Drug Monograph
Myrbetriq (Mirabegron)
mirabegron extended-release tablets
Pharmacokinetic Profile
Half-Life
~50 h (adults)
Metabolism
Multiple pathways (CYP3A4, CYP2D6, UGT, BChE)
Protein Binding
~71%
Bioavailability
29% (25 mg); 35% (50 mg)
Volume of Distribution
1670 L (Vss)
Clinical Information
Drug Class
Beta-3 Adrenergic Agonist
Available Doses
25 mg, 50 mg ER tablets; granules for oral suspension (8 mg/mL)
Route
Oral
Renal Adjustment
Max 25 mg if eGFR 15–29; not recommended if <15
Hepatic Adjustment
Max 25 mg (Child-Pugh B); not recommended in C
Pregnancy
No adequate human data
Lactation
Unknown excretion; present in rat milk
Schedule
Prescription only (not scheduled)
Generic Available
Yes (approved 2024)
CYP2D6 Inhibition
Moderate inhibitor
Indications
| Indication | Approved Population | Therapy Type | Status |
|---|---|---|---|
| Overactive bladder (OAB) — urge urinary incontinence, urgency, urinary frequency | Adults | Monotherapy | FDA Approved |
| OAB — combination therapy with solifenacin succinate 5 mg | Adults | Combination (with solifenacin) | FDA Approved |
| Neurogenic detrusor overactivity (NDO) | Pediatric ≥3 years, ≥35 kg (tablets); ≥3 years (granules) | Monotherapy | FDA Approved |
Mirabegron is the first beta-3 adrenergic receptor agonist approved for overactive bladder, representing a fundamentally different mechanism from the antimuscarinic class. Initially approved by the FDA in June 2012 for adult OAB, it gained an additional indication for combination therapy with solifenacin in 2021, as well as approval for pediatric neurogenic detrusor overactivity. Across three pivotal 12-week trials involving over 4,100 patients, mirabegron demonstrated statistically significant reductions in incontinence episodes, micturition frequency, and urgency compared with placebo.
Off-Label Uses
Neurogenic detrusor overactivity in adults: Used in adults with spinal cord injury or multiple sclerosis who have detrusor overactivity, either alone or as add-on to antimuscarinics, based on extrapolation from adult OAB data and emerging evidence. Evidence quality: Moderate.
Brown adipose tissue activation / metabolic research: Mirabegron has been investigated for its thermogenic effects via beta-3 receptor activation of brown adipose tissue. This remains an investigational application. Evidence quality: Low.
Dosing
Adult Dosing — Overactive Bladder
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| OAB — monotherapy, treatment-naive adult | 25 mg once daily | 25–50 mg once daily | 50 mg/day | May increase to 50 mg after 4–8 weeks if needed Swallow whole with water; do not crush, chew, or divide; take with or without food |
| OAB — combination with solifenacin 5 mg | 25 mg once daily + solifenacin 5 mg | 25–50 mg + solifenacin 5 mg once daily | 50 mg + solifenacin 5 mg/day | Increase mirabegron to 50 mg after 4–8 weeks if needed; solifenacin dose remains fixed at 5 mg |
| OAB — severe renal impairment (eGFR 15–29) | 25 mg once daily | 25 mg once daily | 25 mg/day | Do not exceed 25 mg Not recommended if eGFR <15 or on dialysis |
| OAB — mild renal impairment (eGFR 30–89) | 25 mg once daily | 25–50 mg once daily | 50 mg/day | No dose adjustment required |
| OAB — moderate hepatic impairment (Child-Pugh B) | 25 mg once daily | 25 mg once daily | 25 mg/day | Do not exceed 25 mg Not recommended in Child-Pugh C; no adjustment for Child-Pugh A |
Pediatric Dosing — Neurogenic Detrusor Overactivity
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| NDO — child ≥3 years, weight ≥35 kg (tablets) | 25 mg once daily | 25–50 mg once daily | 50 mg/day | Increase after 4–8 weeks if needed Must take with food; swallow whole |
| NDO — child ≥3 years, weight ≥35 kg (granules) | 6 mL (48 mg) once daily | 6–10 mL once daily | 10 mL (80 mg)/day | Oral suspension 8 mg/mL Must take with food |
| NDO — child ≥3 years, weight 22 to <35 kg (granules) | 4 mL (32 mg) once daily | 4–8 mL once daily | 8 mL (64 mg)/day | Weight-based dosing; granules only Must take with food |
| NDO — child ≥3 years, weight 11 to <22 kg (granules) | 3 mL (24 mg) once daily | 3–6 mL once daily | 6 mL (48 mg)/day | Weight-based dosing; granules only Must take with food |
Clinical Pearl: Non-Anticholinergic Advantage
Mirabegron offers a distinct advantage over antimuscarinic agents in patients where anticholinergic side effects are a concern. The PILLAR study, a phase IV trial specifically in adults aged 65 and older, demonstrated that mirabegron 25–50 mg improved OAB symptoms without the cognitive side effects associated with antimuscarinic agents. This positions mirabegron as a preferred first-line pharmacotherapy in elderly patients, patients with cognitive impairment risk, and those intolerant of anticholinergic dry mouth or constipation.
