BETMIGA Mirabegron 50mg Prolonged Release Tablet 1's
RXDRUG-DR-XY46351-1pc
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Features
Brand
Betmiga
Full Details
Dosage Strength
50 mg
Drug Ingredients
- Mirabegron
Drug Packaging
Prolonged Release Tablet 1's
Generic Name
Mirabegron
Dosage Form
Prolonged Release Tablet
Registration Number
DR-XY46351
Drug Classification
Prescription Drug (RX)
Description
Indications/Uses
Symptomatic treatment of urgency, increased micturition frequency &/or urgency incontinence as may occur in adult patients w/ overactive bladder (OAB) syndrome.
Dosage/Direction for Use
Adults (including elderly patients): The recommended dose is 50 mg once daily with or without food.
Posology: Special populations: Renal and hepatic impairment: Mirabegron (Betmiga) has not been studied in patients with end stage renal disease (GFR < 15 mL/min/1.73 m2 or patients requiring haemodialysis) or severe Gender: No dose adjustment is necessary according to gender.
Paediatric population: The safety and efficacy of Mirabegron (Betmiga) in children below 18 years of age have not yet been established. No data are available.
Method of administration: The tablet is to be taken once daily, with liquids, swallowed whole and is not to be chewed, divided, or crushed.hepatic impairment (Child-Pugh Class C) and it is therefore not recommended for use in these patient populations (see Pharmacology: Pharmacodynamics under Actions and Precautions).
Posology: Special populations: Renal and hepatic impairment: Mirabegron (Betmiga) has not been studied in patients with end stage renal disease (GFR < 15 mL/min/1.73 m2 or patients requiring haemodialysis) or severe Gender: No dose adjustment is necessary according to gender.
Paediatric population: The safety and efficacy of Mirabegron (Betmiga) in children below 18 years of age have not yet been established. No data are available.
Method of administration: The tablet is to be taken once daily, with liquids, swallowed whole and is not to be chewed, divided, or crushed.hepatic impairment (Child-Pugh Class C) and it is therefore not recommended for use in these patient populations (see Pharmacology: Pharmacodynamics under Actions and Precautions).
Overdosage
Mirabegron (Betmiga) has been administered to healthy volunteers at single doses up to 400 mg. At this dose, adverse events reported included palpitations (1 of 6 subjects) and increased pulse rate exceeding 100 beats per minute (bpm) (3 of 6 subjects). Multiple doses of Mirabegron (Betmiga) up to 300 mg daily for 10 days showed increases in pulse rate and systolic blood pressure when administered to healthy volunteers.
Treatment for overdose should be symptomatic and supportive. In the event of overdose, pulse rate, blood pressure, and ECG monitoring is recommended.
Treatment for overdose should be symptomatic and supportive. In the event of overdose, pulse rate, blood pressure, and ECG monitoring is recommended.
Administration
May be taken with or without food: Swallow whole, do not chew/divide/crush.
Contraindications
Mirabegron (Betmiga) is contraindicated in patients with: Hypersensitivity to the active substance or to any of the excipients listed in Description.
Severe uncontrolled hypertension defined as systolic blood pressure ≥180 mm Hg and/or diastolic blood pressure ≥110 mm Hg.
Severe uncontrolled hypertension defined as systolic blood pressure ≥180 mm Hg and/or diastolic blood pressure ≥110 mm Hg.
Special Precautions
Renal impairment: Mirabegron (Betmiga) has not been studied in patients with end stage renal disease (GFR <15 mL/min/1.73 m2 or patients requiring haemodialysis) and, therefore, it is not recommended for use in this patient population. Data are limited in patients with severe renal impairment (GFR 15 to 29 mL/min/1.73 m2); based on a pharmacokinetic study (see Pharmacodynamics: Pharmacokinetics under Action) a dose reduction to 25 mg is recommended in this population. Mirabegron (Betmiga) is not recommended for use in patients with severe renal impairment (GFR 15 to 29 mL/min/1.73 m2) concomitantly receiving strong CYP3A inhibitors (see Interactions).
Hepatic impairment: Mirabegron (Betmiga) has not been studied in patients with severe hepatic impairment (Child-Pugh Class C) and, therefore, it is not recommended for use in this patient population. Mirabegron (Betmiga) is not recommended for use in patients with moderate hepatic impairment (Child-Pugh B) concomitantly receiving strong CYP3A inhibitors (see Interactions).
