Medications · October 3, 2026 · Memios · 23 min read

Tadalafil

Tadalafil does not create arousal; it amplifies a signal that only appears when nitric oxide is already being released.

TadalafilCialisAdcircaAlyqmedicine research
Photograph for Tadalafil: plain unmarked tablets in a dish beside a glass of water on pale linen.

TLDR

  • Well established. Tadalafil does not create arousal; it amplifies a signal that only appears when nitric oxide is already being released.
  • What it is: Tadalafil is a small synthetic molecule that selectively blocks phosphodiesterase type 5, the enzyme that breaks down cyclic GMP in smooth muscle.
  • Main use: Erectile dysfunction (well supported).
  • Other approved uses: Lower urinary tract symptoms of benign prostatic hyperplasia, alone or with erectile dysfunction (well supported); Pulmonary arterial hypertension (sold as Adcirca and generics) (well supported).
  • Uses NOT supported by research: Duchenne muscular dystrophy.
  • Recommended dose (official position): Dose is set by the prescriber, not by the reader. As a position, the FDA-approved Cialis labelling (Eli Lilly) describes a starting dose of 10 mg before anticipated sexual activity, adjustable to 20 mg or 5 mg, and 2.5 mg for once-daily use.
  • Studied dose (a trial dose, not a recommendation): PHIRST randomised patients with pulmonary arterial hypertension to placebo or tadalafil 2.5, 10, 20 or 40 mg once daily for 16 weeks; only 40 mg met the prespecified significance level. Findings citing that trial: 1 for, 1 against.
  • Upper limit: There is no upper intake level in the nutritional sense.
  • What goes wrong: 4 findings on harm. In the same pooled trials, stopping treatment because of an adverse event was about 1.8 times more likely on tadalafil than on placebo.
  • Interactions: 7 recorded, including Organic nitrates (nitroglycerin, isosorbide mononitrate or dinitrate, amyl nitrite), Riociguat and other guanylate cyclase stimulators, Alcohol, Grapefruit juice.
  • Common myth: Tadalafil is an aphrodisiac that gives you an erection, and the stronger drug is the better drug.

What it is

Tadalafil is a small synthetic molecule that selectively blocks phosphodiesterase type 5, the enzyme that breaks down cyclic GMP in smooth muscle. It is chemically distinct from sildenafil and much longer-acting: the mean terminal half-life is about 17.5 hours, which is why it can be taken either before sex or as a low daily dose. It is cleared mainly by CYP3A4 in the liver and excreted mostly in the faeces. The same molecule is sold under different brand names and strengths for erectile dysfunction, for prostate symptoms and for pulmonary arterial hypertension.

What the research says

Tadalafil does not create arousal; it amplifies a signal that only appears when nitric oxide is already being released. For erectile dysfunction a network meta-analysis of 82 randomised trials in 47,626 men found tadalafil 10 mg gave intermediate efficacy with the lowest overall rate of adverse events among starting doses. For prostate symptoms a meta-analysis of 13 placebo-controlled trials in 3,973 men found tadalafil 5 mg once daily improved symptom scores, though discontinuations for adverse events were more common than on placebo (odds ratio 1.79). For pulmonary arterial hypertension the 405-patient PHIRST trial found only the 40 mg dose reached significance, with a placebo-corrected gain of 33 m in six-minute walk distance and no significant change in WHO functional class. Where it has been tried outside these uses it has failed: a phase 3 trial in 331 boys with Duchenne muscular dystrophy found no effect at all on walking decline. Common adverse effects are headache, indigestion, back pain and muscle ache; rare ones include sudden hearing loss and a small absolute risk of non-arteritic anterior ischaemic optic neuropathy. It must never be combined with nitrates.

Evidence grade: Well established.