Pharmacology
Mechanism of Action
Mirabegron is a selective agonist of the human beta-3 adrenergic receptor (beta-3 AR), a receptor subtype predominantly expressed in the detrusor smooth muscle of the urinary bladder. During the storage phase of the micturition cycle, activation of beta-3 ARs by mirabegron induces smooth muscle relaxation through a cyclic AMP-mediated pathway, increasing functional bladder capacity and reducing the sensation of urgency. This mechanism is fundamentally distinct from antimuscarinic agents, which block the muscarinic receptors responsible for detrusor contraction. Mirabegron demonstrates very low intrinsic activity at the beta-1 and beta-2 adrenergic receptor subtypes at therapeutic doses, though beta-1 stimulation has been observed at supratherapeutic exposures (200 mg), which accounts for the modest blood pressure elevation seen with the drug.
ADME Profile
| Parameter | Value | Clinical Implication |
|---|---|---|
| Absorption | Tmax ~3.5 h; bioavailability 29% (25 mg) to 35% (50 mg); increases more than dose-proportionally; no clinically significant food effect in adults | Dose-dependent bioavailability explains more-than-proportional AUC increase; pediatric patients must take with food (fasted exposure 80–170% higher) |
| Distribution | Vss 1670 L; ~71% protein-bound (albumin and alpha-1 acid glycoprotein); distributes to erythrocytes (~2-fold higher RBC concentration) | Very large volume of distribution; moderate protein binding means drug interactions via displacement are unlikely; extensive tissue distribution |
| Metabolism | Multiple pathways: dealkylation, oxidation, glucuronidation, amide hydrolysis via CYP3A4, CYP2D6, UGT, and butyrylcholinesterase; two major inactive glucuronide metabolites (16% and 11% of exposure); moderate CYP2D6 inhibitor | No single dominant enzyme; not a sensitive CYP3A4 substrate in vivo; CYP2D6 inhibition requires monitoring of co-administered CYP2D6 substrates with narrow therapeutic index |
| Elimination | t½ ~50 h (adults); CLtot 57 L/h; CLR 13 L/h (~25% of CLtot); 55% urine, 34% feces; ~25% unchanged in urine; renal excretion via active tubular secretion and glomerular filtration | Long half-life supports once-daily dosing; steady state at ~7 days; significant renal contribution necessitates dose adjustment in severe renal impairment |
Side Effects
≥10%
Very Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Hypertension | 11.3% (25 mg); 7.5% (50 mg) | Includes BP above normal range and BP increased from baseline; occurs predominantly in patients with baseline hypertension; mean SBP increase ~0.5–1 mmHg above placebo in OAB trials; dose-related increases of ~3.5/1.5 mmHg seen in healthy volunteer studies at 50 mg |
1–10%
Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Nasopharyngitis | 3.5% (25 mg); 3.9% (50 mg) | Common in clinical trials; not clearly drug-related; similar rates observed in long-term studies |
| Urinary tract infection | 4.2% (25 mg); 2.9% (50 mg) | More frequent at 25 mg in 12-week trials; 5.9% in 52-week active-controlled study at 50 mg |
| Headache | 2.1% (25 mg); 3.2% (50 mg) | Usually mild to moderate; one of the most frequent reasons for early discontinuation |
| Constipation | 1.6% (25 mg); 1.6% (50 mg) | Rates are low compared to antimuscarinic agents; not dose-related; 2.8% in 52-week study |
