Tadalafil 5mg tablets
Requires a prescription from a doctor or prescriber
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MHRA alerts for Tadalafil
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Tadalafil
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Tadalafil
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
24 branded products available
Part of the Cialis brand family (generic: Tadalafil)
MHRA licensed products
View all licensed products for Tadalafil on the MHRA register
Cialis 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
Tadalafil 5mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
10 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(2)
Erectile dysfunction: Alprostadil cream (ESNM50)
Erectile dysfunction: avanafil (ESNM45)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 10 · Randomised trials: 34 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
Hartmut Porst, Harin Padma-Nathan, François Giuliano, et al.
Urology, 2003
FRANCESCO MONTORSI, HARIN PADMA NATHAN, ANDREW MCCULLOUGH, et al.
Journal of Urology, 2004
Sanches M, de Amorim L, Moreira M, et al.
2025
Salonia A, Bettocchi C, Burnett A, et al.
2026
- Erectile Dysfunction
- Phosphodiesterase 5 Inhibitors
- Pyrimidines
IntroductionErectile dysfunction (ED) is a multifactorial condition with psychological, vascular, hormonal, neurological, and systemic risk factors. Four phosphodiesterase-5 inhibitors (PDE5is), sildenafil, tadalafil, vardenafil, and avanafil, have been approved by the United States Food and Drug Administration and the European Medicines Agency for the management of ED.ObjectivesWhile several meta-analyses have assessed the efficacy of PDE5is in the management of ED, none have focused on dose-specific outcomes. Hence, the study was conducted to compare the dose-dependent efficacy and safety of four FDA/EMA-approved PDE5is in the treatment of ED using on-demand dosages.MethodsA comprehensive literature search identified randomized, double-blind, placebo-controlled trials. Only on-demand doses of PDE5is were included in the network meta-analysis (NMA), which focused on primary outcomes such as the proportion of participants achieving satisfactory erectile function (EF), defined as an International Index of Erectile Function (IIEF) domain score > 26. A threshold analysis was conducted to evaluate the robustness of treatment recommendations derived from the NMA.ResultsA total of 83 studies with 6029 participants (treatment group: 3457 participants; placebo group: 2572 participants) were included. This dose-response network meta-analysis highlighted better efficacy with sildenafil (sildenafil 100 mg: odds ratio [OR] 9.06, sildenafil 50 mg: OR 7.90) in improving EF compared to that with placebo, followed by tadalafil (tadalafil 20 mg: OR 7.13, tadalafil 10 mg: OR 3.14), vardenafil (vardenafil 10 mg: OR 7.78), and avanafil (avanafil 200 mg: OR 3.42, avanafil 100 mg: OR 1.75). Threshold analysis showed a statistically significant improvement in ED with sildenafil 100 mg [OR 2.20; 95% confidence interval (CI) 1.78-2.63] and 50 mg (OR 2.10; 95% CI 1.69-2.50) compared to placebo. This indicated the robustness of the results, with moderate variations unlikely to alter their comparative ranking within the NMA. The odds of treatment-related adverse events were highest for vardenafil, followed by avanafil and sildenafil, and lowest for tadalafil compared to placebo. However, in some instances, the wide CI showed higher variability and potential uncertainty in effect estimates.ConclusionPDE5is are highly effective, with sildenafil showing a significantly greater efficacy compared with the other PDE5is.
Abstract licence: CC BY-NC
Eshetie S, Ejekpokpo O, Charlick M, et al.
2026
PurposeErectile dysfunction (ED) is a prevalent and distressing consequence of radical prostatectomy (RP) and radiotherapy (RT) for prostate cancer, profoundly impacting quality of life. Despite a wide array of available interventions, their comparative effectiveness remains uncertain in the absence of head-to-head trials.Materials and methodsWe conducted a systematic review and network meta-analysis (NMA) of studies evaluating medical interventions for ED following RP or RT. MEDLINE, Embase, and Scopus were searched for eligible studies. Risk of bias (RoB) was assessed using the Cochrane RoB 2 and ROBINS-I tools. A random-effects NMA was performed, with efficacy expressed as odds ratios (ORs) and 95% confidence intervals (CIs). The certainty of evidence was evaluated using the GRADE framework. The primary outcome was recovery of erectile function, assessed using validated measures or the proportion achieving successful intercourse.ResultsForty-one studies (n=4,157 participants) met inclusion criteria. Following RP, combination therapies were most effective: tadalafil plus intraurethral alprostadil gel (OR 24.8), tadalafil plus vacuum erection device (OR 12.3), and tadalafil plus low-intensity shockwave therapy (OR 8.2) demonstrated the highest odds of functional recovery versus placebo. Following RT, on-demand tadalafil was the most effective intervention (OR 8.0). Pooled analysis of RP studies showed a significant mean improvement in International Index of Erectile Function scores favouring active interventions over control (mean difference 4.5, 95% CI: 2.4-6.5, I²=62%), with longer intervention duration associated with greater improvement. Overall certainty of evidence was low to very low due to RoB, imprecision, and inconsistency.ConclusionsCombination therapies appear most effective for ED recovery after RP, while on-demand phosphodiesterase type 5 inhibitors are most efficacious after RT. These findings provide novel comparative evidence; however, cautious clinical application and further high-quality research are warranted.
