ABHD15 Inhibitors

ABHD15 inhibitors like Orlistat, Triacsin C, Etomoxir, C75, and TOFA directly target enzymes involved in lipid synthesis and breakdown. By inhibiting these enzymes, these chemicals reduce the availability of substrates necessary for lipid metabolism, which is a process that ABHD15 is thought to regulate. This reduction in substrate availability can lead to alterations in lipid homeostasis, which may influence ABHD15's activity.

Other compounds, such as GW9662 and T0070907, antagonize PPARγ, a nuclear receptor that plays a central role in adipocyte differentiation and lipid storage. By blocking PPARγ's activity, these chemicals can impair the differentiation of adipocytes, a process in which ABHD15 may participate. PD98059 and Genistein exert their effects by interfering with signaling pathways, such as the MAPK/ERK pathway and tyrosine kinase-mediated signal transduction, respectively. These pathways are crucial for various cellular functions, including adipogenesis and lipid metabolism, and their inhibition can affect ABHD15's role within these processes. AICAR activates AMPK, a master regulator of energy metabolism, which can lead to changes in lipid metabolism and adipocyte function, processes regulated by ABHD15. Similarly, CL-316,243 stimulates β3-adrenergic receptors, which can induce lipolysis and potentially affect the lipid regulatory roles of ABHD15. Nicotinamide inhibitssirtuins, which are involved in various metabolic processes, including lipid metabolism.