](https://pubmed.ncbi.nlm.nih.gov/16487221/) — substantially longer than the [4 to 5 hours typical of other PDE5 inhibitors](https://pubmed.ncbi.nlm.nih.gov/16780568/). This extended duration underpins its utility for daily dosing and explains why it is the only PDE5 inhibitor approved as a once-daily therapy for erectile dysfunction. Compounded tadalafil troches dissolve sublingually or buccally; the closest available bioavailability evidence comes from orodispersible film studies showing bioequivalence to standard tablets in fasting conditions. Tadalafil-specific troche data is extrapolated from similar formulation research rather than direct troche-versus-tablet trials, and providers account for this when determining dose and formulation. Compounded medications are prepared by a licensed compounding pharmacy and are not FDA-approved. They have not been evaluated by the FDA for safety, efficacy, or quality in the same manner as commercially manufactured branded products. Compounded tadalafil may differ from the branded version in formulation, concentration, and inactive ingredients.

All clinical trial data cited in this article were generated using FDA-approved branded formulations of tadalafil (Cialis, Adcirca), not compounded formulations. Efficacy and safety findings may not be directly transferable to compounded troches or other compounded formulations.

How Tadalafil Works in the Body

PDE5 Inhibition and the cGMP Pathway

Tadalafil's primary action is selective inhibition of phosphodiesterase type 5 (PDE5), an enzyme that degrades cyclic guanosine monophosphate (cGMP) in smooth muscle cells. Normally, sexual stimulation triggers nitric oxide (NO) release from endothelial cells, which activates guanylate cyclase to produce cGMP. cGMP causes smooth muscle relaxation in the corpus cavernosum, allowing blood to fill the erectile tissue. PDE5 terminates this signal by breaking down cGMP. Tadalafil blocks PDE5, allowing cGMP to accumulate and prolonging smooth muscle relaxation. The critical clinical implication is that tadalafil requires endogenous nitric oxide signaling to be active — it enhances a physiological response rather than generating an independent one. A 2021 umbrella review in Frontiers in Pharmacology by Pyrgidis and colleagues — synthesizing 23 systematic reviews encompassing 563 primary studies and 154,796 total participants — confirmed this mechanism as central to PDE5i efficacy across the drug class, while noting that PDE5 inhibitors do not significantly improve endothelial dysfunction in humans despite positive signals in animal models.

Endothelial and Vascular Effects

PDE5 is expressed not only in penile smooth muscle but throughout the vascular endothelium. By sustaining cGMP levels systemically, tadalafil influences vascular tone and endothelial function beyond the localized effects of erection. A 2025 meta-analysis by Zhang and colleagues — pooling 63 RCTs with 3,242 total participants — found that PDE5 inhibitors significantly improved flow-mediated dilation by 2.47% (95% CI: 1.24–3.71; p < 0.001), reduced pulse wave velocity by 0.75 cm/s (95% CI: −1.01 to −0.49; p < 0.001), and lowered systolic blood pressure by 2.80 mmHg (95% CI: −4.24 to −1.37; p < 0.001) compared with placebo. A 2017 study by Ozdabakoglu and colleagues enrolled 30 men with ED (mean age 48.7 years) free from known cardiovascular disease alongside 20 healthy controls and found that a single dose of tadalafil significantly reduced systolic blood pressure (p = 0.001), reduced pulse pressure (p = 0.018), and improved aortic distensibility (p = 0.001), aortic strain (p = 0.003), and both large- and small-artery elasticity indices (p = 0.02 and p = 0.003, respectively), while also improving left ventricular diastolic function. These vascular effects are relevant to the growing interest in PDE5i applications beyond their approved indications, though these uses are not FDA-approved and remain under investigation.

Lower Urinary Tract and Prostatic Effects

PDE5 is also expressed in smooth muscle of the prostate, bladder neck, and urethra. Tadalafil's inhibition of PDE5 in these tissues reduces smooth muscle tone in the lower urinary tract, which is the proposed mechanism for its efficacy in benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS). This mechanism distinguishes tadalafil from alpha-blocker medications like tamsulosin, which act on adrenergic receptors in the same tissues. A 2020 meta-analysis in Medical Science Monitor by Guo and colleagues — pooling 7 RCTs with 1,601 total patients — found no significant difference between tadalafil and tamsulosin in total IPSS, voiding subscores, storage subscores, quality-of-life scores, maximum flow rate (Qmax), or post-void residual urine, but tadalafil was significantly superior on International Index of Erectile Function (IIEF) scores — a clinically meaningful advantage given the high co-occurrence of BPH/LUTS and erectile dysfunction.

