Tadalafil Tablets

Tadalafil is an orally administered phosphodiesterase-5 (PDE5) inhibitor that is compounded in 2.5 mg, 5 mg, 10 mg, and 20 mg immediate-release tablets for prescription use under the supervision of qualified clinicians^[1]. It was originally introduced for erectile dysfunction but is now also employed for benign prostatic hyperplasia (BPH) and selected cases of pulmonary arterial hypertension (PAH).

Chemically, tadalafil is a once-daily, highly selective, reversible inhibitor of PDE5, the cGMP-specific isoenzyme most abundant in corpus cavernosum and other vascular smooth-muscle beds^[2]. Inhibition of PDE5 prevents degradation of cyclic guanosine monophosphate (cGMP), augmenting the nitric-oxide (NO) signaling cascade and facilitating relaxation of smooth muscle throughout the lower urinary tract and pulmonary vasculature^[2].

The broad therapeutic scope of tadalafil reflects this pharmacology. Clinical experience demonstrates meaningful improvements in penile rigidity, symptom scores in BPH, exercise tolerance in PAH, and endothelial function in several vascular beds³. These clinical benefits, however, remain contingent upon intact NO release from nitrergic nerves or endothelial cells, so individual responses may vary^[3].

After oral administration, peak plasma concentrations are usually achieved within two hours; absolute bioavailability approaches 80 %. The drug is 94 % protein-bound and exhibits an apparent volume of distribution of roughly 63 L, indicating extensive tissue penetration^[4]. Metabolism is primarily hepatic via CYP3A4 to the active catechol metabolite, with subsequent glucuronidation and fecal plus renal elimination; the terminal half-life of ≈ 17.5 hours allows for either once-daily or on-demand dosing^[4].

Hemodynamic interaction studies show that the vasodilatory effect is prolonged; coadministration with organic nitrates can precipitate profound hypotension even 48 hours after a single 20 mg dose^[5]. These findings inform strict contraindications and mandatory wash-out intervals when nitrates are part of the therapeutic regimen^[5].

For prescribers utilizing 503A compounded tadalafil, it is critical to note that labeling and stability data follow the United States Pharmacopeia (USP) for compounded oral tablets. The compounded product must meet potency, purity, and content uniformity specifications validated by the pharmacy’s quality program to ensure batch-to-batch consistency before release^[6].

For on-demand treatment of erectile dysfunction, the typical adult starting dose is 10 mg taken at least 30 minutes before anticipated intercourse; depending on tolerance and efficacy, doses may be decreased to 5 mg or increased to 20 mg, not to exceed once per 24 hours^[27].

When a once-daily strategy is chosen for combined management of BPH and erectile dysfunction, 5 mg administered at approximately the same time each day provides continuous PDE5 inhibition; severe renal impairment (CrCl < 30 mL min⁻¹) or concomitant strong CYP3A4 inhibitors warrant a maximum dose of 10 mg every 72 hours^[28]. Dose-adjustment guidance for moderate hepatic impairment allows up to 10 mg on-demand, whereas once-daily use is not recommended; practitioners compounding divided tablets should ensure accuracy of low-dose splits and counsel patients on precise administration^[29].

Tadalafil acts by competitive, selective inhibition of PDE5, preventing hydrolysis of cGMP that is generated after NO activates guanylate cyclase in smooth-muscle cells⁷. The sustained cGMP elevation lowers intracellular calcium, promoting myosin light-chain de-phosphorylation and smooth-muscle relaxation, thereby enhancing arterial inflow to erectile tissue and reducing pulmonary vascular resistance^[7].

Beyond erectile tissue, PDE5 is expressed in bladder, prostate, and vascular endothelium. Selectivity studies confirm >10 000-fold preference for PDE5 over PDE1-4 and ≈ 700-fold over PDE11; this profile minimizes unintended chronotropic or neurologic effects while sparing skeletal muscle and retinal phototransduction^[8].