How it works

Drug class: Phosphodiesterase type 5 (PDE5) inhibitor

Sexual stimulation makes nerve endings and the lining of blood vessels release nitric oxide, which tells smooth muscle to make cyclic GMP. Cyclic GMP relaxes the muscle so blood flows in. PDE5 is the enzyme that destroys cyclic GMP; tadalafil blocks it, so the cyclic GMP signal lasts longer and the relaxation is stronger. Because nitric oxide has to come first, the drug does nothing without sexual stimulation. The same enzyme sits in the smooth muscle of the prostate, the bladder and the lung arteries, which is why one molecule is used for three different conditions, although the label concedes the reason prostate symptoms improve is not established. (Source 1)

What it is used for

  • Large randomised evidence. In a network meta-analysis of 82 trials and 47,626 men, tadalafil 10 mg had intermediate efficacy among PDE5 inhibitors but the lowest overall adverse event rate; sildenafil 50 mg was more effective but less well tolerated. Evidence: established. (Source 2)
  • Thirteen placebo-controlled trials in 3,973 men show symptom scores improve on tadalafil 5 mg once daily over 12 weeks. Discontinuation for adverse events was about 1.8 times more likely than on placebo. The label admits the mechanism for the prostate benefit is not established. Evidence: established. (Source 3)
  • In the 405-patient PHIRST trial only the 40 mg once-daily dose met the prespecified significance level, with a placebo-corrected improvement of 33 m in six-minute walk distance and less clinical worsening. Functional class did not change significantly. Evidence: established. (Source 4)
  • Tested and failed. A phase 3 placebo-controlled trial in 331 boys aged 7 to 14 found no effect on six-minute walk distance or on any secondary outcome, and the authors graded it Class I evidence of no benefit. Evidence: not-supported. (Source 5)

Interactions

  • Organic nitrates (nitroglycerin, isosorbide mononitrate or dinitrate, amyl nitrite) (clinical trial): Absolutely contraindicated. Both drugs push the same nitric oxide pathway, and together they can drop blood pressure dangerously. This applies to regular and occasional nitrate use, including recreational nitrites. (Source 6)
  • Riociguat and other guanylate cyclase stimulators (label): Not to be combined. These drugs also raise cyclic GMP, so blood pressure can fall too far. (Source 6)
  • Alcohol (clinical trial): Both are mild vasodilators, so together they can lower blood pressure more than either alone. The labelling singles out substantial drinking, five units or more, as the point where dizziness, headache, a faster heart rate and a drop in standing blood pressure become more likely. (Source 7)
  • Grapefruit juice (theoretical): Grapefruit juice inhibits CYP3A4, the enzyme that clears tadalafil, so it would be expected to raise tadalafil levels. This is an extrapolation rather than a measured result: the manufacturer states the specific interaction has not been studied. (Source 8)
  • Strong CYP3A4 inhibitors: ritonavir, ketoconazole, itraconazole (pharmacokinetic study): These slow the breakdown of tadalafil, so exposure rises and the labelling caps the dose that may be used. (Source 7)
  • CYP3A4 inducers: rifampin, carbamazepine, phenytoin, phenobarbital (and by the same mechanism St John's wort) (pharmacokinetic study): Enzyme inducers strip tadalafil out of the blood. Rifampin cut single-dose exposure by 88%, and the labelling expects other inducers to do the same and to reduce how well the drug works. St John's wort is a herbal CYP3A4 inducer, but we found no published study of it with tadalafil specifically. (Source 9)
  • Food generally (label): No meaningful interaction. Unlike sildenafil, tadalafil absorption is not altered enough by a meal to matter, so it can be taken with or without food. (Source 10)

Stopping it

  • No dependence or withdrawal syndrome is described for tadalafil in the literature we read. In the as-needed regimen it is taken only before sexual activity, so there is nothing to taper. (Source 11)
  • People do stop it, but mostly not because of side effects. In a systematic review of 44 studies of tadalafil for prostate symptoms, about 12.8% discontinued overall, 4.56% for adverse events and 3.30% for lack of effect. The drug clears quickly once stopped, with a mean terminal half-life of 17.5 hours, so the effect simply wears off. (Source 12)

What goes wrong

In the same pooled trials, stopping treatment because of an adverse event was about 1.8 times more likely on tadalafil than on placebo. (Source 3)

  • Meta-analysis, Moderate certainty.
  • Size: 13 randomised placebo-controlled trials, 3,973 patients.
  • Who: Men with lower urinary tract symptoms, with or without erectile dysfunction.
  • How long: 12 weeks.
  • Result: Discontinuation due to adverse event odds ratio 1.79 (95% CI 1.12 to 2.85, P = 0.01), which the authors nonetheless read as good tolerability.
  • Funding: not stated.