Pulmonary Vascular Effects

PDE5 is highly expressed in pulmonary arterial smooth muscle. In pulmonary arterial hypertension (PAH), elevated pulmonary vascular resistance reduces right heart function and exercise tolerance. Tadalafil inhibits PDE5 in pulmonary vasculature, promoting vasodilation and reducing pulmonary arterial pressure. This is the mechanism underlying the Adcirca indication. Systemic and pulmonary PDE5 activity share the same molecular pathway; the clinical distinction between the ED indication (Cialis) and the PAH indication (Adcirca) reflects different doses, patient populations, and regulatory filings rather than a different mechanism of action.

Pharmacokinetics and the Daily Dosing Advantage

Tadalafil's half-life of 17.5 hours (5th–95th percentile: 11.5–29.6 hours) — confirmed in a 2006 pharmacokinetic study in the British Journal of Clinical Pharmacology by Forgue and colleagues analyzing 237 healthy subjects receiving single doses of 2.5–20 mg — is the longest in the PDE5 inhibitor class. Sildenafil and vardenafil have half-lives of approximately 4 to 5 hours, requiring sexual activity to be timed around dosing. Tadalafil at 5 mg daily reaches steady-state plasma concentrations within approximately 5 days. This enables spontaneous sexual activity without the anticipatory dosing that characterizes other PDE5i. [Food does not affect tadalafil absorption](https://pubmed.ncbi.nlm.nih.gov/16487221/), which also distinguishes it from sildenafil. Steady-state also appears to confer downstream benefits: a 2019 meta-analysis in Sexual Medicine by Zhou and colleagues — pooling 4 RCTs with 1,035 participants treated for at least 24 weeks — found that daily tadalafil produced significantly greater IIEF-EF improvement than on-demand dosing (MD 1.24; 95% CI: 0.03–2.44; p = 0.04), along with significantly higher successful intercourse rates (SEP3 MD 8.19; 95% CI: 2.09–14.29; p = 0.009) and a lower overall incidence of treatment-emergent adverse events (OR 0.73; 95% CI: 0.56–0.96; p = 0.02).

What the Research Shows About Effectiveness

Erectile Dysfunction: Daily vs. On-Demand Dosing

A 2016 integrated analysis in the Journal of Sexual Medicine by Brock and colleagues — pooling 17 on-demand and 4 once-daily placebo-controlled trials with 4,354 men over 12 weeks — found that both tadalafil 5 mg once daily and 10–20 mg on demand significantly improved IIEF erectile function domain scores versus placebo (p < 0.02) across all clinical subgroups, including men with diabetes, cardiovascular disease, hypertension, and hyperlipidemia. For men with erectile dysfunction and concurrent BPH or LUTS, the once-daily 5 mg dose was studied specifically in a 2018 trial in the International Journal of Impotence Research by Bolat and colleagues: in 63 diabetic men with ED over 3 months, both once-daily 5 mg (n = 31) and on-demand 20 mg (n = 32) improved IIEF scores and LUTS symptoms in patients under 65, with daily 5 mg producing significantly greater improvements in ejaculatory function and LUTS than the on-demand regimen. A 2-year post-marketing RCT published in Asian Journal of Andrology in 2024 by Jiang and colleagues enrolled 635 Chinese men with ED, randomized initially to tadalafil 2.5 or 5 mg daily for 3 months before continuing at 5 mg daily for 21 months; at 24 months, IIEF-EF scores improved by a mean of 8.6 points (95% CI: 8.1–9.0; p < 0.001), 48.0% of patients had regained normal erectile function (IIEF-EF score 26 or above), and treatment-emergent adverse events remained stable between month 12 and month 24, confirming durable efficacy and a favorable long-term safety profile.