Hemodynamic investigations reveal that tadalafil reduces mean pulmonary artery pressure and pulmonary vascular resistance without significant changes in systemic vascular resistance, demonstrating organ-specific vasodilatation^[9]. These pulmonary benefits justify its incorporation into PAH management in selected adults and parturients under specialist care^[9].

In the lower urinary tract, PDE5 inhibition relaxes prostatic stromal smooth muscle, detrusor, and bladder neck, potentially improving uroflow and relieving storage symptoms without adversely affecting detrusor contractility¹⁰. Improvement in LUTS is additive to α-blocker therapy and offers sexual function advantages over 5-α-reductase inhibitors^[10].

Pharmacodynamic modeling indicates that exposure-response curves plateau near 20 mg, but the long half-life sustains clinically relevant plasma levels for up to 36 hours, allowing on-demand dosing flexibility and once-daily regimens for chronic indications^[11].

Concurrent administration of any nitrate or NO-donor is absolutely contraindicated because synergistic increases in cGMP can provoke life-threatening hypotension; at least 48 hours should elapse between the last tadalafil dose and nitrate exposure^[12].

Patients with a history of non-arteritic anterior ischemic optic neuropathy (NAION) or pre-existing crowded optic discs may face a heightened risk of vision loss, and tadalafil is not recommended in this population^[13].

Severe hepatic impairment (Child-Pugh C) markedly increases systemic exposure; the manufacturer therefore advises against use in this setting, and alternative therapies should be sought^[14].

Marked hypotension (systolic < 90 mm Hg), unstable angina, recent stroke or myocardial infarction, uncontrolled arrhythmias, severe aortic stenosis, or hypersensitivity to tadalafil or any tablet excipients constitute additional contraindications because the drug can exacerbate cardiovascular instability^[15].

Possible interactions include certain drugs for high blood pressure; certain drugs for the treatment of HIV infection or AIDS; certain drugs used for fungal or yeast infections, like fluconazole, ketoconazole, and voriconazole; certain drugs used for seizures like carbamazepine, phenytoin, and phenobarbital; grapefruit juice; macrolide antibiotics; medicines for prostate problems; rifabutin, rifampin or rifapentine. This list may not describe all possible interactions. Give your health care provider a list of all the medicines, herbs, non-prescription drugs, or dietary supplements you use. Also tell them if you smoke, drink alcohol, or use illegal drugs. Some items may interact with your medicine.

The safety and efficacy of tadalafil administered concurrently with any other phosphodiesterase inhibitors (e.g., vardenafil and sildenafil) has not been studied. The manufacturer of tadalafil recommends to avoid the use of tadalafil with any other phosphodiesterase inhibitors.^[2]

Tadalafil has been shown to potentiate the hypotensive effects of nitrates. This interaction is consistent with tadalafil’s known effects on the nitric oxide/cGMP pathway. Deaths have been reported in men who were using a similar agent, sildenafil, while taking nitrate or nitrite therapy for angina. Tadalafil administration to patients who are concurrently using organic nitrates or nitrites in any form is contraindicated.^[6] It should be noted that during once daily administration of tadalafil, the presence of continuous plasma tadalafil concentrations may change the potential for interactions with other medications such as nitrates.^[6]

