Drug Monograph

Gemtesa (Vibegron)

vibegron tablets

Beta-3 Adrenergic Agonist · Oral · Urinary Antispasmodic
Pharmacokinetic Profile
Half-Life
30.8 h (effective)
Metabolism
Minor role; CYP3A4 predominant in vitro
Protein Binding
~50%
Bioavailability
Greater than dose-proportional
Volume of Distribution
6304 L (apparent)
Clinical Information
Drug Class
Selective Beta-3 Adrenergic Agonist
Available Dose
75 mg tablet (single strength)
Route
Oral (can be crushed)
Renal Adjustment
None (eGFR 15–89); not recommended in ESRD
Hepatic Adjustment
None (Child-Pugh A/B); not recommended in C
Pregnancy
No human data available
Lactation
Unknown; present in rat milk
Schedule
Prescription only (not scheduled)
Generic Available
No
CYP Inhibition
None (does not inhibit CYP2D6)
Rx

Indications

IndicationApproved PopulationTherapy TypeStatus
Overactive bladder (OAB) — urge urinary incontinence, urgency, urinary frequencyAdultsMonotherapyFDA Approved
OAB in males with benign prostatic hyperplasia (BPH) — urge urinary incontinence, urgency, urinary frequency in males on pharmacological BPH therapyAdult males on BPH pharmacotherapyMonotherapy (add-on to BPH medication)FDA Approved

Vibegron is a selective beta-3 adrenergic receptor agonist approved by the FDA in December 2020 for overactive bladder in adults. In December 2024, it received an additional indication for OAB in adult males concurrently receiving pharmacological therapy for benign prostatic hyperplasia, supported by the phase 3 COURAGE trial. Vibegron is the second beta-3 agonist to reach market after mirabegron, but it is distinguished by the absence of CYP2D6 inhibitory activity, no blood pressure warning in the label, a fixed-dose regimen requiring no titration, and the ability to crush the tablet for patients with swallowing difficulty. The pivotal EMPOWUR trial (Study 3003) enrolled over 1,500 patients and demonstrated statistically significant reductions in micturition frequency, urge urinary incontinence episodes, and urgency episodes compared with placebo at 12 weeks.

Off-Label Uses

Neurogenic detrusor overactivity in adults: Limited data exist for vibegron use in adult NDO. Based on its beta-3 agonist mechanism, off-label use may be considered when antimuscarinics and mirabegron are not tolerated. Evidence quality: Low.

Dose

Dosing

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
OAB — treatment-naive adult75 mg once daily75 mg once daily75 mg/dayNo dose titration required
Swallow whole with water, or crush and mix with ~15 mL applesauce; take with or without food
OAB in male with concurrent BPH pharmacotherapy75 mg once daily75 mg once daily75 mg/daySame dose; add to existing BPH medication (alpha-blocker, 5-ARI, or combination)
COURAGE trial demonstrated efficacy in this population
OAB — mild to severe renal impairment (eGFR 15–89)75 mg once daily75 mg once daily75 mg/dayNo dose adjustment required
Not recommended in ESRD (eGFR <15 with or without hemodialysis)
OAB — mild to moderate hepatic impairment (Child-Pugh A/B)75 mg once daily75 mg once daily75 mg/dayNo dose adjustment required
Not studied in severe hepatic impairment (Child-Pugh C); not recommended
OAB — elderly (≥65 years)75 mg once daily75 mg once daily75 mg/dayNo dose adjustment; 46% of trial patients were ≥65 years with no difference in safety or efficacy
Can be crushed for patients with swallowing difficulty
Clinical Pearl: Key Differentiators from Mirabegron

Vibegron offers several practical advantages over mirabegron in specific clinical scenarios. It requires no dose titration (a single 75 mg fixed dose), has no CYP2D6 inhibitory activity (eliminating concern for interactions with metoprolol, flecainide, or tamoxifen), carries no blood pressure warning in the FDA label, and can be crushed and mixed with applesauce for patients who cannot swallow tablets. These characteristics make it particularly suitable for elderly patients on multiple medications and those with dysphagia.