BPH and Lower Urinary Tract Symptoms

A 2021 meta-analysis in Frontiers in Medicine by Cui and colleagues — pooling 15 RCTs with 9,525 total patients (4,937 tadalafil, 4,588 placebo) treated with 5 mg once daily for 12 weeks — found a significant IPSS reduction of 1.97 points versus placebo (95% CI: −2.24 to −1.70; p < 0.00001), though maximum urinary flow rate (Qmax) did not significantly improve (MD 0.11 mL/s; 95% CI: −0.41 to 0.63; p = 0.68). The FDA approved tadalafil for BPH in 2011, making it the only PDE5 inhibitor with a dedicated LUTS indication. Tadalafil is also approved for the combined management of ED and BPH in the same patient, which reflects its unique dual utility in men with both conditions.

Pulmonary Arterial Hypertension: The PHIRST Trial

The PHIRST trial (Pulmonary Arterial Hypertension and Response to Tadalafil), published by Galie and colleagues in Circulation in 2009, was the pivotal RCT for the PAH indication. The trial enrolled 405 patients with idiopathic or associated PAH — both treatment-naive and those on background bosentan therapy — randomizing them to tadalafil 2.5, 10, 20, or 40 mg once daily versus placebo over 16 weeks. The 40 mg group achieved a placebo-corrected improvement of 33 meters in 6-minute walk distance (95% CI: 15–50 m; p < 0.01), with a larger effect in bosentan-naive patients (+44 m; 95% CI: 20–69 m) than in those on background bosentan (+23 m; 95% CI: −2 to 48 m). Tadalafil 40 mg also reduced clinical worsening by 68% (p = 0.038) and significantly improved health-related quality of life (p = 0.041). The 40 mg dose was subsequently approved under the brand name Adcirca. This is a distinctly different population, dose, and indication than the ED and BPH uses of Cialis.

Patient and Partner Preference

A 2017 systematic review and meta-analysis in International Urology and Nephrology by Gong and colleagues — including 16 controlled trials directly comparing tadalafil and sildenafil — found similar overall efficacy and adverse event rates, but tadalafil significantly improved psychological outcomes including sexual confidence, and patients and their partners preferred tadalafil over sildenafil (p < 0.05). A 2024 systematic review in Minerva Urology and Nephrology by Manfredi and colleagues — analyzing 14 RCTs with 6,841 patients — found that 66–73% of patients preferred tadalafil over sildenafil (p < 0.05), primarily because it allowed erections long after dosing (cited by 55–67% of those who preferred it), while 57–59% preferred tadalafil as-needed over fixed-schedule dosing (p < 0.05); however, all included RCTs were assessed as high risk of bias. These preference findings are relevant to treatment adherence, though they do not establish clinical superiority and should be interpreted in the context of different study populations and designs.

Side Effects and What to Expect

Tadalafil's side effect profile is consistent across the PDE5 inhibitor class and is generally dose-dependent. Most adverse effects are mild to moderate and tend to diminish with continued use or dose adjustment.

Common side effects:

• Headache (reported in 15.8% of 1,173 men with ED in a 24-month open-label extension trial by Montorsi and colleagues using tadalafil 5–20 mg as needed; dose-dependent and typically resolving with continued use)
• Flushing (vasodilatory mechanism; more common at higher doses)
• Dyspepsia and indigestion (more common with tadalafil than with other PDE5i due to inhibition of PDE11, which is expressed in the gastrointestinal tract)
• Nasal congestion
• Back pain and myalgia (distinctive to tadalafil; attributed to PDE11 inhibition; typically transient)
• Limb pain

Less common but clinically important:

• Hypotension: tadalafil lowers blood pressure via cGMP-mediated vasodilation. Co-administration with nitrates (including nitroglycerin) is absolutely contraindicated due to risk of severe hypotension. An integrated safety analysis in the Journal of Clinical Hypertension by Kloner and colleagues (2022) — pooling 72 Phase II–IV studies with 22,825 patients with ED or BPH — found that hypotension-related adverse events occurred in only 0.6–1.5% of tadalafil users, with no significant increase in hypotension-related events or major adverse cardiovascular events in patients taking one or more antihypertensive medications concurrently (p values 0.74 or above for all comparisons versus placebo).
• Non-arteritic anterior ischemic optic neuropathy (NAION): rare; patients with a history of NAION should not use PDE5 inhibitors
• Sudden hearing loss: rare; patients should seek immediate medical attention if sudden decrease or loss of hearing occurs
• Priapism (prolonged erection exceeding 4 hours): seek immediate medical attention; failure to treat promptly can result in permanent erectile damage

Providers screen for cardiovascular status, concurrent medications, and relevant comorbidities before prescribing. The contraindication with nitrate medications is absolute and requires careful medication reconciliation at baseline.