Concurrent use of phosphodiesterase (PDE5) inhibitors and alpha-blockers may lead to symptomatic hypotension in some patients. Tadalafil, other PDE5 inhibitors, and alpha-blockers are systemic vasodilators which can lower blood pressure. If vasodilators are used in combination, an additive effect on blood pressure is anticipated. Because the efficacy of concurrent use of tadalafil and alpha-blockers in the treatment of benign prostatic hyperplasia (BPH) has not been adequately studied, and due to the potential vasodilatory effects of combination treatment, tadalafil is not recommended for use with alpha-blockers when treating BPH. Patients receiving alpha-blocker therapy for BPH prior to tadalafil initiation should discontinue the alpha-blocker at least one day prior to beginning tadalafil treatment. When tadalafil is co-administered with an alpha-blocker in a patient receiving tadalafil for erectile dysfunction (ED), the patient should be stable on alpha-blocker therapy before starting PDE5 inhibitor therapy. If hemodynamic instability is evident on alpha-blocker therapy alone, there is an increased risk of symptomatic hypotension with concomitant PDE5 inhibitor therapy. For patients with ED who are stable on alpha-blocker therapy, PDE5 inhibitors should be started at the lowest recommended dose. If a patient with ED is currently receiving an optimized dose of a PDE5 inhibitor, alpha-blocker therapy should be initiated at the lowest dose. Stepwise increases in the alpha-blocker dose may be associated with further hypotension when taking a PDE5 inhibitor. Other variables, such as intravascular volume depletion and other antihypertensive drugs, may affect the safety of concomitant use of PDE5 inhibitors and alpha-blockers. Studies have been conducted to determine the effects of tadalafil on the potentiation of the blood-pressure-lowering effects of the alpha-blockers doxazosin and tamsulosin. When tadalafil 20 mg was administered to healthy subjects taking doxazosin (8 mg daily), an alpha-1-blocker, there was significant augmentation of the hypotensive effects of doxazosin. In contrast, coadministration of a single 20-mg dose of tadalafil to healthy subjects taking either 0.4 mg tamsulosin once-daily or 10 mg alfuzosin once daily, both of which are selective alpha-1A-blockers, resulted in no significant decreases in blood pressure. It should be noted that during once daily administration of tadalafil for ED or other indications, the presence of continuous plasma tadalafil concentrations may change the potential for interactions with medications such as alpha-blockers.^[6]

Particular caution should be used when prescribing phosphodiesterase type 5 (PDE5) inhibitors, such as tadalafil, to patients receiving certain protease inhibitors such as atazanavir, darunavir, ritonavir, amprenavir, fosamprenavir, indinavir, tipranavir, nelfinavir, or saquinavir.^[2]

Tadalafil is metabolized predominantly by CYP3A4. Efavirenz induces CYP3A4 and may decrease serum concentrations of drugs metabolized by this enzyme.^[7][6] Similar precautions apply to combination products containing efavirenz such as efavirenz; emtricitabine; tenofovir.

Particular caution should be used when prescribing phosphodiesterase type 5 (PDE5) inhibitors to patients receiving delavirdine. Coadministration of delavirdine with these drugs is expected to substantially increase their plasma concentrations and may result in increased associated adverse events including hypotension, syncope, visual changes, and prolonged erection. The manufacturer of tadalafil recommends that in patients receiving concomitant potent CYP3A4 inhibitors, the ‘as needed’ dose for erectile dysfunction should not exceed 10 mg within a 72 hour time period, and the ‘once-daily’ dose for erectile dysfunction or benign prostatic hyperplasia should not exceed 2.5 mg (see Dosage).6 It should be noted that during once daily administration of tadalafil, the presence of continuous plasma tadalafil concentrations may change the potential for interactions with potent inhibitors of CYP3A4. When used for pulmonary arterial hypertension, tadalafil should not be co-administered with potent CYP3A inhibitors.^[6]

Tadalafil is metabolized predominantly by CYP3A4. Inhibitors of CYP3A4 may reduce tadalafil clearance. In theory, CYP3A4 inhibitors which may interact with tadalafil include amiodarone, cimetidine, clarithomycin or products containing clarithomycin, conivaptan, diltiazem, erythromycin or products containing erythromycin, fluconazole, fluoxetine or combination products with fluoxetine, fluvoxamine, ketoconazole, imatinib, STI-571, itraconazole, mibefradil, nefazodone, quinidine or combination products with quinidine, troleandomycin, voriconazole, zafirlukast, and zileuton. Increased systemic exposure to tadalafil may result in increased associated adverse events including hypotension, syncope, visual changes, and prolonged erection. The manufacturer of tadalafil recommends that in patients receiving concomitant potent CYP3A4 inhibitors, the ‘as needed’ dose for erectile dysfunction should not exceed 10 mg within a 72 hour time period, and the ‘once-daily’ dose for erectile dysfunction or benign prostatic hyperplasia should not exceed 2.5 mg (see Dosage).^[6]