| Upper respiratory tract infection | 2.1% (25 mg); 1.5% (50 mg) | Common in clinical trials; not clearly drug-related |
| Tachycardia | 1.6% (25 mg); 1.2% (50 mg) | Reflects beta-adrenergic activity; not clearly dose-dependent; palpitations also reported (<1%) |
| Arthralgia | 1.6% (25 mg); 1.3% (50 mg) | Mild; no specific intervention required |
| Diarrhea | 1.2% (25 mg); 1.5% (50 mg) | Usually self-limiting; consider other causes |
| Fatigue | 1.4% (25 mg); 1.2% (50 mg) | Mild; not clearly dose-related |
| Abdominal pain | 1.4% (25 mg); 0.6% (50 mg) | More common at lower dose in trials; assess for GI causes if persistent |
Serious
Serious Adverse Effects (Regardless of Frequency)
| Adverse Effect | Estimated Frequency | Typical Onset | Required Action |
|---|---|---|---|
| Angioedema | Rare (postmarketing) | Hours after first dose or after multiple doses | Immediately discontinue; provide emergency airway management; permanent discontinuation required |
| Severe hypertension / hypertensive crisis | Rare | Days to weeks | Discontinue or reduce dose; initiate antihypertensive therapy; not recommended if SBP ≥180 or DBP ≥110 |
| Urinary retention | Rare (postmarketing) | Variable; higher risk with BOO or concurrent antimuscarinic use | Discontinue if unable to void; catheterisation may be needed; use caution with concurrent antimuscarinics |
| Atrial fibrillation | 0.2% (pivotal trials) | Variable | Evaluate cardiac rhythm; cardiology referral; consider discontinuation based on clinical context |
| Stevens-Johnson syndrome | Very rare (single case report) | Variable | Immediate discontinuation; dermatology and intensive care consultation; reported with concurrent herbal medication |
| Cerebrovascular accident | 0.4% (52-week study, 50 mg) | Variable | Emergency care; reassess cardiovascular risk; causality not established |
Discontinuation
Discontinuation Rates
12-Week Monotherapy Trials
Low (≤0.2% per event)
Top reasons: Nausea, headache, hypertension, diarrhea, constipation, dizziness, tachycardia (each ≤0.2%)
52-Week Active-Controlled (Study 4)
Constipation 0.9%
Other reasons >0.4%: Headache (0.6%), dizziness (0.5%), hypertension (0.5%), dry eyes (0.4%), nausea (0.4%)
| Reason for Discontinuation | Incidence (52-week) | Context |
|---|---|---|
| Constipation | 0.9% | Most frequent cause in long-term study; lower than rates seen with antimuscarinic comparator |
| Headache | 0.6% | Usually mild to moderate; resolves after discontinuation |
| Hypertension | 0.5% | Worsening of pre-existing hypertension in a minority of patients |
Managing Blood Pressure Elevation
The blood pressure increase with mirabegron is modest in OAB patients (mean ~0.5–1 mmHg above placebo at 50 mg) but was greater in healthy volunteer studies (~3.5/1.5 mmHg at 50 mg). Pre-existing hypertension was the main risk factor. Measure blood pressure before initiating treatment and periodically thereafter. The drug is not recommended in patients with severe uncontrolled hypertension (SBP ≥180 and/or DBP ≥110 mmHg). Worsening of pre-existing hypertension was infrequent in clinical trials.
Drug Interactions
Mirabegron is metabolised by multiple pathways with no single dominant enzyme. It is a moderate inhibitor of CYP2D6, which is the most clinically significant interaction pathway. Mirabegron does not inhibit CYP1A2, 2C9, 2C19, or 3A4, and does not induce CYP1A2 or CYP3A at clinically relevant concentrations.
