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β3-Adrenergic Receptor Agonists

β3-adrenergic receptor agonists are the contemporary companion class to antimuscarinics for overactive bladder (OAB), working through the opposite arm of autonomic bladder physiology. Two agents are FDA-approved: mirabegron (Myrbetriq) and vibegron (Gemtesa).[7][23] Both activate bladder β3-adrenoceptors and improve OAB urgency and voided volume, with efficacy comparable to antimuscarinics and lower rates of dry mouth and constipation without anticholinergic burden; the contribution of direct detrusor relaxation to clinical benefit remains uncertain.[1][2][3][4]

The 2024 AUA/SUFU OAB guideline recommends offering either a β3-agonist or an antimuscarinic within a menu of options rather than a fixed step sequence. It also cites a SUFU white paper advising a β3-agonist trial before an antimuscarinic when drug therapy is chosen, particularly where anticholinergic burden or cognitive risk matters.[4]

Mechanism of Action​

β3-adrenoceptor mRNA is abundant in human detrusor, and receptor expression has been reported in other bladder tissues; experimental studies link β3 activation to cAMP signaling, with observed or proposed effects including:[2][3][5]

  • Direct detrusor smooth muscle relaxation during the storage phase
  • Decreased afferent signaling from the bladder
  • Improved bladder compliance during filling
  • Increased functional bladder capacity
  • Suppression of detrusor micro-contractions via effects on detrusor smooth muscle cells and suburothelial interstitial cells

Secondary mechanism — cholinergic inhibition​

Experimental human-donor and rat bladder work suggests a prejunctional pathway: β3 stimulation can promote EPAC1/PKC-dependent adenosine release and inhibit cholinergic nerve signaling.[6] Its contribution to clinical OAB efficacy has not been established.

The dominant clinical mechanism is not settled: therapeutic mirabegron plasma concentrations are considerably below the in-vitro EC50 for direct relaxation of human detrusor preparations, so the demonstrated relaxant effect may not fully account for the clinical benefit. This motivates continued interest in the prejunctional and micro-contraction-suppression pathways above as contributors, without establishing which pathway predominates.[3]

FDA-Approved Agents​

Mirabegron (Myrbetriq)​

First-in-class: FDA-approved 2012.[7]

PropertyDetail
IndicationsOAB in adults, alone or with solifenacin; neurogenic detrusor overactivity in pediatric patients age ≥3 years (granules with labeled dosing from 11 kg; tablets from 35 kg)[7]
Adult dosingStart 25 mg PO daily; can increase to 50 mg after 4–8 weeks
Pediatric dosingFor NDO age ≥3 years: usual granule doses are 24→48 mg/day at 11–<22 kg and 32→64 mg/day at 22–<35 kg; at ≥35 kg, tablets 25→50 mg/day or granules 48→80 mg/day. Increase after 4–8 weeks if needed; give either pediatric product with food. The formulations are not interchangeable mg-for-mg; renal or hepatic impairment may lower the maximum dose. Monitor BP, particularly at ages 3–<12 years.[7]
Onset of efficacy4–8 weeks; sustained through 52 weeks
Key cautionsSevere uncontrolled HTN (SBP ≥180 and/or DBP ≥110 mm Hg) — not recommended; eGFR below 15 or dialysis — not recommended; Child-Pugh C hepatic impairment — not recommended; lower dose ceiling with Child-Pugh B or eGFR 15–29
Drug interactionsModerate CYP2D6 inhibitor — caution with metoprolol, desipramine, flecainide, thioridazine, propafenone; digoxin levels rise, so start digoxin at the lowest dose and monitor levels

Vibegron (Gemtesa)​

FDA-approved 2020 (OAB); 2024 expansion to OAB in men on BPH pharmacotherapy (COURAGE trial).[8][9][23]

PropertyDetail
IndicationsOAB (adults); OAB in adult males on BPH pharmacologic therapy (α-blocker ± 5-ARI)
Dose75 mg PO daily (no titration required)[23]
Onset of efficacyWithin 4 weeks; sustained 52+ weeks
BP effectsMinimal — ambulatory BP monitoring shows no clinically meaningful changes[10]
Drug interactionsFewer than mirabegron; no CYP2D6 inhibition. Digoxin levels rise — check levels before and during coadministration[23]