PK

Pharmacology

Mechanism of Action

Vibegron is a selective agonist of the human beta-3 adrenergic receptor. Like mirabegron, vibegron relaxes detrusor smooth muscle during the bladder filling phase by activating beta-3 receptors, thereby increasing functional bladder capacity and reducing the sensation of urgency. Vibegron demonstrates high selectivity for the beta-3 receptor subtype relative to beta-1 and beta-2 adrenergic receptors. Unlike mirabegron, vibegron does not inhibit CYP2D6, which translates into a cleaner drug interaction profile. In a dedicated ambulatory blood pressure monitoring study, vibegron 75 mg was not associated with clinically significant blood pressure changes in OAB patients, and the drug does not prolong the QT interval at a dose 5.3 times the approved recommended dose.

ADME Profile

ParameterValueClinical Implication
AbsorptionTmax 1–3 h; Cmax and AUC increase greater than dose-proportionally up to 600 mg; no clinically significant food effect; can be crushed with applesauce without affecting PKRapid absorption; fixed 75 mg dose is effective without titration; flexibility in administration route supports patients with dysphagia
DistributionApparent Vd 6304 L; ~50% plasma protein-bound; blood-to-plasma ratio 0.9Very large volume of distribution indicates extensive tissue distribution; moderate protein binding makes displacement interactions unlikely
MetabolismMetabolism plays a minor role in elimination; CYP3A4 is the predominant enzyme in vitro; does not inhibit CYP1A2, 2B6, 2C8, 2C9, 2C19, 2D6, or 3A4; does not induce CYP1A2, 2B6, or 3A4; P-gp substrate but does not inhibit P-gp or other transportersClean interaction profile: no CYP2D6 inhibition (key difference from mirabegron); unlikely to cause clinically significant PK interactions with most co-administered drugs
EliminationEffective t½ 30.8 h; 59% feces (54% unchanged), 20% urine (19% unchanged); steady state in ~7 days; accumulation ratio 1.7 (Cmax) and 2.4 (AUC0-24)Primarily excreted as unchanged drug in feces, suggesting biliary/intestinal secretion is the dominant elimination pathway; half-life supports once-daily dosing
SE

Side Effects

1–10% Common (Study 3003 — OAB Adults, 12 Weeks)
Adverse EffectIncidence (Vibegron)PlaceboClinical Note
Headache4.0%2.4%Most common adverse reaction; usually mild to moderate
Nasopharyngitis2.8%1.7%Common in clinical trials; not clearly drug-related
Diarrhea2.2%1.1%Usually self-limiting
Nausea2.2%1.1%Usually mild; taking with food may help
Upper respiratory tract infection2.0%0.7%Not clearly drug-related
<2% Less Common (<2% in Study 3003)
Adverse EffectIncidenceClinical Note
Dry mouth<2%Notably lower than antimuscarinic agents; not dose-related since only one dose studied
Constipation<2%Much lower than rates seen with antimuscarinics; reported at >2% in long-term extension only
Residual urine volume increased<2%Monitor in patients with BOO or concurrent antimuscarinic use
Urinary retention<2%Risk higher with concurrent antimuscarinics or BOO
Hot flush<2%Beta-adrenergic class effect
≥2% Long-Term Extension and BPH Population
Adverse EffectIncidenceClinical Note
Urinary tract infection (52-week extension)6.6%Emerged with longer treatment duration; not reported at ≥2% in the 12-week study
Bronchitis (52-week extension)2.9%Reported in long-term use; unclear causal relationship
Hypertension (BPH study, 24 weeks)9.0% vs 8.3% placeboBroadly defined in COURAGE trial; rates comparable to placebo; the dedicated ABPM study showed no significant BP effect at 75 mg
UTI (BPH study, 24 weeks)2.5% vs 2.2% placeboSimilar rates to placebo in male BPH population
Serious Serious Adverse Effects (Regardless of Frequency)
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
AngioedemaRare (postmarketing)Hours after first dose or after multiple dosesImmediately discontinue; provide emergency airway management; permanent discontinuation required; contraindication added to label Oct 2024
Urinary retentionRare (postmarketing)Variable; higher risk with BOO or concurrent antimuscarinic useDiscontinue vibegron; catheterisation may be needed; listed as a warning and precaution in the FDA label
Hypersensitivity reactions (urticaria, pruritus, rash, drug eruption)Rare (postmarketing)VariableDiscontinue if significant; provide appropriate treatment
Discontinuation Discontinuation Rates
EMPOWUR 12-Week Study
1.7% vs 1.1% placebo
Context: Lower discontinuation rate than the active control (tolterodine 3.3%); favourable tolerability profile
52-Week Extension
85.7% completion
Context: Of 182 patients who continued vibegron from the initial study, 85.7% completed the additional 40-week extension
Blood Pressure Profile