Safety assessments included discontinuations due to adverse event (odds ratio (OR) = 1.79, 95% CI = 1.12-2.85, P = 0.01) indicated that tadalafil 5 mg once-daily was well tolerated.

Pooled observational data found no overall link between PDE5 inhibitor use and sudden ischaemic optic nerve damage, but the tadalafil subgroup showed roughly a doubling of risk. (Source 13)

  • Meta-analysis, Very low certainty.
  • Size: 5 articles with 6 clinical observations, all observational.
  • Who: Men exposed to PDE5 inhibitors, compared with unexposed periods or people.
  • How long: Risk assessed within a 1-month window of use.
  • Result: Overall unadjusted RR 1.16 (95% CI 0.98 to 1.39, P = .09); tadalafil subgroup RR 2.14 (95% CI 1.20 to 3.84, P = .01); sildenafil RR 2.25 (1.29 to 3.94)
  • Funding: not stated.

Limit of this finding: This meta-analysis does not agree with itself. The headline result is "no significant higher risk" (RR 1.16, 95% CI 0.98 to 1.39), yet both drug-specific subgroups are reported as significant and their point estimates (tadalafil 2.14, sildenafil 2.25) lie outside that overall interval, which should not normally happen. The pooled figures are also unadjusted for age, diabetes, blood pressure and smoking, all of which independently raise the risk of this eye condition. Neither half should be quoted alone: the honest reading is that the observational data are unsettled.

Subgroup analyses indicated 2 PDE5-Is were significantly related to NAION (tadalafil: RR = 2.14, 95% CI = 1.20-3.84, P = .01; sildenafil: RR = 2.25, 95% CI = 1.29-3.94, P = .004).

In the placebo-controlled daily-dosing trials, 4.1% of men on tadalafil stopped because of adverse events compared with 2.8% on placebo. (Source 14)

  • Official position, Certainty not rated.
  • Size: Three placebo-controlled trials pooled in the labelling.
  • Who: Men with erectile dysfunction, mean age 58 (range 21 to 82)
  • How long: 12 or 24 weeks.
  • Result: Discontinuation for adverse events 4.1% on tadalafil versus 2.8% on placebo in the three once-daily trials; in the label's once-daily table the reactions reported by at least 2% of men were headache (5 mg 6%, 2.5 mg 3%, placebo 5%), dyspepsia (5%, 4%, 2%), nasopharyngitis (3%, 4%, 4%), back pain (3%, 3%, 1%), upper respiratory tract infection (3%, 3%, 1%) and flushing (3%, 1%, 1%)
  • Funding: manufacturer data summarised in regulator-approved labelling.

Limit of this finding: These percentages come from the label's once-daily table (2.5 mg and 5 mg), not from the as-needed table for 10 mg and 20 mg, where the figures are higher - headache 11% to 15% and dyspepsia 8% to 10% against 5% and 1% on placebo. The label heads the once-daily table "more frequent on drug than placebo", yet nasopharyngitis is listed at 3% on 5 mg against 4% on placebo, so the table does not entirely match its own heading.

the discontinuation rate due to adverse events in patients treated with tadalafil was 4.1%, compared to 2.8% in placebo-treated patients.

Sudden partial or total hearing loss has been reported in time association with PDE5 inhibitors including tadalafil, though causation is not established. (Source 15)

  • Official position, Very low certainty.
  • Size: Spontaneous reports; no rate given.
  • Who: Users of PDE5 inhibitors.
  • How long: Not stated.
  • Result: No frequency given; events may be accompanied by tinnitus and dizziness, and the labelling states it is not possible to determine whether they are directly drug-related.
  • Funding: regulator-approved labelling.

Physicians should advise patients to stop taking PDE5 inhibitors, including CIALIS, and seek prompt medical attention in the event of sudden decrease or loss of hearing.

What the evidence supports

Among PDE5 inhibitor starting doses, tadalafil 10 mg gave intermediate efficacy for erectile dysfunction with the lowest overall rate of adverse events. (Source 2)

  • Meta-analysis, Moderate certainty.
  • Size: 82 trials with 47,626 patients for efficacy; 72 trials with 20,325 patients for adverse events.
  • Who: Men with erectile dysfunction in randomised trials against placebo or another PDE5 inhibitor.
  • How long: Varied by trial.
  • Result: Sildenafil 50 mg had the greatest efficacy and the highest overall adverse event rate; tadalafil 10 mg had intermediate efficacy and the lowest overall adverse event rate; vardenafil 10 mg and avanafil 100 mg had similar adverse events to sildenafil 50 mg but markedly lower global efficacy.
  • Funding: not stated.

