The observed embryofetal toxicity occurred at doses associated with maternal toxicity. The study population consisted of approximately 48% antimuscarinic treatment naïve patients as well as approximately 52% patients previously treated with antimuscarinic medicinal products. Most adverse reactions were mild to moderate in severity.The most common adverse reactions reported for patients treated with Betmiga 50 mg during the three 12-week phase 3 double blind, placebo controlled studies are tachycardia and urinary tract infections. Follow all directions on your prescription label. Multiple doses of mirabegron 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.
Betmiga(mirabegron): Symptomatic treatment of urgency, increased micturition frequency &/or urgency incontinence as may occur in adult w/ overactive bl Betmiga has not been studied in patients with end stage renal disease (GFR < 15 mL/min/1.73 m 2 or patients requiring haemodialysis) and, therefore, it is not recommended for use in this patient population. Mirabegron 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 females administered mirabegron at the 50 mg dose, the mean difference from placebo on QTcI interval at 5 hours post dose was 3.67 msec (upper bound of the one-sided 95% CI 5.72 msec). The effect of co-administered medicinal products on the pharmacokinetics of mirabegron and the effect of mirabegron on the pharmacokinetics of other medicinal products was studied in single and multiple dose studies. No dose adjustment is needed for mirabegron when administered with therapeutic doses of rifampicin or other CYP3A or P-gp inducers.CYP2D6 genetic polymorphism has minimal impact on the mean plasma exposure to mirabegron (see section 5.2). Mirabegron is the major circulating component following a single dose of In healthy subjects who are genotypically poor metabolisers of CYP2D6 substrates (used as a surrogate for CYP2D6 inhibition), mean CThe pharmacokinetics of mirabegron are not influenced by race.Following single dose administration of 100 mg Betmiga in volunteers with mild renal impairment (eGFR-MDRD 60 to 89 mL/min/1.73 mFollowing single dose administration of 100 mg Betmiga in volunteers with mild hepatic impairment (Child-Pugh Class A), mean mirabegron CPre-clinical studies have identified target organs of toxicity that are consistent with clinical observations. A single 400 mg dose of moxifloxacin was used as a positive control.
Multiple once daily dosing of mirabegron IR resulted in a 90% increase in CCaution is advised if mirabegron is co-administered with medicinal products with a narrow therapeutic index and significantly metabolised by CYP2D6, such as thioridazine, Type 1C antiarrhythmics (e.g., flecainide, propafenone) and tricyclic antidepressants (e.g., imipramine, desipramine). Rating: 1 - 6 review(s) advertisement.
Betmiga has not been studied in patients with end stage renal disease (GFR < 15 mL/min/1.73 mThe following table provides the daily dosing recommendations for subjects with renal or hepatic impairment in the absence and presence of strong CYP3A inhibitors (see sections 4.4, 4.5 and 5.2).2. Caution is also advised if mirabegron is co-administered with CYP2D6 substrates that are individually dose titrated.Mirabegron is a weak inhibitor of P-gp. Do not take this medicine in larger or smaller amounts or for longer than recommended.Do not crush, chew, or break an extended-release tablet.