Clinical Efficacy​

Mirabegron — phase 3 data[7][11]​

OutcomeMirabegron 50 mgPlacebo
Micturition frequency reduction−1.6 to −1.9 episodes / 24 h−1.0 to −1.3
Incontinence reduction−1.4 to −1.6 episodes / 24 h−1.1 to −1.2
Volume per void, adjusted mean change at week 12+18 to +24 mL+7 to +12 mL[7]

Network meta-analysis: mirabegron 50 mg has comparable overall efficacy to most antimuscarinics, with significantly better tolerability on dry mouth (better than 21/22 active comparators), constipation (9/20), and urinary retention (7/10).[12]

Vibegron — EMPOWUR trial (1,518 patients)[8][13]​

OutcomeVibegron 75 mgPlacebo
Micturition frequency reduction−1.8 episodes / 24 h−1.3
Incontinence reductionAmong participants with urge incontinence, −2.0 versus −1.4 episodes/24 h at week 12 (P<0.0001)[8]—
Volume per voidSignificantly greater increase (P<0.0001)—

In the 40-week extension, 506 EMPOWUR completers entered active treatment (505 treated: 273 vibegron, 232 tolterodine); vibegron and tolterodine participants continued their assignments, and placebo participants were re-randomized 1:1 to vibegron or tolterodine. Symptom improvements were maintained among participants receiving vibegron for 52 weeks; there was no placebo comparison after week 12.[13]

Vibegron vs. mirabegron​

Three short Japanese trials in women directly compared mirabegron and vibegron at 50 mg/day.[27] Two overlapping 2025 meta-analyses found no statistically significant difference in overall OAB symptom score or total adverse events; one found a small urgency-incontinence score difference favoring vibegron.[27][28] Indirect comparisons add:

  • Indirect treatment comparison (Kennelly 2021): vibegron may have slightly greater efficacy for total incontinence episodes at 4 and 52 weeks and volume voided at 12 and 52 weeks[14]
  • 2025 network meta-analysis (Huang): vibegron outperformed mirabegron and antimuscarinics in reducing micturition frequency; vibegron 100 mg (dose higher than FDA-approved 75 mg) showed the greatest reduction[15]
  • Vibegron has simpler US dosing (75 mg daily without titration) and lacks mirabegron's CYP2D6 inhibition.[7][23]

Special Populations​

Men with BPH — the COURAGE trial​

Vibegron's 2024 FDA expansion for OAB in men on BPH therapy is backed by the COURAGE trial (1,105 men on α-blocker ± 5-ARI):[9]

Outcome at 12 weeksVibegron effect
Daily micturitionsPlacebo-adjusted least-squares difference −0.74/day at week 12 (95% CI −1.02 to −0.46; P<0.001)
Urgency episodesSignificantly reduced vs. placebo
IPSS-storage subscoreSignificantly improved vs. placebo
Retention / safetyComparable to placebo

This is the first β3-agonist approved specifically for the "prostate-with-OAB" phenotype, a common clinical scenario where antimuscarinics are often avoided due to retention concerns. The AUA BPH guideline (2026) states that clinicians may offer a β3 agonist alone or with an α-blocker for moderate-to-severe predominant storage LUTS ; in the PLUS trial, add-on mirabegron in men taking tamsulosin had adverse-event rates similar to tamsulosin alone, and in a 12-week placebo-controlled study of mirabegron alone in men with obstruction it did not worsen Qmax or detrusor pressure at Qmax.[25]

Elderly population​

  • Real-world data: in one single-center retrospective series (35 β3-agonist recipients), β3-agonist recipients were older (mean age 77.4 years versus 69.2 for antimuscarinics)[16]
  • This likely reflects preference for β3-agonists in patients vulnerable to anticholinergic side effects
  • In a Japanese claims cohort of adults ≥65 years, anticholinergic users had higher observed dementia incidence than β3-agonist users (adjusted HR 1.22, 95% CI 1.15–1.30).[24] A Danish new-user active-comparator analysis instead found lower observed dementia incidence with antimuscarinics than mirabegron (IRR 0.82, 95% CI 0.74–0.92).[29] Both are observational, and comparative long-term cognitive risk remains uncertain.[24][29]
  • Avoiding anticholinergic burden is a practical advantage.