Vibegron is the only beta-3 agonist without a blood pressure warning in its FDA label. In the dedicated ambulatory blood pressure monitoring study (n=200 OAB patients), 75 mg daily vibegron was not associated with clinically significant blood pressure changes. In the EMPOWUR trial, rates of hypertension with vibegron (1.7%) were identical to placebo (1.7%), while the tolterodine comparator arm reported a 1.7% rate. This blood pressure neutrality is a significant clinical differentiator from mirabegron, which carries a specific blood pressure monitoring requirement.

Int

Drug Interactions

Vibegron has a notably clean drug interaction profile. It does not inhibit or induce any CYP enzymes (including CYP2D6) or major drug transporters at clinically relevant concentrations. The only clinically meaningful interaction identified in the FDA label is with digoxin. Vibegron is a CYP3A4 substrate and a P-gp substrate, but co-administration with ketoconazole (strong CYP3A4 and P-gp inhibitor), diltiazem (moderate CYP3A4 inhibitor), or rifampicin (strong CYP3A4 inducer) did not produce clinically significant changes in vibegron exposure.

ModerateDigoxin
MechanismUncertain; vibegron does not inhibit P-gp at clinically relevant concentrations in vitro, but increased digoxin exposure was observed in vivo
EffectDigoxin Cmax increased 21% and AUC increased 11%
ManagementMeasure serum digoxin concentrations before initiating vibegron; monitor during therapy and titrate digoxin to clinical effect; continue monitoring after vibegron discontinuation
FDA PI
MinorCYP2D6 substrates (metoprolol, flecainide, tamoxifen, etc.)
MechanismNo interaction — vibegron does not inhibit CYP2D6
EffectNo clinically significant changes in metoprolol pharmacokinetics observed in clinical studies
ManagementNo dose adjustment or monitoring required; key advantage over mirabegron which inhibits CYP2D6
FDA PI
MinorWarfarin
MechanismNo CYP-mediated interaction
EffectNo clinically significant changes in warfarin pharmacokinetics
ManagementNo dose adjustment or additional INR monitoring required
FDA PI
MinorKetoconazole / CYP3A4 inhibitors
MechanismVibegron is a CYP3A4 and P-gp substrate, but metabolism plays a minor role in overall elimination
EffectNo clinically significant changes in vibegron pharmacokinetics with ketoconazole (strong CYP3A4/P-gp inhibitor) or diltiazem (moderate CYP3A4 inhibitor)
ManagementNo dose adjustment of vibegron required
FDA PI
MinorRifampicin / CYP3A4 inducers
MechanismCYP3A4 induction; metabolism is a minor elimination pathway for vibegron
EffectNo clinically significant changes in vibegron pharmacokinetics with rifampicin
ManagementNo dose adjustment of vibegron required
FDA PI
ModerateMuscarinic antagonists (antimuscarinic OAB drugs)
MechanismPharmacodynamic: additive risk of urinary retention when combining beta-3 agonist with anticholinergic
EffectIncreased risk of urinary retention; no significant PK interaction with tolterodine in clinical studies
ManagementMonitor for signs and symptoms of urinary retention when combining; discontinue vibegron if retention develops
FDA PI
Mon

Monitoring

  • Digoxin LevelsBefore initiation; during therapy; after discontinuation
    Trigger-based
    Vibegron increases digoxin Cmax 21% and AUC 11%; measure serum digoxin before starting, monitor during treatment, and continue monitoring after vibegron is stopped to guide dose adjustment
  • Symptom Response4–12 weeks; then every 6–12 months
    Routine
    Assess OAB symptoms using voiding diary or validated questionnaire; no dose titration available (fixed 75 mg dose); periodically reassess continued need for therapy
  • Post-Void ResidualBaseline if BOO suspected; as needed
    Trigger-based
    Monitor in patients with BOO or concurrent antimuscarinic medications; discontinue vibegron if urinary retention develops
  • Renal FunctionBaseline
    Routine
    Assess eGFR before initiation; no dose adjustment for eGFR 15–89; not recommended in ESRD (eGFR <15 or dialysis)
  • Hepatic FunctionBaseline
    Routine
    No adjustment for Child-Pugh A/B; not studied and not recommended in Child-Pugh C
CI

