Vibegron

Vibegron (MK-4618) is a selective and potent β3-adrenergic receptor agonist used in research related to overactive bladder (OAB). Vibegron showed an EC₅₀ of 1.1 nM for human β3-AR, with IC₅₀ values >20 μM for both β1-AR and β2-AR.

β3-adrenoceptor:1.1 nM (EC₅₀), CHO cells:0.57 nM (EC₅₀)

Method: Using CHO cells stably expressing human β3-AR, β1-AR, or β2-AR, vibegron was co-incubated with the cells for 30 min. Intracellular cAMP levels were measured using time-resolved fluorescence resonance energy transfer (TR-FRET) to evaluate its agonistic activity toward β3-AR and selectivity over β1/β2-AR.
Result: Vibegron showed an EC50 of 1.1 nM (84% activation) for human β3-AR, with IC50 values >20 μM for both β1-AR and β2-AR, demonstrating a selectivity of more than 10,000-fold ^[1].

Method: Female Sprague-Dawley rats (250-350 g) were anesthetized via urethral meatus, and bladder overactivity was induced by continuous intravesical infusion of 0.25% acetic acid in saline. Vibegron was administered intravenously, and intravesical pressure was recorded to evaluate changes in functional bladder capacity and micturition pressure.
Result: Vibegron dose-dependently increased functional bladder capacity in acetic acid-induced rats and reduced micturition pressure, indirectly reflecting a relaxant effect on the detrusor muscle ^[1].
Method: Female C57BL/6N mice underwent Th8-9 spinal cord transection and were orally administered vibegron (30 mg/kg) daily from 2 to 4 weeks post-injury. mRNA expression levels of fibrosis and ischemia-related markers in bladder tissue were detected using RT-PCR.
Result: Vibegron significantly downregulated the mRNA expression levels of collagen types 1 and 3, TGF-β1, and HIF-1α ^[2].

DMSO: 76 mg/mL (170.97 mM), Sonication is recommended.