Pediatric NDO​

Mirabegron is FDA-approved for neurogenic detrusor overactivity in pediatric patients age ≥3 years; use weight-based granules from 11 kg to <35 kg, and tablets or granules at ≥35 kg according to their separate labeled regimens.[7]

Neurogenic LUT dysfunction​

Separate symptoms from urodynamic risk. EAU 2026 gives a strong recommendation to use antimuscarinics or β3 agonists for neurogenic OAB, and a strong recommendation against using β3 agonists with the intention of reducing urodynamically proven NDO (level 1a evidence that mirabegron does not improve urodynamic parameters in NDO).[22] Reassess pressure and compliance when these drive treatment.[22] Mirabegron's pediatric NDO indication does not confer an adult NDO indication; adult use for NDO is off-label. See NLUTD for risk-based surveillance.[7]

Adverse Effects​

Common[7][8][13][17][23]​

AEMirabegronVibegron
HypertensionMirabegron: 7.5% at 50 mg vs 7.6% placebo and 11.3% at 25 mg in pooled 12-week OAB trials; see BP effects below[7]Vibegron: 9.0% vs 8.3% placebo over 24 weeks in men on BPH therapy (COURAGE)[9]; 1.7% vs 1.7% over 12 weeks in EMPOWUR[8]
UTI2.9–4.2% with mirabegron in pooled 12-week trials and 5.9% at 52 weeks[7]2.5% with vibegron in 24-week COURAGE, 5.0% in 12-week EMPOWUR, and 6.6% in its extension[9][8][13]
Headache2.1–3.2% with mirabegron in pooled 12-week trials and 4.1% at 52 weeks[7]4.0% with vibegron in 12-week EMPOWUR and 5.5% in its extension[8][13]
Nasopharyngitis3.5–3.9% in adult mirabegron OAB trials[7]2.8% in 12-week EMPOWUR and 4.8% in its extension[8][13]
Dry mouth≈2–3% (2.8% at 52 weeks vs 8.6% with tolterodine in the label's active-controlled study)[7]1.7% with vibegron vs 0.9% placebo in 12-week EMPOWUR[8]
ConstipationLower than antimuscarinicsLower than antimuscarinics
Discontinuation for AELow1.7% with vibegron vs 3.3% with tolterodine in 12-week EMPOWUR[8]; 1.5% vs 3.4% among extension-study participants[13]

Serious / unexpected adverse effects (pharmacovigilance)​

A FAERS disproportionality analysis identified the following mirabegron reporting signals:[18]

  • Cardiac arrhythmias: atrial fibrillation, tachycardia, palpitations
  • Neurological events: dementia, TIA, Parkinson's disease
  • Vascular: ANCA-positive vasculitis
  • Angioedema: lip or tongue swelling

Urinary retention​

Japanese JADER adverse event database analysis showed urinary retention as the most frequently reported AE:[19]

  • Mirabegron crude ROR: 62.1
  • Vibegron crude ROR: 250 (spontaneous-report disproportionality signals)
  • With mirabegron, retention reports were more frequent during concomitant antimuscarinic use and in men with a BPH history; about half of β3-agonist retention reports occurred within 15 days of initiation.[19]

In COURAGE, men on stable BPH pharmacotherapy without prior retention or Qmax <5 mL/s had urinary-retention adverse events in 5/553 (0.9%) with vibegron and 3/551 (0.5%) with placebo over 24 weeks.[9] Vibegron is approved for OAB in men on BPH pharmacotherapy.[23]

Cardiovascular safety​

Vibegron specifically: a dedicated 28-day placebo-controlled ambulatory BP study found no clinically meaningful differences in BP or HR.[10][20] EMPOWUR: hypertension incidence with vibegron 1.7% versus placebo 1.7%.[10]

Mirabegron: the label reports mean BP increases of about 0.5–1 mm Hg over placebo at 50 mg in OAB patients (about 3.5/1.5 mm Hg in healthy volunteers), and the volunteer studies showed dose-related rises. Worsening of pre-existing hypertension was reported infrequently. Check BP periodically, especially in hypertensive patients.[7]

Contraindications and Precautions​

Known hypersensitivity to mirabegron or its formulation components contraindicates mirabegron; known hypersensitivity to vibegron or its components contraindicates vibegron.[7][23]

Mirabegron[7]​

Not recommended for:

  • Severe uncontrolled hypertension: mirabegron is not recommended when adult systolic BP is ≥180 or diastolic BP is ≥110 mm Hg; in pediatric NDO, the label uses BP above the age-, sex-, and stature-specific 99th percentile plus 5 mm Hg.[4][7]
  • eGFR below 15 mL/min/1.73 m² or dialysis[7]
  • Child-Pugh C hepatic impairment

The adult maximum is 25 mg/day with eGFR 15–29 or Child-Pugh B impairment. With CYP2D6 substrates (particularly narrow-therapeutic-index drugs such as flecainide, thioridazine and propafenone), monitor and consider adjustment of the substrate drug. Use the lowest digoxin dose when starting with mirabegron and monitor digoxin levels. Mirabegron also carries a retention caution in clinically significant bladder outlet obstruction and with concomitant antimuscarinics.[7] Tongue, hypopharyngeal, or laryngeal angioedema requires prompt discontinuation and airway management.[7]

Vibegron​

  • No adjustment is recommended for eGFR 15–89 mL/min/1.73 m² or mild or moderate hepatic impairment. Not recommended with eGFR below 15 (including dialysis) or severe hepatic impairment.[23]
  • Digoxin requires level monitoring before and during coadministration, and after stopping vibegron; adjust digoxin as needed.[23]
  • Vibegron does not inhibit CYP2D6.[23]
  • Monitor for urinary retention with bladder outlet obstruction or concomitant antimuscarinic use; discontinue vibegron if retention develops. Angioedema involving the upper airway requires immediate discontinuation and airway treatment. The label carries no blood pressure warning; pediatric safety and effectiveness are unestablished.[23]

General precautions​

  • BP monitoring: particularly for mirabegron, particularly in hypertensive patients
  • Urinary retention risk assessment: consider baseline PVR with emptying symptoms or a history of retention, enlarged prostate, neurologic disease, incontinence or prostate surgery, or long-standing diabetes.[4] Monitor for new retention early after treatment starts; about half of cases reported in JADER occurred within 15 days.[19]
  • Concomitant antimuscarinic: increases retention risk

Combination Therapy​

EAU 2026 (non-neurogenic female LUTS) offers a β3 agonist to women with OAB who fail conservative management and lists a β3 agonist, alone or with an anticholinergic, as an option when an anticholinergic proves ineffective . It rates mirabegron and vibegron as effective for OAB/UUI with adverse-event rates similar to placebo, and as effective as antimuscarinics with less dry mouth (level 1a); its panel review found β3 agonists more effective than antimuscarinics for nocturia episodes. It suggests adding mirabegron rather than escalating solifenacin 5 mg .[26]

Mirabegron 25–50 mg + solifenacin 5 mg improved outcomes in wet OAB trials: SYNERGY II tested mirabegron 50 mg plus solifenacin 5 mg in adults with wet OAB and found fewer daily incontinence episodes and micturitions than with either monotherapy; in BESIDE, patients remaining incontinent on solifenacin 5 mg received add-on mirabegron, which improved incontinence versus solifenacin 5 mg, was noninferior to solifenacin 10 mg for the number of incontinence episodes in a 3-day diary at week 12, and improved micturition frequency versus 10 mg.[12][15][21][31][4][32] The AUA/SUFU guideline offers a different-class combination after inadequate single-drug response .[4] The trade-off: increased anticholinergic side effects (dry mouth, constipation) compared with β3-agonist monotherapy.

  • BESIDE and SYNERGY are the trials cited by the AUA/SUFU panel for a combination principle it considered likely generalizable within each class; SYNERGY II tested the combination over 12 months.[4][32]
  • Evidence for combinations beyond mirabegron plus solifenacin is limited. AUA/SUFU considers the class-combination principle likely generalizable, but the size of benefit and harms of other pairings remain uncertain.[4]

Clinical Positioning​

2024 AUA/SUFU framework[4]​

β3-agonists are positioned as:

  • Offered alongside antimuscarinics as an oral OAB option , with side-effect profile and shared decision-making guiding the choice[4]
  • The guideline notes lower rates of dry mouth and constipation and likely less effect on PVR:
    • Elderly
    • Cognitive impairment
    • Dry-mouth intolerance
    • Constipation-prone
    • Narrow-angle glaucoma, impaired gastric emptying or prior retention (where the guideline urges extreme caution with antimuscarinics)
    • Men with OAB receiving pharmacologic BPH therapy (vibegron is FDA-approved for this population; monitor for retention with bladder outlet obstruction)[4][23]
  • Alternative when antimuscarinics are contraindicated or not tolerated
  • Add-on therapy for patients with inadequate response to antimuscarinics