MajorCYP2D6 substrates (narrow TI): thioridazine, flecainide, propafenone
MechanismMirabegron is a moderate CYP2D6 inhibitor; increases systemic exposure of CYP2D6 substrates
EffectDesipramine Cmax increased 79% and AUC increased 241% (with 100 mg mirabegron OCAS); metoprolol Cmax increased 90% and AUC increased 229% (with 160 mg IR mirabegron)
ManagementAppropriate monitoring and dose adjustment of CYP2D6 substrates, especially narrow therapeutic index drugs; avoid thioridazine co-administration
FDA PIMajorDigoxin
MechanismInhibition of P-glycoprotein-mediated drug transport and/or intestinal absorption
EffectDigoxin Cmax increased 29% and AUC increased 27% with mirabegron monotherapy; Cmax +14% and AUC +10% with mirabegron+solifenacin combination
ManagementInitiate digoxin at the lowest dose when starting mirabegron; monitor serum digoxin concentrations and titrate to clinical effect
FDA PIModerateMetoprolol and other CYP2D6-metabolised beta-blockers
MechanismCYP2D6 inhibition by mirabegron increases beta-blocker exposure
EffectMetoprolol Cmax increased 90% and AUC increased 229% (with 160 mg IR mirabegron); may enhance bradycardic and hypotensive effects
ManagementMonitor heart rate and blood pressure; consider reducing metoprolol dose or using a beta-blocker not primarily metabolised by CYP2D6 (e.g., bisoprolol, atenolol)
FDA PIModerateTamsulosin (with mirabegron + solifenacin combination)
MechanismCYP2D6 inhibition by mirabegron increases tamsulosin exposure
EffectTamsulosin AUC increased 47.5% and Cmax increased 54.3% when co-administered with mirabegron 50 mg + solifenacin 5 mg
ManagementMonitor for tamsulosin adverse effects (orthostatic hypotension, dizziness); dose reduction may be needed
FDA PIModerateWarfarin
MechanismPotential CYP2D6-mediated interaction; single-dose interaction study only; multiple-dose effect not fully characterised
EffectFull pharmacodynamic interaction (INR, prothrombin time) with multiple warfarin doses not fully investigated
ManagementMonitor INR closely when initiating or adjusting mirabegron in patients on warfarin
FDA PIMinorKetoconazole (strong CYP3A4 inhibitor)
MechanismCYP3A4 inhibition reduces mirabegron first-pass metabolism
EffectMirabegron Cmax increased 45% and AUC increased 80% with ketoconazole 400 mg daily
ManagementNo dose adjustment recommended; mirabegron is not considered a sensitive CYP3A4 substrate in vivo (<2-fold AUC increase)
FDA PIMonitoring
- Blood PressureBaseline, then periodically
RoutineMeasure before initiation and at each follow-up visit; particularly important in patients with pre-existing hypertension; not recommended if SBP ≥180 and/or DBP ≥110 mmHg; higher BP increases may occur in pediatric patients - Renal FunctionBaseline
RoutineEstimate GFR before initiation; max dose 25 mg if eGFR 15–29; not recommended if eGFR <15 or on dialysis; reassess periodically in patients with progressive renal disease - Hepatic FunctionBaseline
RoutineAssess Child-Pugh classification before initiation; max 25 mg in Child-Pugh B; not recommended in Child-Pugh C; rare transaminase elevations (>10-fold) reported in 52-week study (0.3%), resolved while continuing drug - Symptom Response4–8 weeks; then every 6–12 months
RoutineReassess OAB symptoms at 4–8 weeks to determine if dose escalation to 50 mg is needed; periodically reassess continued need for therapy - Digoxin LevelsAfter initiating mirabegron in digoxin-treated patients
Trigger-basedMirabegron increases digoxin Cmax 29% and AUC 27%; start with lowest digoxin dose; monitor serum digoxin and titrate to clinical effect - CYP2D6 SubstratesAfter initiating mirabegron
Trigger-basedMonitor patients receiving narrow therapeutic index CYP2D6 substrates (e.g., flecainide, propafenone, thioridazine) for increased drug effect or toxicity; consider dose adjustment - Post-Void ResidualBaseline if BOO suspected; as needed
Trigger-basedMonitor in patients with BOO or taking concurrent antimuscarinic medications; urinary retention reported in postmarketing experience
Contraindications & Cautions
Absolute Contraindications
- Known hypersensitivity: Hypersensitivity to mirabegron or any inactive ingredient of the tablet or oral suspension formulation, including angioedema or anaphylaxis
Relative Contraindications (Specialist Input Recommended)
- Severe uncontrolled hypertension: Not recommended when SBP ≥180 mmHg and/or DBP ≥110 mmHg; mirabegron can further increase blood pressure via beta-adrenergic stimulation
- End-stage renal disease (eGFR <15 or dialysis): Not recommended due to insufficient safety data and expected drug accumulation
- Severe hepatic impairment (Child-Pugh C): Not recommended; hepatic metabolism contributes significantly to drug clearance