Who Is Tadalafil Typically Prescribed For?

Erectile Dysfunction

Tadalafil is FDA-approved for erectile dysfunction in adult men. Providers typically consider it for individuals who have confirmed erectile dysfunction affecting quality of life and who have been evaluated for underlying cardiovascular health, since erectile dysfunction is often an early vascular signal. A 2020 network meta-analysis in World Journal of Urology by Madeira and colleagues — encompassing 179 RCTs with 50,620 patients — ranked tadalafil 10 mg and 20 mg among the most effective PDE5 inhibitors for improving IIEF scores (73% and 76% probability of being among the best treatments, respectively), while concluding that sildenafil at low doses and tadalafil should be first-line therapeutic options based on combined efficacy and safety profiles. Providers evaluate candidacy based on cardiovascular status, concurrent medications, and underlying causes of erectile dysfunction. Tadalafil is FDA-approved for erectile dysfunction, BPH, and pulmonary arterial hypertension. Any use outside these approved indications is the independent clinical judgment of the prescribing physician. Any off-label use is the independent clinical judgment of the prescribing physician.

Benign Prostatic Hyperplasia and LUTS

Tadalafil is FDA-approved for the signs and symptoms of BPH and for co-management of BPH and erectile dysfunction in men with both conditions. Providers typically consider it for men with confirmed lower urinary tract symptoms where the dual benefit on erectile function and LUTS is clinically relevant. At the approved 5 mg once-daily dose, it is appropriate for long-term use, with the 2-year Jiang trial providing safety data extending beyond most short-term trials. Tadalafil is not a substitute for clinical evaluation of BPH, including appropriate PSA monitoring to rule out prostate cancer.

Pulmonary Arterial Hypertension

Tadalafil is FDA-approved as Adcirca (40 mg once daily) for pulmonary arterial hypertension in adults to improve exercise ability and delay clinical worsening. This indication is managed by specialists in pulmonary medicine or cardiology. The dose, patient population, and clinical monitoring requirements for this indication differ substantially from those for erectile dysfunction or BPH use. Superpower's provider network is not a specialist PAH service; individuals with PAH should be managed by qualified specialists.

Who Should Not Take Tadalafil

A licensed provider will evaluate individual risk factors before prescribing tadalafil. The following are recognized contraindications or conditions requiring significant clinical scrutiny:

• Concurrent use of organic nitrates in any form (including nitroglycerin, isosorbide mononitrate, isosorbide dinitrate, amyl nitrite): risk of severe, potentially life-threatening hypotension
• Concurrent use of soluble guanylate cyclase stimulators (e.g., riociguat): additive blood pressure lowering
• Hypersensitivity to tadalafil or any component of the formulation
• Severe hepatic impairment (Child-Pugh Class C): tadalafil is hepatically metabolized; impaired clearance increases drug exposure
• Severe renal impairment (creatinine clearance less than 30 mL/min): dose adjustment required; not recommended for once-daily use in this population
• Cardiovascular instability: men for whom sexual activity is inadvisable due to cardiovascular status (e.g., unstable angina, recent myocardial infarction, uncontrolled arrhythmia) should not use tadalafil without specialist clearance
• Prior non-arteritic anterior ischemic optic neuropathy (NAION): risk of recurrence
• Significant hypotension (blood pressure below 90/50 mmHg): risk of dangerous blood pressure reduction
• Concomitant use of potent CYP3A4 inhibitors (e.g., ketoconazole, ritonavir): substantially increases tadalafil plasma levels; providers adjust dose accordingly

This is not an exhaustive list. A licensed provider will evaluate the full clinical picture, including medication list, cardiovascular history, and comorbidities, before prescribing. Alpha-blocker co-administration requires particular care due to additive hypotensive effects; providers typically initiate at the lowest tadalafil dose in patients on stable alpha-blocker therapy.