Other treatment options​

Discuss minimally invasive therapy when medication is ineffective, poorly tolerated or inconsistent with the patient’s preferences. The AUA/SUFU guideline permits these options through shared decision-making without requiring prior medication trials.[4] Options include:

  • Intradetrusor onabotulinumtoxinA (100 U for adults with OAB and urge urinary incontinence, or 200 U for adults with urinary incontinence due to neurologic detrusor overactivity, after inadequate response to or intolerance of an anticholinergic)[30]
  • Sacral neuromodulation (InterStim, Axonics)
  • Posterior tibial nerve stimulation (PTNS, eCoin, Revi)

See Also​

References​

1. Wei JT, Dauw CA, Brodsky CN. Lower urinary tract symptoms in men. JAMA. 2025;334(9):809–821. doi:10.1001/jama.2025.7045

2. Andersson KE, Martin N, Nitti V. Selective β3-adrenoceptor agonists for the treatment of overactive bladder. J Urol. 2013;190(4):1173–80. doi:10.1016/j.juro.2013.02.104

3. Igawa Y, Aizawa N, Michel MC. β3-adrenoceptors in the normal and diseased urinary bladder — what are the open questions? Br J Pharmacol. 2019;176(14):2525–2538. doi:10.1111/bph.14658

4. Cameron AP, Chung DE, Dielubanza EJ, et al. The AUA/SUFU guideline on the diagnosis and treatment of idiopathic overactive bladder. J Urol. 2024;212(1):11–20. doi:10.1097/JU.0000000000003985

5. Hennenberg M, Michel MC. Adrenoceptors in the lower urinary tract. Handb Exp Pharmacol. 2024;285:333–367. doi:10.1007/164_2023_678

6. Silva I, Magalhães-Cardoso MT, Ferreirinha F, et al. β adrenoceptor-induced cholinergic inhibition in human and rat urinary bladders involves the exchange protein directly activated by cyclic AMP 1 favoring adenosine release. Br J Pharmacol. 2020;177(7):1589–1608. doi:10.1111/bph.14921

7. Astellas Pharma US. Myrbetriq / Myrbetriq Granules (mirabegron): prescribing information. Sections 1.1–1.2. Manufacturer prescribing information; DailyMed label. Accessed September 11, 2026.

8. Staskin D, Frankel J, Varano S, et al. 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. doi:10.1097/JU.0000000000000807

9. Staskin D, Owens-Grillo J, Thomas E, et al. 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. doi:10.1097/JU.0000000000003999

10. Frankel J, Staskin D, Varano S, et al. An evaluation of the efficacy and safety of vibegron in the treatment of overactive bladder. Ther Clin Risk Manag. 2022;18:171–182. doi:10.2147/TCRM.S310371

11. Deeks ED. Mirabegron: a review in overactive bladder syndrome. Drugs. 2018;78(8):833–844. doi:10.1007/s40265-018-0924-4

12. Kelleher C, Hakimi Z, Zur R, et al. Efficacy and tolerability of mirabegron compared with antimuscarinic monotherapy or combination therapies for overactive bladder: a systematic review and network meta-analysis. Eur Urol. 2018;74(3):324–333. doi:10.1016/j.eururo.2018.03.020

13. Staskin D, Frankel J, Varano S, et al. Once-daily vibegron 75 mg for overactive bladder: long-term safety and efficacy from a double-blind extension study of the international phase 3 trial (EMPOWUR). J Urol. 2021;205(5):1421–1429. doi:10.1097/JU.0000000000001574

14. Kennelly MJ, Rhodes T, Girman CJ, et al. Efficacy of vibegron and mirabegron for overactive bladder: a systematic literature review and indirect treatment comparison. Adv Ther. 2021;38(11):5452–5464. doi:10.1007/s12325-021-01902-8

15. Huang W, Zheng X, Luo J, Chen Y, Xu Y. Comparative efficacy and adverse effects of β3-agonists and antimuscarinics in overactive bladder: a network and component network meta-analysis. Eur J Clin Pharmacol. 2025. doi:10.1007/s00228-025-03855-1

16. Huang CK, Lin CC, Lin AT. Effectiveness of antimuscarinics and a beta-3 adrenoceptor agonist in patients with overactive bladder in a real-world setting. Sci Rep. 2020;10(1):11355. doi:10.1038/s41598-020-68170-4