Etravirine is an inducer of CYP3A4; coadministration may result in decreased tadalafil concentrations. Dosage adjustments may be needed based on clinical efficacy.^[8]

Tadalafil is metabolized via the CYP3A4 isozyme. Grapefruit juice (food) has been reported to decrease the metabolism of drugs metabolized via this enzyme. Grapefruit juice contains a furano-coumarin compound, 6,7-dihydroxybergamottin that inhibits CYP3A4 in enterocytes in the GI tract. Tadalafil levels may increase; it is possible that tadalafil-induced side effects could also be increased in some individuals.^[6]

Although specific interaction studies have not been performed, CYP3A4 inducers such as barbiturates, bosentan, carbamazepine, dexamethasone, phenytoin or fosphenytoin, nevirapine, rifabutin, troglitazone, rifampin, or isoniazid would likely decrease tadalafil AUC since tadalafil is primarily metabolized by CYP3A4.^[6] Patients should be monitored for loss of efficacy of tadalafil during concurrent use

Mifepristone, RU-486 inhibits CYP3A4 in vitro.^[9][10] Coadministration of mifepristone may lead to an increase in serum levels of drugs metabolized via CYP3A4, such as tadalafil. Due to the slow elimination of mifepristone from the body, such interactions may be observed for a prolonged period after mifepristone administration.

The combination of tadalafil and substantial consumption of ethanol can increase the potential for orthostatic signs and symptoms, including increase in heart rate, decrease in standing blood pressure, dizziness, and headache. Ethanol and PDE5 inhibitors, including tadalafil, are mild systemic vasodilators. As reported by the manufacturer, the interaction of tadalafil with ethanol was evaluated in 3 clinical pharmacology studies. In 2 of the studies, ethanol was administered at a dose of 0.7 g/kg, which is equivalent to approximately 6 ounces of 80-proof vodka in an 80-kg male, and tadalafil was administered at a dose of 10 mg in 1 study and 20 mg in another. In both of these studies, all patients consumed the entire ethanol dose within 10 minutes of starting. In one of these studies, blood ethanol concentrations of 0.08% were confirmed. In these two studies, more patients had clinically significant decreases in blood pressure on the combination of tadalafil and ethanol as compared to ethanol alone. Some subjects reported postural dizziness, and orthostatic hypotension was observed in some subjects. When tadalafil 20 mg was administered with a lower dose of ethanol (0.6 g/kg, which is equivalent to approximately 4 ounces of 80-proof vodka, administered in less than 10 minutes), orthostatic hypotension was not observed, dizziness occurred with similar frequency to ethanol alone, and hypotensive effects of ethanol were not potentiated. Tadalafil did not affect ethanol plasma concentrations and ethanol did not affect tadalafil plasma concentrations. It should be noted that during once daily administration of tadalafil, the presence of continuous plasma tadalafil concentrations may change the potential for an interaction when a substantial amount of ethanol is consumed.^[6]

Nilotinib is a competitive inhibitor of CYP3A4, and tadalafil is a CYP3A4 substrate.^[11][12] Concurrent administration of the CYP3A4 substrate midazolam with nilotinib increased midazolam exposure by 30%. Caution should be exercised when coadministering nilotinib with CYP3A4 substrates, especially substrates with a narrow therapeutic index.^[12]

Sapropterin acts as a cofactor in the synthesis of nitric oxide and may cause vasorelaxation. Caution should be exercised when administering sapropterin in combination with drugs that affect nitric oxide-mediated vasorelaxation such as tadalafil. When given together these agents may produce an additive reduction in blood pressure. The combination of sapropterin and a phosphodiesterase inhibitor did not significantly reduce blood pressure when administered concomitantly in animal studies. The additive effect of these agents has not studied been in humans.^[13]