- Concurrent use of narrow therapeutic index CYP2D6 substrates (thioridazine): Risk of significant elevation of thioridazine levels and QT prolongation; avoid combination
Use with Caution
- Bladder outlet obstruction: Urinary retention reported postmarketing in patients with BOO; monitor for retention symptoms
- Concurrent antimuscarinic OAB medications: Increased risk of urinary retention when mirabegron is combined with antimuscarinic agents, including the approved combination with solifenacin
- Patients taking digoxin: Initiate digoxin at the lowest dose and monitor serum levels due to increased digoxin exposure
- Pre-existing hypertension: Blood pressure increases may be more clinically significant; periodic monitoring recommended
- Patients on CYP2D6-metabolised medications: Moderate CYP2D6 inhibition may increase exposure to co-administered substrates; dose adjustment may be needed
FDA Safety Advisory
Blood Pressure Monitoring Required
Mirabegron can increase blood pressure in both adult and pediatric patients. The FDA PI specifically warns that periodic blood pressure determinations are recommended, especially in hypertensive patients. In pediatric patients, blood pressure increases may be larger in children (3 to <12 years) than in adolescents (12 to <18 years). The drug is not recommended in patients with severe uncontrolled hypertension.
Patient Counselling
Purpose of Therapy
Mirabegron works by a different mechanism from older bladder medications. Rather than blocking the nerve signals that cause the bladder to squeeze, it activates receptors that help the bladder muscle relax during filling, allowing it to hold more urine. This reduces the frequency of urination, the urgency sensation, and episodes of leakage. Symptom improvement typically becomes noticeable within 4 to 8 weeks.
How to Take
Swallow the tablet whole with water. Do not crush, chew, or divide the tablet, as this would disrupt the extended-release coating. Adults can take it with or without food. If you miss a dose and more than 12 hours have passed, skip the missed dose and take the next one at the regular time.
Blood Pressure
Tell patientMirabegron can cause a small increase in blood pressure. If you have high blood pressure, it is especially important to monitor it at home and keep your regular follow-up appointments. Continue taking your blood pressure medications as prescribed.
Call prescriberIf you develop a severe headache, visual disturbances, chest pain, or if home blood pressure readings are consistently elevated above your usual range.
Urinary Tract Infections
Tell patientUTIs were reported in clinical trials. Stay well hydrated and maintain good urinary hygiene. Symptoms to watch for include burning on urination, increased frequency with small volumes, cloudy or foul-smelling urine, or fever.
Call prescriberIf you develop symptoms of a urinary tract infection, particularly fever, back or flank pain, or blood in urine.
Allergic Reactions
Tell patientRarely, mirabegron can cause serious allergic reactions including swelling of the face, lips, tongue, or throat. This can happen after the first dose or after taking the medication for some time.
Call prescriberStop the medication immediately and seek emergency medical attention if you experience swelling of the tongue or throat, difficulty breathing, or widespread rash with hives.
Difficulty Urinating
Tell patientAlthough rare, mirabegron may cause difficulty emptying the bladder, especially if you have a condition that already affects urine flow (such as an enlarged prostate) or if you take other bladder medications at the same time.
Call prescriberIf you notice difficulty starting urination, very weak stream, inability to urinate, or abdominal discomfort from a full bladder.
Other Medications
Tell patientMirabegron can affect how certain other medications work by changing the way your body processes them. Always tell your doctor, pharmacist, or prescriber about all medications you take, including heart medications (such as metoprolol, digoxin, flecainide), antidepressants, and blood thinners.
Call prescriberIf you start or stop any other medication while taking mirabegron, so your prescriber can check for potential interactions.
Sources
Regulatory (PI / SmPC)
- Myrbetriq (mirabegron extended-release tablets) / Myrbetriq Granules (mirabegron for extended-release oral suspension) — Full Prescribing Information. Astellas Pharma US, Inc. Revised April 2021. Astellas US PIPrimary regulatory source for adult OAB and pediatric NDO indications, dosing tables, adverse reaction data (Tables 8–12), PK parameters, and drug interaction studies.
