Mitochondrial function, cell viability, pharmacokinetics and molecular simulation studies reveal the impact of CX-6258 HCl, a pan-Pim kinase inhibitor, on adipocytes

Obesity leads to the development of several diseases and chronic death worldwide. Mitochondrial dysfunction is one of the vital causes to develop obesity. Targeting mitochondrial uncoupling protein 1 (UCP1) may well be a potential therapeutic approach against obesity or mitochondrial dysfunction-related illnesses. To assess the significance of mitochondrial adenosine triphosphate (ATP) synthesis, mitochondrial DNA quantity and <i>in vitro</i> pharmacodynamics and pharmacokinetics, we used CX-6258 HCl (pan-Pim kinase inhibitor) in this work. CX-6258 HCl significantly reduces ATP production both in white and brown adipocytes and, therefore, improves thermogenesis, which helps to reduce fat in adipocytes. On the HEK293T cell line, no appreciable cell growth was seen. The <i>in silico</i> analysis identifies a potential interaction between CX-6258 HCl and the UCP1 protein. To treat disorders linked to mitochondrial dysfunction or obesity, CX-6258 HCl may be a promising therapeutic option. The role of pan-Pim kinase inhibitor on obesity and mitochondrial dysfunction-related disorders remains unknown. Further investigation will be leading to the development of the mechanism of action and therapeutic potential of CX-6258 HCl (pan-Pim kinase inhibitor).