Nifedipine can have additive hypotensive effects when administered with phosphodiesterase inhibitors (PDE 5 inhibitors).^[14] The patient should be monitored carefully and the dosage should be adjusted based on clinical response. Vardenafil (20 mg) did not affect the AUC or Cmax of slow-release nifedipine (30 or 60 mg daily), which is metabolized by CYP3A4.^[15] Nifedipine did not alter plasma levels of vardenafil.^[15] In patients whose hypertension was controlled with nifedipine, vardenafil produced mean additional supine systolic/diastolic blood pressure reductions of 6/5 mm Hg compared to placebo.^[15]

Potent inhibitors of CYP3A4, such as telithromycin, may reduce tadalafil clearance; tadalafil is metabolized predominantly by CYP3A4. Increased systemic exposure to tadalafil may result in increased associated adverse events including hypotension, syncope, visual changes, and prolonged erection. The manufacturer of tadalafil recommends that in patients receiving concomitant potent CYP3A4 inhibitors, the ‘as needed’ dose for erectile dysfunction should not exceed 10 mg within a 72 hour time period, and the ‘once-daily’ dose for erectile dysfunction or benign prostatic hyperplasia should not exceed 2.5 mg (see Dosage). It should be noted that during once daily administration of tadalafil, the presence of continuous plasma tadalafil concentrations may change the potential for interactions with potent inhibitors of CYP3A4. When used for pulmonary arterial hypertension, tadalafil should not be co-administered with potent CYP3A inhibitors.^[6][16]

Tadalafil, when used for pulmonary arterial hypertension (PAH), is contraindicated with telaprevir. Coadministration of telaprevir with phosphodiesterase type 5 (PDE5) inhibitors is expected to substantially increase their plasma concentrations and may result in increased associated adverse events including hypotension, syncope, visual changes, and prolonged erection. Telaprevir can be used cautiously with tadalafil for erectile dysfunction; use tadalafil at a reduced dose of 10 mg no more frequently than every 72 hours with increased monitoring for adverse reactions.^[3][17]

Studies have shown that tadalafil does not inhibit or induce cytochrome P450 (CYP) enzymes 1A2, 3A4, 2C9, 2C19, 2D6, and 2E1. Therefore, tadalafil is not expected to cause clinically significant inhibition or induction of the clearance of drugs metabolized by CYP enzymes. When tadalafil was administered with theophylline, a CYP1A2 substrate, a small augmentation (3 beats per minute) of the increase in heart rate associated with theophylline was observed. However, tadalafil had no clinically significant effect on the pharmacokinetics of theophylline. Tadalafil had no clinically significant on the AUCs of the CYP3A4 substrates midazolam or lovastatin. Additionally, no clinically significant effect was observed on S-warfarin and R-warfarin AUC when coadministered with tadalafil; prothrombin time changes induced by warfarin were not affected by tadalafil.^[6]

Tadalafil and other PDE5 inhibitors are mild systemic vasodilators. Studies were conducted to assess the interaction of tadalafil 10 mg and sustained-release metoprolol (25 to 200 mg daily), bendroflumethiazide (2.5 mg daily), or enalapril (10 to 20 mg daily). Following dosing of tadalafil with metoprolol, the mean reduction in supine systolic/diastolic blood pressure was 5/3 mmHg, compared to placebo. After dosing of tadalafil with bendroflumethiazide, the mean reduction in supine systolic/diastolic blood pressure was 6/4 mmHg, compared to placebo. Following dosing of tadalafil with enalapril, the mean reduction in supine systolic/diastolic blood pressure was 4/1 mmHg, compared to placebo.^[6]

Tadalafil and other PDE5 inhibitors are mild systemic vasodilators. A study was conducted to assess the interaction of tadalafil 20 mg and angiotensin II receptor blockers. Study subjects were taking any marketed angiotensin II receptor blocker, either alone, as a component of a combination product, or as part of a multiple antihypertensive regimen. Following dosing, ambulatory measurements of blood pressure revealed differences between tadalafil and placebo of 8/4 mmHg in systolic/diastolic blood pressure.^[6]

The increase in pH associated with nizatidine administration had no significant effect on tadalafil pharmacokinetics. Additionally, simultaneous administration of an antacid (magnesium hydroxide; aluminum hydroxide) and tadalafil reduced the apparent rate of absorption of tadalafil without altering the AUC of tadalafil.^[6]

Post-marketing data list headache, flushing, nasal congestion, dyspepsia, and back pain among the most frequently reported adverse events and these tend to be dose-dependent and self-limited^[20].

