We supply Mirabegron API

We're proud to offer Mirabegron API, a medicinal- grade substance that has a proven track record in treating hyperactive bladder( OAB) in grown-ups. it is of the loftiest quality, and our strict quality control measures insure that it's free from any contaminations and pollutants. With our dependable force chain and competitive pricing, we're committed to meeting our guests' requirements and delivering ontime.However, look no further than us, If you are looking for a trusted supplier of Mirabegron. communicate us moment to learn further about our products and services.

What's Mirabegron?

Mirabegron was developed by Japanese pharmaceutical company Astellas and was listed in Japan on September 16, 2011. It was approved by the US Food and Drug Administration( FDA) on June 28, 2012 for use in the treatment of hyperactive bladder( OAB) in grown-ups. Mirabelone is the first β 3 adrenergic receptor agonist medicine used to treat bladder overactivity, and its successful launch fills the gap in the treatment of bladder overactivity with β adrenergic receptor agonists.

Basic Information

Product Name: Mirabegron

CAS: 223673-61-8

MF:C21H24N4O2S

MW:396.51

EINECS:800-126-3

MDL No.:MFCD11100356

Melting point:138-140°C

Boiling point:690.0±55.0 °C(Predicted)

Structural formula:

Application: Overactive Bladder Treatment; Prostaglandin Antagonists/Antagonist

Origin: China

Delivery Time: in stock

Technical Specification

Package: 1kg; 10kg; or according to your demands

Storage conditions:2-8℃, protected from light and moisture, sealed and dry

Transportation conditions: 2-8 ℃ transportation

Shelf Life:24 months

Application

Mirabegron API is a drug primarily used for the treatment of hyperactive bladder( OAB). It works by widely cranking beta- 3 adrenergic receptors in the detrusor muscle of the bladder, leading to relaxation of the muscle and increased bladder capacity. Then are some crucial applications of Mirabegron:

Treatment of hyperactive Bladder( OAB): it is used in the expression of specifics aimed at treating symptoms of OAB, similar as urgency, frequence, and prompt incontinence. It provides an indispensable treatment option for cases who may not tolerate or respond well to other specifics like antimuscarinics.

Single and Combination remedy: it can be used as monotherapy or in combination with antimuscarinic agents for a synergistic effect in managing OAB symptoms. This combination approach allows for individualized treatment grounded on patient response and forbearance.

enhancement of Bladder Function: By cranking beta- 3 adrenergic receptors, it helps to relax the detrusor muscle, thereby adding bladder capacity and reducing the frequence of involuntary condensation that contribute to OAB symptoms.

exploration and Development: Beyond its current suggestions, it is also studied for implicit applications in affiliated conditions similar as urinary incontinence and other bladder dysfunctions. Research continues to explore its efficacity and safety biographies in colorful patient populations.

Market Applications:  Pharmaceutical companies use it to develop oral phrasings, generally in the form of tablets or extended- release capsules, icing accessible dosing and case compliance.

In summary, it serves as the foundation for specifics that effectively manage symptoms of hyperactive bladder by targeting beta- 3 adrenergic receptors. Its application extends to both standalone and combination curatives, contributing to bettered bladder function and quality of life for cases with OAB.

Pharmacological action

Mirabegron relaxes the bladder detrusor muscle and increases its stability substantially by acting on β3 receptors. Three β receptor subtypes( β1, B2 and β3) are set up in mortal detrusor cells and urethral epithelial cells. The mRNA of β3 receptor is substantially expressed in mortal detrusor smooth muscle cells, counting for 97 of β receptor mRNA in bladder towel. The expression of β receptor mRNA and the function of its signaling pathway suggest that β3 receptor plays a mainstay part in normal and diseased bladders.

Drug interactions

Mirabegron is prone to interact with clinically applicable medicines that are cytochrome CYP2D6 substrates and CYP3A4 impediments. Studies have shown that it increases the tube exposure of desipramine and metoprolol( CYP2D6 substrate medicines), reversibly dragging the medicine half- life. Other studies have shown that different boluses of ketoconazole( a strong CYP3A4 asset) can inhibit the concurrence of mirabegron in healthy grown-ups, while repeated boluses of rifampicin( an converting CYP3A4 metabolism) can lead to a moderate drop in mirabegron tube attention.

Synthesis method

Mirabegron is synthesized by using p- nitrophenylethylamine hydrochloride( 1) as a raw material, condensing with( R)- styrene oxide to gain amino alcohol( 2),( 2) is amino defended, nitro reduced, condensed with 2-( 2- aminothiazol-4-yl) acetic acid, and deprotected to gain mirabegron. The response is as follows

Biological activity

Mirabegron( YM178) is a picky beta3- adrenoceptor( β3 adrenoceptor) agonist with an EC50 of22.4 nM.

Target

Target                                  Value

β3- adrenoceptor               22.4 nM( EC50)

In vitro research

Mirabegron increases cAMP accumulation in CHO cells expressing mortal B adrenaline receptors( ARs) in a attention-dependent manner, with anI.A. of0.8. it has a minor negative effect on 1- and 2- ARs.it relaxes rat and mortal bladder smooth muscle bands in a attention-dependent manner, 10Mirabegron is a time-dependent asset of CYP2D6, with an IC50 value in mortal liver microsomes dwindling from 13 to4.3 μM after 30- nanosecond preincubation in the presence of NADPH. it is to some extent an unrecoverable orquasi-irreversible metabolic-dependent CYP2D6 asset.

In vivo research

Mirabegron reduces the frequence of metrical bladder condensation in anesthetized rats in a cure-dependent manner. Mirabegron at a cure of 3 mg/ kg intravenously inhibits the frequence of bladder condensation to 2 times/ 10 twinkles. it doesn't reduce the breadth of metrical bladder condensation. it reduces primary bladder sensational exertion and bladder microcontractions in rats. Mirabegron(0.3 and 1 mg/ kg) inhibits the exertion of mechanosensitive unit afferents( SAAs) of Aδ filaments in response to bladder stuffing. SAAs of C filaments were reduced only under 1 mg/ kg Mirabegron treatment. it administration inhibited mean bladder pressure and the number of microcontractions under isovolumetric conditions. it is effective in promoting bladder storehouse. Mirabegron cure- dependently reduced resting intravesical pressure. it cure- dependently reduced the frequence of nonemptying condensation, considered an index of abnormal responses in bladder storehouse. it had no significant effect on the breadth of nonemptying condensation, starting pressure, voided volume, residual volume, or bladder capacity.

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