In the trade-off analysis of starting dosages, sildenafil 50mg had the greatest efficacy but also had the highest rate of overall adverse events. Tadalafil 10mg had intermediate efficacy but had the lowest overall rate of all adverse events.

Tadalafil 5 mg once daily improved prostate symptom scores and erectile function against placebo in pooled randomised trials. (Source 3)

  • Meta-analysis, Moderate certainty.
  • Size: 13 randomised double-blind placebo-controlled trials, 3,973 patients.
  • Who: Men with lower urinary tract symptoms suggestive of benign prostatic hyperplasia, with or without erectile dysfunction.
  • How long: 12 weeks.
  • Result: Total IPSS standardised mean difference -2.02 (95% CI -2.52 to -1.53, P < 0.00001); BPH Impact Index SMD -0.58 (95% CI -0.84 to -0.33); IIEF erectile function domain SMD 5.18 (95% CI 4.13 to 6.23)
  • Funding: not stated.

Thirteen publications involving a total of 3973 patients were used in the analysis, including 13 RCTs that compared tadalafil 5 mg once-daily with placebo.

In pulmonary arterial hypertension only the 40 mg dose met the prespecified significance level, improving six-minute walk distance by 33 m over placebo. (Source 4)

  • Randomized trial, Moderate certainty.
  • Size: 405 patients randomised to placebo or tadalafil 2.5, 10, 20 or 40 mg once daily.
  • Who: Patients with idiopathic or associated pulmonary arterial hypertension, treatment-naive or on background bosentan.
  • How long: 16 weeks double-blind, with an optional long-term extension.
  • Result: Mean placebo-corrected treatment effect 33 m (95% CI 15 to 50 m); 44 m (20 to 69) in bosentan-naive patients versus 23 m (-2 to 48) on background bosentan; time to clinical worsening improved (P=0.041) with a 68% relative risk reduction in incidence (P=0.038)
  • Funding: not stated in the recorded passage; PHIRST was a manufacturer-sponsored registration trial.

Overall, the mean placebo-corrected treatment effect was 33 m (95% confidence interval, 15 to 50 m).

What the evidence does not support

In the same trial, WHO functional class did not improve significantly, and the lower doses did not reach the prespecified significance level. (Source 4)

  • Randomized trial, Moderate certainty.
  • Size: 405 patients across five arms.
  • Who: Patients with pulmonary arterial hypertension.
  • How long: 16 weeks.
  • Result: Only the 40 mg dose met the prespecified level of statistical significance (P<0.01); changes in WHO functional class were not statistically significant.
  • Funding: not stated in the recorded passage.

The changes in World Health Organization functional class were not statistically significant.

Tadalafil did not slow the loss of walking ability in boys with Duchenne muscular dystrophy. (Source 5)

  • Randomized trial, High certainty.
  • Size: 331 participants randomised to tadalafil 0.3 mg/kg/day, 0.6 mg/kg/day or placebo.
  • Who: Boys aged 7 to 14 with Duchenne muscular dystrophy taking glucocorticoids.
  • How long: 48 weeks.
  • Result: 48-week decline in six-minute walk distance 51.0 +/- 9.3 m on placebo, 64.7 +/- 9.8 m on low-dose tadalafil (p = 0.307) and 59.1 +/- 9.4 m on high dose (p = 0.538); no effect on secondary outcomes; graded Class I evidence of no benefit.
  • Funding: not stated in the recorded passage; conducted as a registration-scale phase 3 programme.

Tadalafil had no effect on the primary outcome: 48-week declines in 6MWD were 51.0 ± 9.3 m with placebo, 64.7 ± 9.8 m with low-dose tadalafil (p = 0.307 vs placebo), and 59.1 ± 9.4 m with high-dose tadalafil (p = 0.538 vs placebo).

Where the evidence is mixed

The authors of that meta-analysis warned their own result should be read cautiously because only observational studies were available and confounding could not be controlled. (Source 16)

  • Meta-analysis, Very low certainty.
  • Size: 5 observational articles.
  • Who: PDE5 inhibitor users.
  • How long: Not applicable.
  • Result: No overall association; the authors called for prospective comparative studies with larger samples and more rigorous designs.
  • Funding: not stated.

