Vibegron 75mg tablets
Requires a prescription from a doctor or prescriber
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Vibegron
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.
View Drug Analysis Profile
Browse all Drug Analysis Profiles A–Z
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
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.
View EudraVigilance report
Suspected adverse reactions reported for Vibegron
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
MHRA licensed products
View all licensed products for Vibegron on the MHRA register
Obgemsa 75mg 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)
75 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(4)
Vibegron for treating symptoms of overactive bladder syndrome (TA999)
Lower urinary tract symptoms in men: management (CG97)
Urinary incontinence in neurological disease: assessment and management (CG148)
Urinary incontinence and pelvic organ prolapse in women: management (NG123)
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
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
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: 22 · Randomised trials: 14 · 2015–2025
Showing the 50 most relevant studies, sorted by most relevant.
Wenjuan He, Yuqian Zhang, Guangliang Huang, et al.
LUTS Lower Urinary Tract Symptoms, 2023
- Urinary Bladder, Overactive
- Network Meta-Analysis
- Acetanilides
Jiankun Zhang, Junpeng Chi, Keyuan Lou, et al.
PLoS ONE, 2025
- Acetanilides
- Pyridines
- Thiazoles
Hirotaka Asakura, Takashi Asakura, Toshiaki Shinojima
Urology, 2025
Wei-Zhen Bai, Shi-Yu Zhou, Yi Mou, et al.
Medicine, 2025
- Acetanilides
- Pyridines
- Pyrimidinones
BACKGROUND: This updated meta-analysis aimed to compare the efficacy, safety, and treatment adherence of mirabegron and vibegron in patients with overactive bladder with head-to-head trials. METHODS: A systematic literature search was conducted in PubMed, Embase, ClinicalTrials.gov, and the Cochrane Library from January 1, 2016 to July 6, 2025. Comparative studies evaluating mirabegron versus vibegron were included. Study selection followed the PICOS framework, and quality assessment was performed using the Cochrane Handbook for randomized controlled trials (RCTs) and the Newcastle-Ottawa Scale for non-RCTs. Outcomes included changes in voiding diary parameters, urodynamic measures, overactive bladder symptom scores, adverse events, and treatment adherence. Statistical analyses were conducted using Review Manager 5.3. RESULTS: Six studies met the inclusion criteria. Vibegron was associated with a greater reduction in daily urgency episodes (standardized mean difference [SMD] = 0.37, P = .0006) and urinary urge incontinence (UUI) episodes (SMD = 0.33, P = .006) compared to mirabegron. However, no significant differences were found in other efficacy parameters or overall safety profiles. Vibegron demonstrated better adherence, with a higher continuation rate and lower discontinuation rate. CONCLUSION: Recent data indicated that vibegron demonstrated superior efficacy in reducing urgency and UUI episodes while maintaining a safety profile comparable to mirabegron. Furthermore, vibegron is associated with improved treatment adherence. However, additional RCTs are necessary to confirm these findings.
Abstract licence: CC BY 4.0
Fishberg SE, Matta R
2025
AimsTo summarize current evidence on β3-adrenoceptor agonists for managing neurogenic lower urinary tract dysfunction (NLUTD), focusing on their efficacy, safety, and clinical role in optimizing bladder storage and protecting upper tracts.MethodsEvidence from randomized controlled trials, meta-analyses, and observational studies in spinal cord injury (SCI), multiple sclerosis (MS), and spina bifida populations was reviewed. Outcomes included bladder storage parameters, patient-reported measures, and cardiovascular and cognitive safety profiles.Resultsβ3-adrenoceptor agonists such as Mirabegron improve cystometric capacity, reduce detrusor pressure, and enhance quality of life. A recent individual-patient meta-analysis confirmed these benefits. Early data on Vibegron in SCI and spina bifida show increased bladder compliance and capacity without new safety concerns. Cardiovascular safety signals are reassuring: one randomized trial in SCI/MS and a large multinational cohort both showed no excess risk. Observational studies continue to associate antimuscarinics with cognitive adverse effects, whereas β3-agonists demonstrate a more favorable tolerability profile.Conclusionsβ3-adrenoceptor agonists represent a safe, effective, and well-tolerated first-line option in NLUTD management. They preserve bladder safety and continence with fewer systemic side effects. OnabotulinumtoxinA remains an important escalation therapy for refractory cases but carries higher procedural and retention risks. A β3-agonist-based strategy offers a rational, patient-centered foundation for treatment.
Abstract licence: CC BY-NC-ND
M. Kennelly, R. Wielage, Denise D Shortino, et al.
Drugs in Context, 2020
Shunye Su, Liqin Liang, Jinlei Lin, et al.
