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, administered in various doses and methods, shows significant therapeutic effects in muscle recovery and protection. At a dose of 3 nmol, it enhances muscle repair in mice injected with Cardiotoxin. When administered at 30 μM and 100 μL, it effectively counters Dexamethasone-induced muscle atrophy. Furthermore, a 100-μL dose of 30 μM IBS008738, delivered intramuscularly immediately and again on day 2 post-traumatic brain injury (TBI), results in decreased expression of pro-inflammatory markers TNF α and IL-6, while simultaneously increasing anti-inflammatory IL-10 mRNA levels in muscles. These findings were observed in six-week-old female BALB/cByJ mice, where the compound was injected into the tibialis anterior (TA) muscle to stimulate muscle repair, and into the TA and gastrocnemius (GM) muscles to prevent muscle atrophy, showcasing IBS008738's potential in mitigating muscle damage and promoting repair in various injury models.