Limit of this finding: The authors call their own result "no association" even though the two drug subgroups they report were statistically significant, so their conclusion and their numbers do not sit comfortably together. The pooled risk ratios were also unadjusted for other risk factors, which the conclusion does not mention.

Although we found no association between NAION and PDE5-I use, our results should be interpreted cautiously because we included only observational studies and could not control for potential confounders.

The pooled risk ratios in that meta-analysis were not adjusted for other risk factors. (Source 17)

  • Meta-analysis, Very low certainty.
  • Size: 5 observational articles with 6 clinical observations.
  • Who: Men prescribed PDE5 inhibitors in observational datasets.
  • How long: Risk assessed within a 1-month window after exposure.
  • Result: Summarised risk ratios were unadjusted; the review followed MOOSE guidance and was registered in PROSPERO as CRD42017080865.
  • Funding: not stated.

Limit of this finding: "Unadjusted" means the figures take no account of how men prescribed these drugs differ from men who are not - older age, diabetes, high blood pressure, smoking - and every one of those independently raises the risk of this eye condition. An unadjusted number can therefore overstate or understate the drug's own contribution, and should not be read as the effect of tadalafil itself.

Summarized unadjusted risk ratios (RRs) with 95% CIs were calculated for the strength of this association.

About one in eight men on tadalafil for prostate symptoms stopped treatment, most often for reasons other than adverse events. (Source 18)

  • Systematic review, Low certainty.
  • Size: 44 studies including 1,724 patients who discontinued.
  • Who: Men treated with tadalafil alone or with an alpha-blocker for lower urinary tract symptoms, with or without erectile dysfunction.
  • How long: Varied by study, to May 2022.
  • Result: Combined discontinuation rate 12.78% (95% CI 9.89 to 15.98); discontinuation for adverse events 4.56% (3.39 to 5.90); for lack of efficacy 3.30% (1.53 to 5.72)
  • Funding: not stated.

The combined discontinuation rate was 12.78% (95% confidence interval (CI) 9.89-15.98%), and the discontinuation rates because of adverse events and lack of efficacy were 4.56% (95% CI 3.39-5.90%) and 3.30% (95% CI 1.53-5.72%), respectively.

Where the research disagrees

Whether tadalafil raises the risk of sudden ischaemic damage to the optic nerve (NAION) - a disagreement inside a single meta-analysis, whose pooled risk ratios were unadjusted for other risk factors

  • Liu and colleagues, Sexual Medicine 2018, headline result, meta-analysis of 5 observational studies: No significant higher risk of NAION was observed after the use of PDE5-Is within a 1-month period (RR = 1.16, 95% CI = 0.98-1.39, P = .09). (Source 13)
  • The same meta-analysis, drug-specific subgroup, subgroup of the same observational data, unadjusted: Subgroup analyses indicated 2 PDE5-Is were significantly related to NAION (tadalafil: RR = 2.14, 95% CI = 1.20-3.84, P = .01; sildenafil: RR = 2.25, 95% CI = 1.29-3.94, P = .004). (Source 13)

Whether tadalafil's tolerability in prostate-symptom trials should be called good

  • Gong and colleagues, Lower Urinary Tract Symptoms 2018, meta-analysis of 13 placebo-controlled RCTs: Safety assessments included discontinuations due to adverse event (odds ratio (OR) = 1.79, 95% CI = 1.12-2.85, P = 0.01) indicated that tadalafil 5 mg once-daily was well tolerated. (Source 3)
  • FDA-approved Cialis labelling (Eli Lilly), pooled manufacturer trial data as a regulatory position: the discontinuation rate due to adverse events in patients treated with tadalafil was 4.1%, compared to 2.8% in placebo-treated patients. (Source 14)