Contraindications & Cautions

Absolute Contraindications

  • Known hypersensitivity: Hypersensitivity to vibegron or any component of the formulation; includes patients with prior angioedema with vibegron (contraindication updated October 2024)

Relative Contraindications (Specialist Input Recommended)

  • End-stage renal disease (eGFR <15, with or without hemodialysis): Not studied; not recommended by the FDA label
  • Severe hepatic impairment (Child-Pugh C): Not studied; not recommended by the FDA label

Use with Caution

  • Bladder outlet obstruction: Urinary retention has been reported; monitor PVR and symptoms of retention
  • Concurrent antimuscarinic OAB medications: Increased risk of urinary retention with pharmacodynamic combination; monitor closely; discontinue vibegron if retention develops
  • Patients taking digoxin: Modest increase in digoxin exposure (Cmax +21%, AUC +11%); measure digoxin levels before and during treatment
FDA Label Update — October 2024 Angioedema Warning Added

In October 2024, the FDA updated the Gemtesa label to include a warning for angioedema (section 5.2) and added hypersensitivity reactions, including angioedema, to the contraindications (section 4). Angioedema of the face and/or larynx has been reported in postmarketing experience, occurring hours after the first dose or after multiple doses. Angioedema associated with upper airway swelling may be life-threatening. Clinicians should immediately discontinue vibegron if tongue, hypopharynx, or larynx involvement occurs and provide appropriate airway management.

Pt

Patient Counselling

Purpose of Therapy

Vibegron helps manage overactive bladder symptoms by activating receptors that relax the bladder muscle during filling, allowing the bladder to hold more urine. This reduces the urgent need to urinate, the frequency of bathroom visits, and accidental leakage episodes. It works differently from older anticholinergic bladder medications and does not cause the dry mouth or constipation commonly seen with those drugs.

How to Take

Take one 75 mg tablet once daily with a glass of water. The tablet can be taken with or without food, at the same time each day. If you have difficulty swallowing, the tablet can be crushed and mixed with approximately one tablespoon (15 mL) of applesauce, then taken immediately with a glass of water. If a dose is missed and more than 12 hours have passed, skip the missed dose and take the next one at the regular time.

Difficulty Urinating
Tell patientAlthough vibegron treats bladder overactivity, it can rarely make it harder to empty the bladder. This risk is higher if you already have trouble with urine flow (such as from an enlarged prostate) or if you take other bladder-calming medications at the same time.
Call prescriberIf you notice difficulty starting urination, a weak stream, feeling that your bladder is not emptying fully, or inability to urinate at all.
Allergic Reactions
Tell patientRarely, vibegron can cause serious allergic reactions including swelling of the face or throat (angioedema). This can happen after the first dose or after you have been taking the medication for some time.
Call prescriberStop the medication immediately and seek emergency medical attention if you experience swelling of the face, lips, tongue, or throat, difficulty breathing, or severe skin reactions such as widespread rash or hives.
Other Medications
Tell patientVibegron has fewer drug interactions than some other bladder medications. However, if you take digoxin (a heart medication), your doctor will need to check your digoxin blood level before starting vibegron and monitor it during treatment. Always inform your healthcare provider about all medications you are taking.
Call prescriberIf you start or stop any medication while taking vibegron, particularly heart medications.
Crushable Tablet
Tell patientIf you have difficulty swallowing tablets, vibegron can be crushed and mixed with a tablespoon of applesauce. Take the mixture immediately after preparation, followed by a glass of water. This has been shown not to affect how the medication works.
Call prescriberIf you have questions about alternative methods of taking this medication or if you experience any difficulty with administration.
Ref