What to Test Before Starting Tadalafil

Establishing a baseline before starting provides the clinical context that makes any changes during use interpretable. The following markers are relevant to tadalafil candidacy and monitoring:

• Cardiovascular biomarkers (lipid panel, ApoB): Erectile dysfunction is strongly associated with early atherosclerotic vascular disease. A full lipid panel including LDL cholesterol and ApoB establishes cardiovascular risk context before starting any vasoactive medication. Providers use this to inform the overall clinical picture.
• Blood pressure: Tadalafil lowers blood pressure through its vasodilatory mechanism. Baseline blood pressure establishes whether there is pre-existing hypotension that would require dosing adjustments. Not a blood test, but clinically essential.
• hs-CRP: Elevated systemic inflammation is associated with endothelial dysfunction, one of the upstream drivers of erectile dysfunction. Baseline hs-CRP contextualizes whether vascular inflammation may be contributing to symptoms.
• eGFR (estimated glomerular filtration rate): Tadalafil dosing must be adjusted in renal impairment. Once-daily use is not recommended in patients with creatinine clearance below 30 mL/min. Baseline eGFR is essential for safe prescribing.
• Liver function tests (ALT, AST, GGT): Tadalafil is primarily metabolized by CYP3A4 in the liver. Hepatic impairment increases drug exposure and requires dose modification or avoidance. Baseline liver function confirms adequate hepatic clearance. Relevant context available through liver health biomarker testing.
• Total testosterone and free testosterone: Erectile dysfunction in men is often multifactorial, and hypogonadism is a common contributing factor. Testosterone levels should be evaluated before attributing erectile dysfunction solely to a vascular or psychogenic cause. Low testosterone may require concurrent management.
• Total PSA: Required before initiating tadalafil in men with BPH symptoms. Tadalafil use is associated with small reductions in PSA values; establishing a pre-treatment baseline is essential for prostate cancer surveillance. Providers factor this in when monitoring PSA during therapy.
• Fasting glucose and HbA1c: Diabetes is among the [most common comorbidities associated with erectile dysfunction](https://pubmed.ncbi.nlm.nih.gov/28722225/) due to both vascular and neurogenic mechanisms. Establishing glycemic status at baseline informs whether metabolic contributors need concurrent management.

What Your Bloodwork May Show While on Tadalafil

Providers monitoring response to tadalafil typically track several markers over time. PSA is one of the most important to watch: unlike 5-alpha reductase inhibitors, tadalafil does not significantly alter PSA values, but pre-treatment baseline values are still necessary for accurate prostate cancer screening interpretation during therapy. Testosterone levels are typically [stable on tadalafil](https://pubmed.ncbi.nlm.nih.gov/16839328/) (it does not directly modulate the HPG axis), but retesting if symptoms change provides useful context. Renal function (eGFR, creatinine) and liver enzymes provide ongoing safety checks, particularly relevant if dose adjustment or long-term use is anticipated. Lipid and cardiovascular markers tracked over time can contextualize the broader vascular picture in men where erectile dysfunction was an early cardiovascular signal.

That principle — establish a baseline, then track how the data changes — is central to Superpower's approach to preventive health. Tadalafil is a well-characterized medication with a robust evidence base; knowing your relevant biomarkers before starting makes the clinical story interpretable at every step.

Frequently Asked Questions

How long does tadalafil last?

Tadalafil has a half-life of approximately 17.5 hours, the longest among PDE5 inhibitors. A single on-demand dose (typically 10 or 20 mg) maintains [therapeutic plasma levels for up to 36 hours](https://pubmed.ncbi.nlm.nih.gov/15866997/). Once-daily dosing at 2.5 to 5 mg reaches [steady-state concentrations within approximately 5 days](https://pubmed.ncbi.nlm.nih.gov/16487221/), providing continuous effect without the need to time activity around dosing.

What is the difference between tadalafil and sildenafil?

