Home Neuronal Signaling Adrenergic Receptor agonist Mirabegron

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Mirabegron Adrenergic Receptor agonist

Cat.No.S4009

Mirabegron (YM 178) is a selective β3-adrenoceptor agonist with EC50 of 22.4 nM.
Mirabegron Adrenergic Receptor agonist Chemical Structure

Chemical Structure

Molecular Weight: 396.51

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Quality Control

Batch: S400901 DMSO]79 mg/mL]false]Ethanol]8 mg/mL]false]Water]Insoluble]false Purity: 99.8%
99.8

Solubility

In vitro
Batch:

DMSO : 79 mg/mL (199.23 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 8 mg/mL

Water : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 396.51 Formula

C21H24N4O2S

 Storage (From the date of receipt)
CAS No. 223673-61-8 Download SDF Storage of Stock Solutions

Synonyms YM 178 SMILES C1=CC=C(C=C1)C(CNCCC2=CC=C(C=C2)NC(=O)CC3=CSC(=N3)N)O

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Mechanism of Action

Targets/IC50/Ki
β3-adrenoceptor
22.4 nM(EC50)
In vitro
Mirabegron concentration-dependently increases the accumulation of cAMP in CHO cells expressing human 3-adrenoceptors (ARs) with I.A. of 0.8. This compound has little agonistic effect on 1- and 2-ARs. It concentration-dependently relaxes rat and Human bladder smooth muscle strips precontracted with 10-6 M or 10-7 M carbachol with EC50 values of 5.1 μM and 0.78 μM, respectively. The maximal relaxant effects of this chemical are 94.0 % and 89.4% that of carbachol, respectively. It is a time-dependent inhibitor of CYP2D6 in the presence of NADPH as the IC50 value in human liver microsomes decreased from 13 to 4.3 μM after 30 min preincubation. This compound acts partly as an irreversible or quasi-irreversible metabolism-dependent inhibitor of CYP2D6.
In vivo
Mirabegron produces a dose-dependent decrease in the frequency of rhythmic bladder contraction in anesthetized rats. 3 mg/kg i.v. this compound suppresses the frequency to 2 counts/10 min. It does not decrease the amplitude of rhythmic bladder contraction. This chemical decreases primary bladder afferent activity and bladder microcontractions in rats. It (0.3 and 1 mg/kg) inhibits mechanosensitive single-unit afferent activities (SAAs) of Aδ fibers in response to bladder filling. SAAs of C-fibers decrease only at 1 mg/kg this compound treatment. Its administration suppresses the mean bladder pressure and the number of microcontractions during an isovolumetric condition of the bladder. It is efficient on facilitation of bladder storage. This compound dose-dependently decreases the resting intravesical pressure. It dose dependently decreases the frequency of nonvoiding contractions, considered an index of abnormal response in bladder storage. It exhibits no significant effects on the amplitude of nonvoiding contractions, micturition pressure, threshold pressure, voided volume, residual volume, or bladder capacity.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/23224420/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-07-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
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VA Office of Research and Development
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NCT07114640 NOT_YET_RECRUITING
Urinary Bladder, Overactive
Far Eastern Memorial Hospital
 2025-08-07 PHASE3
NCT07566208 NOT_YET_RECRUITING
Ventricular Arrhythmias and Cardiac Arrest
Cedars-Sinai Medical Center
 2026-05 PHASE2
NCT07585513 NOT_YET_RECRUITING
Postural Orthostatic Tachycardia Syndrome (POTS)
Cedars-Sinai Medical Center
 2026-05 PHASE2

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