Sources

Regulatory (PI / SmPC)
  1. Gemtesa (vibegron) tablets — Full Prescribing Information. Sumitomo Pharma America, Inc. Revised February 2025. Gemtesa PICurrent regulatory source including Dec 2024 BPH indication, Oct 2024 angioedema warning, adverse reaction Tables 1–2, PK data, and digoxin interaction.
  2. Gemtesa (vibegron) tablets — Original FDA Approval Label (December 2020). FDA LabelOriginal FDA-approved label for adult OAB; source for Study 3003 adverse reaction data and pharmacokinetic parameters.
  3. Gemtesa — DailyMed label. National Library of Medicine. DailyMedNLM-hosted label confirming fixed 75 mg dosing, renal/hepatic recommendations, and drug interaction guidance.
Key Clinical Trials
  1. Staskin D, Frankel J, Varano S, Shortino D, Jankowich R, Mudd PN Jr. International phase III, randomized, double-blind, placebo and active controlled study to evaluate the safety and efficacy of vibegron in patients with symptoms of overactive bladder: EMPOWUR. J Urol. 2020;204(2):316–324. PubMed: 32068483Pivotal phase III trial (Study 3003) in 1,515 OAB patients demonstrating vibegron 75 mg superiority over placebo for micturition frequency, UUI episodes, and urgency at 12 weeks.
  2. Staskin D, Varano S, Frankel J, Shortino D, Jankowich R, Mudd PN Jr. Once-daily vibegron 75 mg for overactive bladder: long-term safety and efficacy from a double-blind extension study of the phase 3 EMPOWUR trial. J Urol. 2021;205(5):1421–1429. PubMed: 3335647940-week extension of EMPOWUR confirming sustained efficacy and tolerability of vibegron 75 mg over 52 weeks; 85.7% completion rate in vibegron continuers.
  3. Staskin D, Owens-Grillo J, Thomas E, Rovner E, Cline K, Mujais S. Efficacy and safety of vibegron for persistent symptoms of overactive bladder in men being pharmacologically treated for benign prostatic hyperplasia: results from the phase 3 randomized controlled COURAGE trial. J Urol. 2024;212(2):256–266. PubMed: 38717901Phase 3 COURAGE trial (Study 3005) supporting the Dec 2024 BPH indication; demonstrated vibegron efficacy in males with OAB symptoms on BPH pharmacotherapy.
  4. Yoshida M, Takeda M, Gotoh M, et al. Vibegron, a novel potent and selective beta-3 adrenoceptor agonist, for the treatment of patients with overactive bladder: a randomized, double-blind, placebo-controlled phase 3 study. Eur Urol. 2018;73(5):783–790. PubMed: 29217216Japanese phase 3 trial confirming vibegron 50 mg and 100 mg efficacy in Asian OAB patients; the 75 mg dose subsequently selected for the global programme.
Guidelines
  1. Lightner DJ, Gomelsky A, Souter L, et al. Diagnosis and treatment of overactive bladder (non-neurogenic) in adults: AUA/SUFU guideline amendment 2019. J Urol. 2019;202(3):558–563. PubMed: 31039103AUA/SUFU guideline positioning oral pharmacotherapy (antimuscarinics and beta-3 agonists) as second-line treatment for OAB after behavioural interventions.
  2. American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria. J Am Geriatr Soc. 2023;71(7):2052–2081. PubMed: 37139824Lists antimuscarinics as potentially inappropriate in older adults; beta-3 agonists including vibegron are not on the Beers list, supporting preferential use in elderly OAB.
Mechanistic / Basic Science
  1. Edmondson SD, Zhu C, Kar NF, et al. Discovery of vibegron: a potent and selective beta-3 adrenergic receptor agonist for the treatment of overactive bladder. J Med Chem. 2016;59(2):609–623. PubMed: 26709102Describes the medicinal chemistry optimisation of vibegron, its beta-3 receptor selectivity profile, and the preclinical pharmacology supporting clinical development.
Pharmacokinetics / Special Populations
  1. Mudd PN Jr, Girard F, Bhatt DL. Clinical pharmacokinetics of vibegron in healthy adult subjects. Clin Pharmacokinet. 2021;60(1):85–95. PubMed: 32557249Population PK analysis describing vibegron absorption, distribution, elimination, and the absence of clinically significant food effects or CYP-mediated interactions.
  2. Mudd PN Jr, Mazzei A, Engel E, et al. Pharmacokinetics and safety of vibegron in subjects with renal or hepatic impairment. Clin Pharmacol Drug Dev. 2021;10(9):1060–1070. PubMed: 33559344Renal and hepatic impairment PK study confirming no dose adjustment needed for eGFR 15–89 or Child-Pugh A/B, supporting the simplified dosing regimen.