Abstract licence: CC BY-NC
Broul M, Liegertová M, Hujová A, et al.
2026
IntroductionPeyronie's disease (PD) is an acquired fibrotic disorder of the tunica albuginea that can cause pain, curvature, deformity, erectile dysfunction, and substantial psychosexual burden. Management is usually guided by disease phase, yet active disease remains inconsistently defined, and no oral regimen has shown high-certainty disease-modifying efficacy. We synthesize clinical, mechanistic, guideline, outcome-measure, traction, and public-data evidence relevant to active or progressive PD as a target for early antifibrotic trials.MethodsWe conducted a targeted narrative translational review of full-text sources on active-phase definitions, PDE5 inhibitor/selective estrogen receptor modulator (SERM) pharmacology, tadalafil-based clinical studies, placebo-controlled tamoxifen evidence, current recommendations, non-surgical evidence reviews, patient-reported outcome measures, traction therapy, and PD transcriptomic or single-cell studies. We selected sources through targeted database searching, citation chasing, and full-text evidence audit; no protocol-registered systematic review was performed. Clinical studies were heterogeneous and largely non-randomized; therefore, we did not attempt a pooled efficacy estimate.ResultsActive and stable PD remain clinically useful categories, although their operational definitions vary across studies. Experimental PD models identify fibroblast-to-myofibroblast transformation as a pharmacologically accessible process, with PDE5 inhibitors and SERMs showing timing-dependent antifibrotic effects. Retrospective PDE5 inhibitor studies and clinical audits of PDE5 inhibitor plus tamoxifen therapy report mixed observations on progression and pain, but interpretation is constrained by non-randomized design, small or imbalanced controls, confounding, and heterogeneous endpoints. Placebo-controlled monotherapy evidence remains negative or neutral for tamoxifen, especially when disease duration is broad or not stratified by active inflammatory features. Guidelines and evidence reviews support individualized conservative care without endorsing PDE5 inhibitor/SERM therapy as standard practice.ConclusionActive/progressive PD is a defensible setting for early antifibrotic trials. PDE5 inhibitor/SERM therapy is among the best-developed mechanistic candidates, but remains investigational. Clinical adoption requires prospective, randomized, stage-defined studies with standardized curvature assessment, plaque imaging, erectile-function measurement, pain assessment, co-intervention documentation, adverse-event capture, and PD-specific patient-reported outcomes.
Abstract licence: CC BY
Pinkus P, Farsi S, Strickland WD, et al.
2026
IntroductionSudden sensorineural hearing loss (SSNHL) can significantly impact quality of life. Recent studies propose a link between the use of phosphodiesterase-5 inhibitors (PDE-5is) and SSNHL emergence.ObjectiveTo clarify the relationship between PDE-5i use and the risk of SSNHL development.Data synthesisFollowing the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, two independent reviewers searched the PubMed, Embase, and Web of Science databases for articles up to December 2023 on hearing loss in PDE-5i users. Out of 190 abstracts initially identified, 6 met the inclusion criteria, totaling 54 patients aged between 37 and 62 years. One study involved 4 female participants, while the rest focused on 50 male patients. Sildenafil, vardenafil, and tadalafil were the most commonly used PDE-5is. All patients experienced sensorineural hearing loss, ranging from moderate to profound, with 4 patients (7%) noting tinnitus and 3 patients (5%), vertigo, in addition to the hearing loss. One patient experienced bilateral hearing loss 15 days after initiating sildenafil consumption. Corticosteroid therapy was the exclusive treatment in all cases. The long-term outcomes following the cessation of the medication were available in 7 cases: 4 patients (57%) had no improvement, 2 patients (29%) fully recovered, and 1 patient (14%) had incomplete resolution of the hearing loss.ConclusionThe current systematic review underscores the importance of monitoring hearing in PDE5i patients and advising them about the potential risk. Further research with larger samples and control groups is needed to establish a definitive causal link.
Abstract licence: CC BY
E. Grünig, P. Jansa, F. Fan, et al.
Journal of the American College of Cardiology, 2024
Zhongbao Zhou, Xuesong Zheng, Jitao Wu, et al.