Medicine, 2021
- Pyrimidinones
- Pyrrolidines
- Muscarinic Antagonists
BACKGROUND: Vibegron is a new β3-adrenergic receptor agonist which has been demonstrated for the treatment of overactive bladder (OAB). We carried out meta-analysis to evaluate the efficiency of vibegron vs antimuscarinic monotherapy for treating OAB. METHODS: Randomized controlled trials (RCTs) of Vibegron vs antimuscarinic monotherapy for OAB were searched systematically by using EMBASE, MEDLINE, and the Cochrane Controlled Trials Register. The RevMan version 5.3.0. was used to analysis the data. RESULTS: Three RCTs involving a total of 1751 patients were studied in the Systematic review and Meta-analysis. Efficacy end points: the mean number of micturitions episodes/d (P = .16); the mean number of urgency episodes/d (P = .05); mean number of urgency incontinence episodes/d (P = .11) and mean number of incontinence episodes/d (P = .14) indicated that vibegron and antimuscarinic had no significant differences in terms of OAB treatment. Mean volume voided/micturition showed a distinct difference in the two groups (P = .009). With regard to dry mouth and drug related treatment-emergent adverse event (TEAE), vibegron showed better tolerance than antimuscarinic. Serious adverse event (SAE) and discontinuations due to adverse event (AE) did not show a significant difference between the two groups. CONCLUSIONS: The therapeutic effect of vibegron is similar to that of antimuscarinic, but vibegron does not increase the risk of AE.
Abstract licence: CC BY-NC 4.0
Zhongyu Jian, Chi Yuan, Hong Li, et al.
International Urology and Nephrology, 2021
- Urinary Bladder, Overactive
- Algorithms
- Meat
Chaofan Xie, Guo Jiang, Tao Wu
Neurourology and Urodynamics, 2020
David Staskin, Janet Owens‐Grillo, Elizabeth Thomas, et al.
The Journal of Urology, 2024
- Prostatic Hyperplasia
- Adrenergic alpha-Antagonists
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
None known
Half-life
60 to 70 hours
Mechanism
Overactive bladder is characterized by symptoms of urge urinary incontinence, urgency, and urinary frequency.
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1-3 hours
[L28305]
Half-life
60 to 70 hours
[A226065]
The effective half-life is 30.8 hours.
[L28305]
Protein binding
49.6–51.3%
[A226065]
Volume of distribution
6304 L
[L28305]
…
Metabolism
[L28305]
…
Elimination
59%
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Vibegron is the second beta-3 adrenergic agonist approved for the treatment of overactive bladder following [mirabegron], which was approved in 2012. Unlike mirabegron, vibegron is less likely to be associated with drug-drug interactions involving the CYP3A4, 2D6, or 2C9 enzymes.[A226065]
[L28305]
It is additionally indicated for the treatment of adult male patients with OAB who are undergoing pharmacologic treatment for benign prostatic hyperplasia (BPH).
[L52305]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 165 interactions
[L28305]
Beta-3 adrenergic receptors (β3ARs) are expressed in the kidneys and lower urinary tract, including ureters, urethra, prostate, and bladder. Vibegron is a selective agonist at β3AR. One vibegron binds to the receptor, β3AR is stimulated and undergoes a conformation change and activates adenylyl cyclases (AC), which promotes the formation of cyclic adenosine monophosphate (cAMP). Increased intracellular cAMP concentration leads to the activation of cAMP-dependent protein kinase A (PKA), which subsequently phosphorylates myosin light chains that are responsible for inhibiting the interaction of actin with myosin dependent on calcium – calmodulin complex.[A226065][A226080] In clinical trials, vibegron increased cAMP levels in a dose-proportional manner. There is evidence that β3AR agonists may also work via sensory mechanisms without directly affecting detrusor muscle motor function.[A226065]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L28305]
[A226065]
The effective half-life is 30.8 hours.
[L28305]
[A226065]
[L28305]
According to tissue distribution studies in animals, vibegron does not penetrate the blood-brain barrier, suggesting limited potential for CNS toxicity in humans.
[A226065]
[L28305]
Two predominant metabolic pathways are oxidation and glucuronidation to form two oxidative metabolites and three glucuronide metabolites.
[A226065]
Metabolites have not been fully characterized.
[L28305]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
ATC G04BD15
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Vibegron
Additional database identifiers
ChemSpider
28528047
BindingDB
50146154
ZINC
ZINC000084757336
HUGO Gene Nomenclature Committee (HGNC)
HGNC:288
GenAtlas
ADRB3
GeneCards
ADRB3
GenBank Gene Database
M29932
GenBank Protein Database
178896
Guide to Pharmacology
30
UniProt Accession
ADRB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_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