Musculoskeletal discomfort (myalgia, limb pain) usually surfaces 12-24 hours after dosing, peaks at 48 hours, and resolves within 72 hours; proposed mechanisms include PDE11 inhibition in skeletal muscle and transient vasodilatation^[21].

Ocular events are rare but clinically important. Case reports link tadalafil to NAION, characterized by painless unilateral visual loss and optic-disc edema, most often within 24-48 hours of dosing; at-risk individuals require counseling about prodromal visual phenomena^[22].

The FDA has mandated label warnings for sudden sensorineural hearing loss after accumulating reports in users of PDE5 inhibitors, including tadalafil; audiologic evaluation is imperative if acute hearing changes occur^[23].

Under the Pregnancy and Lactation Labeling Rule, tadalafil lacks adequate human data; animal reproduction studies show no embryotoxicity or teratogenicity at exposures up to eight times the maximum recommended human dose, yet placental transfer has been demonstrated in animal models, so human fetal risk cannot be ruled out^[24].

Experimental work in a rat model of pre-eclampsia suggests that maternal tadalafil improves uteroplacental blood flow and reduces fetal growth restriction, but translation to clinical practice remains investigational and off-label^[25].

Excretion into human milk is undetermined; however, molecular weight and protein binding predict minimal passage. Until robust data are available, lactating patients should be advised to weigh therapeutic necessity against potential infant exposure^[26].

Tadalafil tablets should be stored at controlled room temperature, 20-25 °C (68-77 °F), with excursions permitted to 15-30 °C; containers must be moisture-tight and protected from excessive light to prevent hydrolysis and polymorphic conversion^[30].