American Journal of Men's Health, 2019
R. Victor, H. Sweeney, R. Finkel, et al.
Neurology, 2017
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
72 found
Half-life
15-17.5h
Mechanism
Tadalafil is a selective phosphodiesterase-5 (PDE5) inhibitor that produces seve…
Food interactions
3 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.5-6h
Half-life
15-17.5h
Protein binding
94%
[A242270][L39095][L39100]
Volume of distribution
63L
Metabolism
Elimination
61%
[A242270][L39095][L39100]
These metabolites are mainly excreted in the feces (61%) and…
Clearance
2.5-3.4L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L39095][L39439]
It is also indicated for the treatment of pulmonary arterial hypertension (PAH) both alone and in combination with [macitentan] or other endothelin-1 antagonists.
[L39100][L39105][L50622]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1228 interactions
[L39095][L39100]
Standard supportive care is recommended. Hemodialysis is not expected to contribute significantly to tadalafil clearance.
In PAH, blood pressure in the pulmonary arteries is raised due to a variety of mechanisms stemming from endothelial dysfunction.[A242377] Decreased production of NO and prostacyclin reduce vasodilatory signaling while overproduction of endothelin-1 and thromboxane increase vasoconstriction. Inflammation, thromboses, and hypoxia later contribute to vascular remodeling which further reduces luminal size. The resultant increase in blood pressure reduces the capacity for gas exchange and increases afterload at the right ventricle, producing symptoms of dyspnea, fatigue, and dizziness as well as leading to right-sided heart failure. Tadalafil exerts its therapeutic effect in PAH through boosting NO-cGMP signaling to contribute to smooth muscle relaxation as with ED.
Lastly, tadalafil is used to treat BPH.[L39095] BPH produces urinary dysfunction through hyperproliferation of the epithelial and smooth muscle layers of the prostate.[A242382] The increased size of the prostate blocks urine flow through the urethra resulting in higher residual volumes due to incomplete emptying. Tadalafil does not appear to exert its benefit via smooth muscle relaxation of the prostate. It may instead exert its effect through a mix of increased oxygenation and decreased inflammation, which decreases tissue remodeling, and inhibition of cell proliferation through the cGMP cascade.
The decreased affinity for PDE6 compared to other PDE5 inhibitors may explain the decreased incidence of visual side effects as PDE6 is present in the eye and contributes to color vision.[L39100][L39105][A242287]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A242270][L39095]
The tmax in adults with PAH is reported as 2-8h with a median of 4h.
[L39100]
There does not appear to be a significant effect on absorption when tadalafil is taken with food.
[A242270]
[A242270][L39095][L39100]
The mean half-life of elimination in adults with PAH is reported as 35h.
[L39100]
[A242270][L39095][L39100]
[A242270][L39095]
The mean apparent volume of distribution is reported as 77L in adults with PAH.
[L39100]
[A242270][A242387][L39095][L39100]
This catechol metabolite undergoes subsequent methylation and glucuronidation with the methyl-glucuronide metabolite becoming the primary metabolite in circulation. None of the known metabolites are considered to be active.
[A242270][L39095][L39100]
These metabolites are mainly excreted in the feces (61%) and to a lesser extent in the urine (36%)
[A242270][L39095][L39100]
The mean apparent oral clearance in adults with PAH is reported as 3.5L/h
Proteins and enzymes this drug interacts with in the body
PMID:15489334 PMID:9714779
Specifically regulates nitric-oxide-generated cGMP PMID:15489334
PMID:10725373 PMID:10906126 PMID:11050148 PMID:16330539
Catalyzes the hydrolysis of both cAMP and cGMP to 5'-AMP and 5'-GMP, respectively PMID:10725373 PMID:10906126 PMID:11050148
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC G04BE08
ATC C02KX52
ATC G04CB51
ATC G04CA54
ATC C02KX54
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Tadalafil
Additional database identifiers
Drugs Product Database (DPD)
12346
ChemSpider
99301
BindingDB
14777
PDB
CIA
ZINC
ZINC000003993855
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8784
GenAtlas
PDE5A
GeneCards
PDE5A
GenBank Gene Database
AF043731
GenBank Protein Database
3420185
Guide to Pharmacology
1304
UniProt Accession
PDE5A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8773
GeneCards
PDE11A
GenBank Gene Database
AB036704
GenBank Protein Database
10716052
Guide to Pharmacology
1311
UniProt Accession
PDE11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8789
GeneCards
PDE6G
GenBank Gene Database
M36476
GenBank Protein Database
189703
UniProt Accession
CNRG_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72