IBS008738, a potent TAZ activator, stabilizes TAZ, elevates the unphosphorylated TAZ level, enhances the interaction of MyoD with the myogenin promoter, upregulates gene transcription regulated by MyoD, and competes with myostatin in C2C12 cells. Additionally, IBS008738 promotes myogenesis in C2C12 cells and facilitates muscle repair in a model of muscle injury.

IBS008738 (0, 24, 48, 72 h) enhances TAZ expression, with a peak at 24 h[1]. IBS008738 (10 μM; 0, 24, 72 h) enhances mRNAs of myogenic markers but not of myofusion markers[1]. IBS008738 (10 μM; 24h) enhances mRNAs of IL-10 in C2C12 cells[2]. Western Blot Analysis[1]Cell Line: C2C12 cells Concentration: Incubation Time: Treated for 0, 24, 48, 72 h under differentiation conditions after 24 h under growth conditions. Result: Enhanced TAZ expression, with a peak at 24 h. RT-PCR[1]Cell Line: C2C12 cells Concentration: 10 μM Incubation Time: 0, 24, 72 h under differentiation Result: Enhanced mRNAs of myogenic markers but not of myofusion markers.

IBS008738 (3 nmol) facilitates muscle repair in Cardiotoxin-injected muscles[1]. IBS008738 (30 μM, 100 μL) prevents Dexamethasone-induced muscle atrophy[1]. IBS008738 (100-μL volume of 30 μM; intramuscular injection; immediately and on day 2 after TBI) diminishes the expression of TNF α and IL-6 but increases that of IL-10 mRNAs in muscles of traumatic brain injury (TBI)[2]. Animal Model: Six-week-old female BALB/cByJ mice[1]Dosage: 3 nmol (0.3 μL of 10 mM IBS008738 was diluted in 100 μL of PBS) Administration: Injected into the tibialis anterior (TA) muscle of mice under anesthesia. Result: Facilitated muscle repair in Cardiotoxin-injected muscles. Animal Model: Six-week-old female BALB/cByJ mice[1]Dosage: 30 μM (100 μL) Administration: Injected into the tibialis anterior (TA) and gastrocnemius (GM) muscles on days 9, 11, and 13. Result: Prevented Dexamethasone-induced muscle atrophy.