How much

  • Reference intake: Dose is set by the prescriber, not by the reader. As a position, the FDA-approved Cialis labelling (Eli Lilly) describes a starting dose of 10 mg before anticipated sexual activity, adjustable to 20 mg or 5 mg, and 2.5 mg for once-daily use. (Source 12)
  • Upper limit: There is no upper intake level in the nutritional sense. As a position, the Cialis labelling caps as-needed dosing at once per day in most patients, with a maximum of 10 mg every 72 hours for people on strong CYP3A4 inhibitors and 2.5 mg for once-daily use in that situation. (Source 6)
  • Studied: PHIRST randomised patients with pulmonary arterial hypertension to placebo or tadalafil 2.5, 10, 20 or 40 mg once daily for 16 weeks; only 40 mg met the prespecified significance level. (Source 4)
  • Studied: The pooled prostate-symptom trials used tadalafil 5 mg once daily over 12 weeks. (Source 3)
  • Studied: The Duchenne muscular dystrophy trial used weight-based daily dosing of 0.3 and 0.6 mg per kg for 48 weeks. (Source 5)

A common belief, and what the research shows

The belief: Tadalafil is an aphrodisiac that gives you an erection, and the stronger drug is the better drug.

What the research shows: It does neither. The label is explicit that without sexual stimulation there is no nitric oxide release and therefore no drug effect: "Because sexual stimulation is required to initiate the local release of nitric oxide, the inhibition of PDE5 by tadalafil has no effect in the absence of sexual stimulation." And more potency is not automatically better: in a network meta-analysis of 82 trials, "Tadalafil 10mg had intermediate efficacy but had the lowest overall rate of all adverse events." Where the drug has been tested outside its licensed uses it has also failed outright, as in Duchenne muscular dystrophy.

Questions and answers

What is it?

Tadalafil is a synthetic tablet medicine, one of the PDE5 inhibitors, the same family as sildenafil. What sets it apart is how long it lasts: the average half-life is about 17.5 hours, so a single dose can still be working a day or more later, and a low dose can be taken every day instead. The same molecule is sold under one brand name for erection problems and prostate symptoms and another for a lung artery condition. (Source 1)

What does it do in the body?

It protects a chemical messenger rather than creating one. Sexual stimulation releases nitric oxide, which makes cyclic GMP, which relaxes smooth muscle so blood flows in. PDE5 destroys cyclic GMP, and tadalafil blocks PDE5, so the relaxation is stronger and lasts longer. Because the nitric oxide has to come first, nothing happens without stimulation. The same enzyme is present in the prostate, bladder and lung arteries, which is why it is used for those too. (Source 19)

Is it good or bad for you?

Good for what it is licensed for, and the trade-offs are well quantified. Across 82 randomised trials tadalafil at its starting dose was somewhat less effective than sildenafil 50 mg but had the lowest overall adverse event rate of the class. It is dangerous in one specific situation: combined with any nitrate it can cause a serious fall in blood pressure. Outside its licensed uses it has been tested and failed, notably in Duchenne muscular dystrophy. (Source 2)

How do you get more of it?

It is prescription-only, and the amount is decided by a prescriber, not by the reader. As a matter of record, the licensed regimens are an as-needed dose taken before sexual activity or a smaller dose taken every day; the lung artery indication uses a much higher daily dose. There is no food or supplement that contains it, and products sold online as herbal substitutes have no place in this evidence base. (Source 11)

If it is harmful, what reduces it?

It clears itself. Mean oral clearance is 2.5 L per hour and the mean terminal half-life is 17.5 hours, with most of the dose leaving in the faeces, so the effect fades over a day or two after the last tablet with no tapering needed. If the problem is an interaction, the practical answer is not to take it with nitrates or guanylate cyclase stimulators at all. (Source 12)

Why might someone be low in it or missing it?

Nobody is deficient in tadalafil; it is a drug, not a nutrient. Someone may be unable to take it because of a contraindication, chiefly any use of organic nitrates, or a serious hypersensitivity, or use of riociguat. Its effect can also be blunted by enzyme inducers such as rifampin, which cut exposure by 88% in a pharmacokinetic study. (Source 6)

Which whole foods contain it or feed it?

None contain it. The only food that matters in the other direction is grapefruit juice, which inhibits the enzyme that clears tadalafil and would be expected to raise blood levels, though the manufacturer says this has not actually been studied for tadalafil. Otherwise the tablet can be taken with or without a meal. (Source 8)

We searched: We searched Europe PMC for tadalafil food sources and food-effect and grapefruit studies, and read the FDA Cialis labelling sections on use with food and CYP3A4 interactions. Tadalafil is a synthetic molecule with no dietary source.

What happens if you do not have it?