Hypertension: Mirabegron (Betmiga) can increase blood pressure, Blood pressure should be measured at baseline and periodically during treatment with Mirabegron (Betmiga), especially in hypertensive patients. Data are limited in patients with stage 2 hypertension (systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg).
Patients with congenital or acquired QT prolongation: Mirabegron (Betmiga), at therapeutic doses, has not demonstrated clinically relevant QT prolongation in clinical studies (see Pharmacology: Pharmacodynamics). However, since patients with a known history of QT prolongation or patients who are taking medicinal products known to prolong the QT interval were not included in these studies, the effects of Mirabegron (Betmiga) in these patients is unknown. Caution should be exercised when administering mirabegron in these patients.
Patients with bladder outlet obstruction and patients taking antimuscarinics medications for OAB: Urinary retention in patients with bladder outlet obstruction (BOO) and in patients taking antimuscarinic medications for the treatment of OAB has been reported in post marketing experience in patients taking mirabegron. A controlled clinical safety study in patients with BOO did not demonstrate increased urinary retention in patients treated with Mirabegron (Betmiga); however, Mirabegron (Betmiga) should be administered with caution to patients with clinically significant BOO. Mirabegron (Betmiga) should also be administered with caution to patients taking antimuscarinic medications for the treatment of OAB.
Effects on ability to drive and use machines: Mirabegron (Betmiga) has no or negligible influence on the ability to drive and use machines.
Hepatic impairment: Mirabegron (Betmiga) has not been studied in patients with severe hepatic impairment (Child-Pugh Class C) and, therefore, it is not recommended for use in this patient population. Mirabegron (Betmiga) is not recommended for use in patients with moderate hepatic impairment (Child-Pugh B) concomitantly receiving strong CYP3A inhibitors (see Interactions).
Hypertension: Mirabegron (Betmiga) can increase blood pressure, Blood pressure should be measured at baseline and periodically during treatment with Mirabegron (Betmiga), especially in hypertensive patients. Data are limited in patients with stage 2 hypertension (systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg).
Patients with congenital or acquired QT prolongation: Mirabegron (Betmiga), at therapeutic doses, has not demonstrated clinically relevant QT prolongation in clinical studies (see Pharmacology: Pharmacodynamics). However, since patients with a known history of QT prolongation or patients who are taking medicinal products known to prolong the QT interval were not included in these studies, the effects of Mirabegron (Betmiga) in these patients is unknown. Caution should be exercised when administering mirabegron in these patients.
Patients with bladder outlet obstruction and patients taking antimuscarinics medications for OAB: Urinary retention in patients with bladder outlet obstruction (BOO) and in patients taking antimuscarinic medications for the treatment of OAB has been reported in post marketing experience in patients taking mirabegron. A controlled clinical safety study in patients with BOO did not demonstrate increased urinary retention in patients treated with Mirabegron (Betmiga); however, Mirabegron (Betmiga) should be administered with caution to patients with clinically significant BOO. Mirabegron (Betmiga) should also be administered with caution to patients taking antimuscarinic medications for the treatment of OAB.
Effects on ability to drive and use machines: Mirabegron (Betmiga) has no or negligible influence on the ability to drive and use machines.
Use In Pregnancy & Lactation
Use in Pregnancy: There are limited amount of data from the use of Mirabegron (Betmiga) in pregnant women. Studies in animals have shown reproductive toxicity (see Pharmacology: Toxicology: Preclinical safety data under Actions). Mirabegron (Betmiga) is not recommended during pregnancy and in women of childbearing potential not using contraception.
Use in Lactation: Mirabegron (Betmiga) is excreted in the milk of rodents and therefore is predicted to be present in human milk (see Pharmacology: Toxicology: Preclinical safety data under Actions). No studies have been conducted to assess the impact of mirabegron on milk production in humans, its presence in human breast milk, or its effects on the breast-fed child.
Mirabegron (Betmiga) should not be administered during breast-feeding.
Fertility: There were no treatment-related effects of Mirabegron (Betmiga) on fertility in animals (see Pharmacology: Toxicology: Preclinical safety data under Actions). The effect of mirabegron on human fertility has not been established.
Use in Lactation: Mirabegron (Betmiga) is excreted in the milk of rodents and therefore is predicted to be present in human milk (see Pharmacology: Toxicology: Preclinical safety data under Actions). No studies have been conducted to assess the impact of mirabegron on milk production in humans, its presence in human breast milk, or its effects on the breast-fed child.