17. Chapple CR, Cruz F, Cardozo L, et al. Safety and efficacy of mirabegron: analysis of a large integrated clinical trial database of patients with overactive bladder receiving mirabegron, antimuscarinics, or placebo. Eur Urol. 2020;77(1):119–128. doi:10.1016/j.eururo.2019.09.024

18. Wang J, Zhang A, Ye M, Zhang C. Examining the safety of mirabegron: an analysis of real-world pharmacovigilance data from the US FDA Adverse Event Reporting System (FAERS) database. Front Pharmacol. 2024;15:1376535. doi:10.3389/fphar.2024.1376535

19. Kawazoe T, Ishida T, Jobu K, et al. Analysis of urinary retention caused by selective β3-adrenoceptor agonists using the Japanese Adverse Drug Event Report database (JADER). Pharmazie. 2023;78(5):56–62. doi:10.1691/ph.2023.3509

20. Peyronnet B, Brucker BM, De Nunzio C, et al. Vibegron in overactive bladder: a comprehensive review of efficacy, safety and patient-reported outcomes. World J Urol. 2025;43(1):514. doi:10.1007/s00345-025-05799-8

21. Jiang YH, Kuo HC. Current optimal pharmacologic therapies for overactive bladder. Expert Opin Pharmacother. 2023;24(18):2005–2019. doi:10.1080/14656566.2023.2264183

22. European Association of Urology. EAU Guidelines on Neuro-Urology (Limited Update March 2026). Section 3.4.2.d, drug treatment recommendations. Official guideline.

23. Sumitomo Pharma America, Inc. GEMTESA (vibegron): US prescribing information. Revised February 2025. Sections 7, 8.6, 8.7, and 12.3. Manufacturer label. Accessed September 11, 2026.

24. Okita Y, Shimomura Y, Komukai S, et al. Risks of dementia associated with anticholinergic medication compared to beta-3 agonist among older patients with overactive bladder in Japan: the LIFE study. Int J Geriatr Psychiatry. 2025;40(1):e70036. doi:10.1002/gps.70036

25. Goueli R, Badlani GH, Welliver C, et al. Management of lower urinary tract symptoms attributed to benign prostatic hyperplasia (BPH): AUA guideline (2026). Part II: Medical management. J Urol. 2026;216(2):152-160. doi:10.1097/JU.0000000000005098

26. European Association of Urology. EAU Guidelines on Management of Non-Neurogenic Female Lower Urinary Tract Symptoms (LUTS) (Limited Update March 2026). Guideline.

27. Zhang J, Chi J, Lou K, et al. "Comparison of efficacy and safety of mirabegron and vibegron in the treatment of Overactive Bladder (OAB) in older women: A systematic review and meta-analysis." PLoS One. 2025;20(4):e0317550. doi:10.1371/journal.pone.0317550

28. Liang P, Yu L, Xia B, Zhang D. "Comparative efficacy and safety of mirabegron and vibegron in female patients with overactive bladder: a systematic review and meta-analysis of randomized controlled trials." Urology. 2025;199:182–190. doi:10.1016/j.urology.2025.02.018

29. Pourhadi N, Janbek J, Gasse C, et al. "Bladder drugs and risk of dementia: Danish nationwide active comparator study." BMJ Med. 2025;4(1):e001125. doi:10.1136/bmjmed-2024-001125

30. DailyMed. "BOTOX (onabotulinumtoxinA): prescribing information." US label.

31. Drake MJ, Chapple C, Esen AA, et al. "Efficacy and Safety of Mirabegron Add-on Therapy to Solifenacin in Incontinent Overactive Bladder Patients with an Inadequate Response to Initial 4-Week Solifenacin Monotherapy: A Randomised Double-blind Multicentre Phase 3B Study (BESIDE)." Eur Urol. 2016;70(1):136–145. doi:10.1016/j.eururo.2016.02.030

32. Gratzke C, van Maanen R, Chapple C, et al. "Long-term Safety and Efficacy of Mirabegron and Solifenacin in Combination Compared with Monotherapy in Patients with Overactive Bladder: A Randomised, Multicentre Phase 3 Study (SYNERGY II)." Eur Urol. 2018;74(4):501–509. doi:10.1016/j.eururo.2018.05.005