Nothing happens to the body from not taking it, because it is not something the body makes or needs. What persists is the condition. For erectile dysfunction, PDE5 inhibitors are the standard first drug treatment, so without one the difficulty simply continues. For pulmonary arterial hypertension the stakes are higher: in the PHIRST trial the placebo group walked less far and had more clinical worsening than the 40 mg group. (Source 20)

How can you test for it?

There is no blood test for tadalafil in ordinary care, and no level to check. What gets measured is the condition it treats, using validated questionnaires: the International Index of Erectile Function for erections and the International Prostate Symptom Score for prostate symptoms, which are the same instruments the trials used. In pulmonary arterial hypertension the outcome measured is the six-minute walk distance. (Source 3)

References

  1. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - prescribing information. 2026. Read the source
  2. European urology. Phosphodiesterase 5 inhibitors for the treatment of erectile dysfunction: a trade-off network meta-analysis. 2015. PMID 25817916, DOI 10.1016/j.eururo.2015.03.031. Read the source
  3. Lower urinary tract symptoms. Tadalafil 5 mg Once Daily Improves Lower Urinary Tract Symptoms and Erectile Dysfunction: A Systematic Review and Meta-analysis. 2018. PMID 29341503, DOI 10.1111/luts.12144. Read the source
  4. Circulation. Tadalafil therapy for pulmonary arterial hypertension. 2009. PMID 19470885, DOI 10.1161/CIRCULATIONAHA.108.839274. Read the source
  5. Neurology. A phase 3 randomized placebo-controlled trial of tadalafil for Duchenne muscular dystrophy. 2017. PMID 28972192, DOI 10.1212/wnl.0000000000004570. Read the source
  6. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - contraindications, warnings, interactions, pharmacokinetics and dosage sections. 2026. Read the source
  7. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - contraindications, warnings, interactions, pharmacokinetics and dosage sections. 2026. Read the source
  8. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - contraindications, warnings, interactions, pharmacokinetics and dosage sections. 2026. Read the source
  9. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - dosage, use with food, pharmacokinetics and clinical trials adverse event sections. 2026. Read the source
  10. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - dosage, use with food, pharmacokinetics and clinical trials adverse event sections. 2026. Read the source
  11. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - dosage, use with food, pharmacokinetics and clinical trials adverse event sections. 2026. Read the source
  12. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - dosage, use with food, pharmacokinetics and clinical trials adverse event sections. 2026. Read the source
  13. Sexual medicine. The Association Between Phosphodiesterase Type 5 Inhibitor Use and Risk of Non-Arteritic Anterior Ischemic Optic Neuropathy: A Systematic Review and Meta-Analysis. 2018. PMID 29884471, DOI 10.1016/j.esxm.2018.03.001. Read the source
  14. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - dosage, use with food, pharmacokinetics and clinical trials adverse event sections. 2026. Read the source
  15. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - contraindications, warnings, interactions, pharmacokinetics and dosage sections. 2026. Read the source
  16. Sexual medicine. The Association Between Phosphodiesterase Type 5 Inhibitor Use and Risk of Non-Arteritic Anterior Ischemic Optic Neuropathy: A Systematic Review and Meta-Analysis. 2018. PMID 29884471, DOI 10.1016/j.esxm.2018.03.001. Read the source
  17. Sexual medicine. The Association Between Phosphodiesterase Type 5 Inhibitor Use and Risk of Non-Arteritic Anterior Ischemic Optic Neuropathy: A Systematic Review and Meta-Analysis. 2018. PMID 29884471, DOI 10.1016/j.esxm.2018.03.001. Read the source
  18. International journal of clinical practice. Discontinuation Rates of Tadalafil Alone and in Combination with a-Blockers in the Treatment of Male Lower Urinary Tract Symptoms with or without Coexisting Erectile Dysfunction: A Systematic Review and Meta-Analysis. 2022. PMID 36419863, DOI 10.1155/2022/9298483. Read the source
  19. DailyMed / Eli Lilly and Company (FDA label). CIALIS (tadalafil) tablets, for oral use - prescribing information. 2026. Read the source
  20. European urology. Phosphodiesterase 5 inhibitors for the treatment of erectile dysfunction: a trade-off network meta-analysis. 2015. PMID 25817916, DOI 10.1016/j.eururo.2015.03.031. Read the source
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