Mirabegron (Betmiga) should not be administered during breast-feeding.
Fertility: There were no treatment-related effects of Mirabegron (Betmiga) on fertility in animals (see Pharmacology: Toxicology: Preclinical safety data under Actions). The effect of mirabegron on human fertility has not been established.
Adverse Reactions
Summary of the safety profile: The safety of Mirabegron (Betmiga) was evaluated in 8433 patients with OAB, of which 5648 received at least one dose of Mirabegron (Betmiga) in the phase 2/3 clinical program, and 622 patients received mirabegron for at least 1 year (365 days). In the three 12-week phase 3 double blind, placebo controlled studies, 88% of the patients completed treatment with Mirabegron (Betmiga), and 4% of the patients discontinued due to adverse events. Most adverse reactions were mild to moderate in severity.
The most common adverse reactions reported for patients treated with Mirabegron (Betmiga) 50 mg during the three 12-week phase 3 double blind, placebo controlled studies are tachycardia and urinary tract infections.
The frequency of tachycardia was 1.2% in patients receiving mirabegron 50 mg.
Tachycardia led to discontinuation in 0.1% patients receiving Mirabegron (Betmiga) 50 mg. The frequency of urinary tract infections was 2.9% in patients receiving Mirabegron (Betmiga) 50 mg. Urinary tract infections led to discontinuation in none of the patients receiving Mirabegron (Betmiga) 50 mg. Serious adverse reactions included atrial fibrillation (0.2%).
Adverse reactions observed during the 1-year (long term) active controlled (muscarinic antagonist) study were similar in type and severity to those observed in the three 12-week phase 3 double blind, placebo controlled studies.
Tabulated list of adverse reactions: The table below reflects the adverse reactions observed with Mirabegron (Betmiga) in the three 12-week phase 3 double blind, placebo controlled studies.
The frequency of adverse reactions is defined as follows: very common (≥1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100); rare (≥1/10,000 to <1/1,000); very rare (<1/10,000). Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.
The most common adverse reactions reported for patients treated with Mirabegron (Betmiga) 50 mg during the three 12-week phase 3 double blind, placebo controlled studies are tachycardia and urinary tract infections.
The frequency of tachycardia was 1.2% in patients receiving mirabegron 50 mg.
Tachycardia led to discontinuation in 0.1% patients receiving Mirabegron (Betmiga) 50 mg. The frequency of urinary tract infections was 2.9% in patients receiving Mirabegron (Betmiga) 50 mg. Urinary tract infections led to discontinuation in none of the patients receiving Mirabegron (Betmiga) 50 mg. Serious adverse reactions included atrial fibrillation (0.2%).
Adverse reactions observed during the 1-year (long term) active controlled (muscarinic antagonist) study were similar in type and severity to those observed in the three 12-week phase 3 double blind, placebo controlled studies.
Tabulated list of adverse reactions: The table below reflects the adverse reactions observed with Mirabegron (Betmiga) in the three 12-week phase 3 double blind, placebo controlled studies.
The frequency of adverse reactions is defined as follows: very common (≥1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100); rare (≥1/10,000 to <1/1,000); very rare (<1/10,000). Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.
Drug Interactions
In vitro data: Mirabegron (Betmiga) is transported and metabolised through multiple pathways. Mirabegron (Betmiga) is a substrate for cytochrome P450 (CYP) 3A4, CYP2D6, butyrylcholinesterase, uridine diphosphoglucuronosyltransferases (UGT), the efflux transporter P-glycoprotein (P-gp) and the influx organic cation transporters (OCT) OCT1, OCT2, and OCT3. Studies of mirabegron using human liver microsomes and recombinant human CYP enzymes showed that mirabegron is a moderate and time-dependent inhibitor of CYP2D6 and a weak inhibitor of CYP3A. Mirabegron (Betmiga) inhibited P-gp-mediated drug transport at high concentrations.
In vivo data: CYP2D6 polymorphism: CYP2D6 genetic polymorphism has minimal impact on the mean plasma exposure to Mirabegron (Betmiga) (see Pharmacology: Pharmacokinetics under Actions). Interaction of mirabegron with a known CYP2D6 inhibitor is not expected and was not studied. No dose adjustment is needed for mirabegron when administered with CYP2D6 inhibitors or in patients who are CYP2D6 poor metabolisers.