- Myrbetriq — DailyMed label. National Library of Medicine. DailyMedCurrent NLM-hosted label for dosing, CYP2D6 interaction guidance, renal/hepatic adjustment tables, and combination therapy with solifenacin.
Key Clinical Trials
- Khullar V, Amarenco G, Angulo JC, et al. Efficacy and tolerability of mirabegron, a beta-3-adrenoceptor agonist, in patients with overactive bladder: results from a randomised European-Australian phase 3 trial. Eur Urol. 2013;63(2):283–295. PubMed: 23182126Pivotal phase III trial (Study 1/SCORPIO) demonstrating mirabegron 50 mg and 100 mg superiority over placebo for OAB endpoints, with an active tolterodine ER 4 mg comparator arm.
- Nitti VW, Auerbach S, Martin N, et al. Results of a randomized phase III trial of mirabegron in patients with overactive bladder. J Urol. 2013;189(4):1388–1395. PubMed: 23079373North American phase III trial (Study 3/ARIES) confirming efficacy of mirabegron 50 mg and 100 mg versus placebo for incontinence episodes and micturition frequency.
- Herschorn S, Barkin J, Castro-Diaz D, et al. A phase III, randomized, double-blind, parallel-group, placebo-controlled, multicentre study to assess the efficacy and safety of the beta-3 adrenoceptor agonist, mirabegron, in patients with symptoms of overactive bladder. Urology. 2013;82(2):313–320. PubMed: 23769122Phase III trial (Study 2/CAPRICORN) evaluating mirabegron 25 mg and 50 mg in a global population with OAB symptoms.
- Wagg A, Staskin D, Engel E, et al. Efficacy, safety, and tolerability of mirabegron in patients aged ≥65 yr with overactive bladder wet: a phase IV, double-blind, randomised, placebo-controlled study (PILLAR). Eur Urol. 2020;77(2):211–220. PubMed: 31733997First prospective trial specifically in elderly OAB patients, demonstrating efficacy without cognitive adverse effects, supporting mirabegron as preferred therapy in older adults.
- 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. PubMed: 26965560Key trial supporting mirabegron+solifenacin combination therapy; demonstrated superiority of mirabegron 50 mg add-on versus solifenacin 5 mg alone in solifenacin-inadequate responders.
Guidelines
- 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.
- 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; mirabegron is not on the Beers list, supporting its preferential use in elderly patients with OAB.
Mechanistic / Basic Science
- Andersson KE. Pharmacology of the lower urinary tract smooth muscles and penile erectile tissues. Pharmacol Rev. 2001;53(1):63–99. PubMed: 11171940Comprehensive review of adrenergic receptor pharmacology in the lower urinary tract, providing the mechanistic basis for beta-3 agonist development.
- Mirabegron — StatPearls. National Center for Biotechnology Information. Last updated August 2023. StatPearlsClinical reference covering mechanism of action, PK summary, dosing guidance, monitoring recommendations, and CYP2D6 interaction considerations.
Pharmacokinetics / Special Populations
- Eltink C, Lee J, Schaddelee M, et al. Single dose pharmacokinetics and absolute bioavailability of mirabegron, a beta-3-adrenoceptor agonist for treatment of overactive bladder. Int J Clin Pharmacol Ther. 2012;50(11):838–850. PubMed: 22943933Definitive PK study establishing absolute bioavailability (29% at 25 mg to 45% at 150 mg), Vss (1670 L), CLtot (57 L/h), and dose-dependent oral exposure.
- Krauwinkel W, van Dijk J, Schaddelee M, et al. Role of cytochrome P450 isoenzymes 3A and 2D6 in the in vivo metabolism of mirabegron. Clin Drug Investig. 2013;33(8):579–595. PubMed: 23625188Interaction studies with ketoconazole and rifampicin defining CYP3A4 and CYP2D6 contribution to mirabegron metabolism; establishes mirabegron as a non-sensitive CYP3A4 substrate.
- Dickinson J, Lewand M, Sawamoto T, et al. Effect of renal or hepatic impairment on the pharmacokinetics of mirabegron. Clin Drug Investig. 2013;33(1):11–23. PubMed: 23208320Pharmacokinetic study in renal and hepatic impairment populations providing the basis for dose adjustment recommendations in the FDA label.