1. U.S. Food and Drug Administration. (2011). CIALIS (tadalafil) tablets, for oral use: Prescribing information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/021368s20s21lbl.pdf 2.Wikipedia contributors. (2025, July 9). PDE5 inhibitor. https://en.wikipedia.org/wiki/PDE5_inhibitor 3.Pachankis, A. (2023, December 14). How does Cialis (tadalafil) work? Verywell Health. https://www.verywellhealth.com/this-is-how-cialis-works-7967620 4.Siddiqui, D. et al. (2025, April 16). What are the pharmacokinetics of tadalafil (Cialis)? DrOracle.ai. https://www.droracle.ai/articles/76845/what-are-the-pharmacokinetics-of-tadalafil 5.Kloner, R. A., & Zusman, R. M. (2003). Time course of the interaction between tadalafil and nitrates. Journal of the American College of Cardiology, 42, 1855-1859. https://doi.org/10.1016/S0735-1097(03)01293-2 6.DailyMed. (2025). Tadalafil tablets: Label information (set ID 34684fe8-9bf3-47fd-e063-6394a90ac80f). https://dailymed.nlm.nih.gov/dailymed/downloadpdffile.cfm?setId=34684fe8-9bf3-47fd-e063-6394a90ac80f 7.Sims, C. et al. (2009). Tadalafil therapy for pulmonary arterial hypertension. Circulation, 120, 982-991. https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.108.839274 8.Elsevier. (2024). Tadalafil - overview. ScienceDirect Topics. https://www.sciencedirect.com/topics/medicine-and-dentistry/tadalafil 9.American College of Cardiology. (2022, April 27). Adverse events associated with co-prescription of PDE5 inhibitors and nitrates. https://www.acc.org/Latest-in-Cardiology/Journal-Scans/2022/04/27/18/47/Adverse-Events-Associated-With-Coprescription 10.Haefner, C. (2014, March 10). Tadalafil helps twice with BPH. Verywell Health. https://www.verywellhealth.com/tadalafil-helps-twice-with-benign-prostatic-hyperplasia-1123906 11.Porst, H. et al. (2005). Safety and efficacy of tadalafil 5 mg dosed once daily. The Journal of Sexual Medicine, 5, 2160-2168. https://academic.oup.com/jsm/article-abstract/5/9/2160/6862525 12.National Institute for Health and Care Excellence. (2025). Tadalafil: Drug interactions. https://bnf.nice.org.uk/interactions/tadalafil/ 13.Pomeranz, H. D. (2002). Tadalafil-associated anterior ischemic optic neuropathy. JAMA Ophthalmology, 120, 1460-1461. https://jamanetwork.com/journals/jamaophthalmology/fullarticle/416888 14.DailyMed. (2025). Tadalafil tablets: Label highlights - hepatic impairment (set ID 2c277890-3c5d-5fd5-e063-6394a90af15b). https://dailymed.nlm.nih.gov/dailymed/fda/fdaDrugXsl.cfm?setid=2c277890-3c5d-5fd5-e063-6394a90af15b 15.Drugs.com. (2025). Cialis disease interactions. https://www.drugs.com/disease-interactions/tadalafil%2Ccialis.html 16.HelloPharmacist. (2024). Ketoconazole-tadalafil interaction. https://hellopharmacist.com/drug-interactions/drugs/ketoconazole/ketoconazole-with-tadalafil 17.Stanley, M. (2016). Drug interactions with CYP3A4: An update. Pharmacy Times. https://www.pharmacytimes.com/view/drug-interactions-with-cyp3a4-an-update 18.Uckert, S. et al. (2006). Hemodynamic interaction of tadalafil with alfuzosin. The Journal of Urology, 176, 1364-1368. https://www.sciencedirect.com/science/article/pii/S009042950600063X 19.Li, Y. et al. (2020). Effect of grapefruit juice on the pharmacokinetics of tadalafil in rats. BioMed Research International, 2020, 1631735. https://doi.org/10.1155/2020/1631735 20.Drugs.com. (2025). Tadalafil side effects. https://www.drugs.com/sfx/tadalafil-side-effects.html 21.Kohler, T. S. et al. (2004). Tadalafil for erectile dysfunction. American Family Physician, 70, 359-366. https://www.aafp.org/pubs/afp/issues/2004/0715/p359.html 22.Miller, D. E. (2023). PDE5 inhibitors and vision changes: More than meets the eye. Chest, 164(4), A54. https://journal.chestnet.org/article/S0012-3692(23)04929-2/fulltext 23.Thompson, C. (2007, October 12). FDA warning: ED drugs and sudden hearing loss. Wired Magazine. https://www.wired.com/2007/10/fda-warning-ere 24.U.S. Food and Drug Administration. (2025). Pregnancy and lactation labeling resources. https://www.fda.gov/drugs/labeling-information-drug-products/pregnancy-and-lactation-labeling-resources 25.Shimada, M. et al. (2020). Prophylactic tadalafil in a rat model of pre-eclampsia. Placenta, 101, 15-22. https://www.sciencedirect.com/science/article/pii/S0143400420301831 26.E-Lactancia. (2017). Tadalafil and breastfeeding. https://www.e-lactation.com/en/tadalafil-pr/ 27.Bridgman, C. (2024, June 1). Tadalafil dosage: Strengths and timing. Medical News Today. https://www.medicalnewstoday.com/articles/drugs-tadalafil-dosage 28.Central Texas Urology. (2024). Maximum dose of tadalafil in 24 hours. https://www.centraltexasurology.com/maximum-dose-of-tadalafil-in-24-hours/ 29.Drugs.com. (2025). Cialis dosage guide. https://www.drugs.com/dosage/cialis.html 30.Salispharm. (2024). How should tadalafil powder be stored? https://www.salispharm.com/knowledge/how-should-tadalafil-powder-be-stored 31.U.S. Food and Drug Administration. (2025). Clinical pharmacology review-NDA 218527. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2025/218527Orig1s000ClinPharmR.pdf 32.Carandang, K. (2022, March 5). 8 medications that could be damaging your ears. AARP. https://www.aarp.org/health/conditions-treatments/medications-that-harm-hearing/ 33.MedEx. (2025). Tadalafil: Pregnancy and lactation. https://medex.com.bd/generics/1029/tadalafil 34.Livestrong Editorial Team. (2023). Grapefruit & Cialis. https://www.livestrong.com/article/488362-grapefruit-cialis/ 35.McGwin, G. (2010). PDE-5 inhibitor use and hearing impairment. JAMA Otolaryngology, 136, 1367-1372. https://jamanetwork.com/journals/jamaotolaryngology/fullarticle/496308 36.WellWisp. (2025). How often can I take tadalafil? https://wellwisp.com/how-often-can-i-take-tadalafil/ 37.PharmaGiant. (2024). Mixing Cialis and alcohol: Risks and precautions. https://pharmagiant.com/cialis-with-alcohol/ 38.Drugs.com. (2025). Ketoconazole and tadalafil interactions. https://www.drugs.com/drug-interactions/ketoconazole-with-tadalafil-1412-0-2144-0.html 39.Tadacip Information Center. (2023). Tadalafil interactions and precautions. https://tadacip.org/interactions-and-precautions/ 40.Kadanu, N. (2018). Interaction between tadalafil and doxazosin/tamsulosin. The Journal of Urology, 199(suppl), e562. https://www.auajournals.org/doi/pdf/10.1016/S0022-5347(18)38432-5 41.Drugs.com. (2025). Tadalafil (pulmonary hypertension) monograph. https://www.drugs.com/monograph/tadalafil-pulmonary-hypertension.html Disclaimer: This compounded medication is prepared under section 503A of the U.S. Federal Food, Drug, and Cosmetic Act. Safety and efficacy for this formulation have not been evaluated by the FDA. Therapy should be initiated and monitored only by qualified healthcare professionals.