Both are PDE5 inhibitors with the same mechanism of action, but their pharmacokinetics differ substantially. Tadalafil has a 17.5-hour half-life; sildenafil's is approximately 4 hours. Tadalafil is not affected by food intake; [high-fat meals can delay sildenafil absorption](https://pubmed.ncbi.nlm.nih.gov/16780568/). Tadalafil is the only PDE5 inhibitor approved for once-daily use and the only one with an FDA approval for BPH. A 2017 systematic review and meta-analysis of 16 head-to-head trials by Gong and colleagues found similar efficacy and adverse event rates between the two drugs, but patients and partners significantly preferred tadalafil (p < 0.05), primarily for sexual confidence and spontaneity, though cross-study comparisons should be interpreted cautiously given differences in populations and study designs.

Can you take tadalafil daily?

Yes. Tadalafil is FDA-approved at 2.5 and 5 mg for once-daily use for erectile dysfunction and BPH. Daily dosing reaches steady-state plasma levels in approximately 5 days and eliminates the need to plan around dosing windows. A 2019 meta-analysis of 4 RCTs (N = 1,035) by Zhou and colleagues found that after at least 24 weeks, daily tadalafil produced significantly greater IIEF-EF improvement than on-demand dosing (MD 1.24; 95% CI: 0.03–2.44; p = 0.04) with a lower overall incidence of treatment-emergent adverse events (OR 0.73; 95% CI: 0.56–0.96; p = 0.02). A provider determines which regimen is appropriate for an individual's clinical picture.

Does tadalafil lower blood pressure?

Tadalafil produces a modest reduction in systolic and diastolic blood pressure through its vasodilatory mechanism, consistent with its PDE5 inhibitor pharmacology. In properly screened patients on stable antihypertensive therapy, tadalafil co-administration has not been shown to cause clinically significant additional hypotension, per an integrated safety analysis of 72 clinical studies (N = 22,825) by Kloner and colleagues, which found no significant increase in hypotension-related events in patients on antihypertensive medications. However, co-administration with nitrates is absolutely contraindicated due to the risk of severe hypotension.

What should I avoid while taking tadalafil?

Nitrates of any form (nitroglycerin, isosorbide mononitrate, amyl nitrite) are absolutely contraindicated with tadalafil due to the risk of severe hypotension. Grapefruit and grapefruit juice inhibit CYP3A4, the enzyme responsible for tadalafil metabolism, and can increase plasma tadalafil levels — an interaction demonstrated in preclinical animal models. Excessive alcohol can lower blood pressure and may amplify tadalafil's hypotensive effects. Potent CYP3A4 inhibitors, including certain antifungals and HIV protease inhibitors, substantially increase tadalafil exposure and require dose adjustment. A provider reviews the full medication list before prescribing.

Does tadalafil affect testosterone levels?

Tadalafil does not act on the hypothalamic-pituitary-gonadal axis and does not directly affect testosterone production or metabolism. However, because low testosterone is a common contributor to erectile dysfunction, providers typically assess testosterone at baseline. In men with both erectile dysfunction and hypogonadism, tadalafil may address the vascular component while testosterone management addresses the hormonal component.

What blood tests should I get before starting tadalafil?

Clinically relevant pre-treatment markers include: eGFR and creatinine (for renal dosing safety), liver function tests (for hepatic metabolism), a lipid panel with ApoB (cardiovascular risk context), total and free testosterone (to assess hormonal contributors to erectile dysfunction), PSA (required before use in men with BPH symptoms), fasting glucose and HbA1c (metabolic context), and baseline blood pressure. A provider determines the appropriate scope of testing based on presentation and indication.

IMPORTANT SAFETY INFORMATION

Tadalafil is an FDA-approved prescription medication. Your licensed healthcare provider will evaluate whether tadalafil is appropriate for you. Superpower connects patients with licensed providers and pharmacies; Superpower does not prescribe or dispense medications.

Do not take tadalafil if you: take nitrates for chest pain (nitroglycerin, isosorbide); take guanylate cyclase stimulators (riociguat); have had a serious allergic reaction to tadalafil.

Warnings: priapism (erection lasting more than 4 hours, seek immediate care); sudden vision loss (NAION); sudden hearing loss; hypotension, especially with alcohol or alpha-blockers. Not for use in women or children.

Common side effects: headache, flushing, indigestion, nasal congestion, back pain, muscle aches, limb pain.

Full prescribing information at dailymed.nlm.nih.gov.