Drug-drug interactions: The effect of co-administered medicinal products on the pharmacokinetics of Mirabegron (Betmiga) and the effect of Mirabegron (Betmiga) on the pharmacokinetics of other medicinal products was studied in single and multiple dose studies. Most drug-drug interactions were studied using a dose of 100 mg Mirabegron (Betmiga) given as oral controlled absorption system (OCAS) tablets. Interaction studies of Mirabegron (Betmiga) with metoprolol and with metformin used mirabegron immediate-release (IR) 160 mg.
Clinically relevant drug interactions between Mirabegron (Betmiga) and medicinal products that inhibit, induce or are a substrate for one of the CYP isozymes or transporters are not expected except for the inhibitory effect of Mirabegron (Betmiga) on the metabolism of CYP2D6 substrates.
In vivo data: CYP2D6 polymorphism: CYP2D6 genetic polymorphism has minimal impact on the mean plasma exposure to Mirabegron (Betmiga) (see Pharmacology: Pharmacokinetics under Actions). Interaction of mirabegron with a known CYP2D6 inhibitor is not expected and was not studied. No dose adjustment is needed for mirabegron when administered with CYP2D6 inhibitors or in patients who are CYP2D6 poor metabolisers.
Drug-drug interactions: The effect of co-administered medicinal products on the pharmacokinetics of Mirabegron (Betmiga) and the effect of Mirabegron (Betmiga) on the pharmacokinetics of other medicinal products was studied in single and multiple dose studies. Most drug-drug interactions were studied using a dose of 100 mg Mirabegron (Betmiga) given as oral controlled absorption system (OCAS) tablets. Interaction studies of Mirabegron (Betmiga) with metoprolol and with metformin used mirabegron immediate-release (IR) 160 mg.
Clinically relevant drug interactions between Mirabegron (Betmiga) and medicinal products that inhibit, induce or are a substrate for one of the CYP isozymes or transporters are not expected except for the inhibitory effect of Mirabegron (Betmiga) on the metabolism of CYP2D6 substrates.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Pharmacodynamics: Mechanism of action: Mirabegron (Betmiga) is a potent and selective beta 3-adrenoceptor agonist. Mirabegron (Betmiga) showed relaxation of bladder smooth muscle in rat and human isolated tissue, increased cyclic adenosine monophosphate (cAMP) concentrations in rat bladder tissue and showed a bladder relaxant effect in rat urinary bladder function models. Mirabegron (Betmiga) increased mean voided volume per micturition and decreased the frequency of non-voiding contractions, without affecting voiding pressure, or residual urine in rat models of bladder overactivity. In a monkey model, mirabegron showed decreased voiding frequency. These results indicate that mirabegron enhances urine storage function by stimulating beta 3-adrenoceptors in the bladder.
During the urine storage phase, when urine accumulates in the bladder, sympathetic nerve stimulation predominates. Noradrenaline is released from nerve terminals, leading predominantly to beta adrenoceptor activation in the bladder musculature, and hence bladder smooth muscle relaxation. During the urine voiding phase, the bladder is predominantly under parasympathetic nervous system control. Acetylcholine, released from pelvic nerve terminals, stimulates cholinergic M2 and M3 receptors, inducing bladder contraction. The activation of the M2 pathway also inhibits beta 3-adrenoceptor induced increases in cAMP. Therefore beta 3-adrenoceptor stimulation should not interfere with the voiding process. This was confirmed in rats with partial urethral obstruction, where mirabegron decreased the frequency of non-voiding contractions without affecting the voided volume per micturition, voiding pressure, or residual urine volume.
During the urine storage phase, when urine accumulates in the bladder, sympathetic nerve stimulation predominates. Noradrenaline is released from nerve terminals, leading predominantly to beta adrenoceptor activation in the bladder musculature, and hence bladder smooth muscle relaxation. During the urine voiding phase, the bladder is predominantly under parasympathetic nervous system control. Acetylcholine, released from pelvic nerve terminals, stimulates cholinergic M2 and M3 receptors, inducing bladder contraction. The activation of the M2 pathway also inhibits beta 3-adrenoceptor induced increases in cAMP. Therefore beta 3-adrenoceptor stimulation should not interfere with the voiding process. This was confirmed in rats with partial urethral obstruction, where mirabegron decreased the frequency of non-voiding contractions without affecting the voided volume per micturition, voiding pressure, or residual urine volume.
MedsGo Class
Drugs for Bladder & Prostate Disorders
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