Can tadalafil cause hearing problems?
Sudden decreases or loss of hearing, sometimes with tinnitus or dizziness, have been reported; any acute auditory change warrants immediate discontinuation and otologic evaluation^[32].

Is tadalafil safe during pregnancy?
Human data are limited and the drug is generally avoided unless potential maternal benefit clearly outweighs theoretical fetal risks^[33].

Why should I avoid grapefruit while on tadalafil?
Compounds in grapefruit juice inhibit metabolism and may raise drug levels, increasing headache or hypotension risk^[34].

How common is sudden hearing loss with PDE5 inhibitors?
Population studies suggest it is rare, but the association is significant enough for regulatory warnings, so vigilance is advised^[35].

How often can I take tadalafil safely?
On-demand regimens should not exceed one dose per 24 hours, while once-daily regimens use lower fixed doses and rely on steady-state exposure^[36].

May I drink alcohol with my dose?
Moderate alcohol may amplify vasodilatation and dizziness; patients should limit intake to two units or less and monitor blood pressure^[37].

Do antifungal agents interact with tadalafil?
Yes-azoles such as ketoconazole markedly increase exposure, so lower tadalafil doses or extended intervals are required^[38].

Can tadalafil be taken with other erectile-dysfunction drugs?
Combining PDE5 inhibitors or adding prostaglandin analogs can raise priapism risk and is generally discouraged unless under specialist supervision^[39].

Is it safe to combine tadalafil with tamsulosin for BPH?
Clinical trials show the combination is usually tolerated if doses are stabilized, but blood-pressure monitoring for additive hypotension is prudent^[40].

Does tadalafil help pulmonary arterial hypertension in all patients?
It may improve exercise capacity and hemodynamics in WHO group I PAH, yet off-label use requires expert evaluation and careful titration^[41].