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Updated: May 28, 2025

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
Mitochondrial function, cell viability, pharmacokinetics and molecular simulation studies reveal the impact of
Md Reyad-Ul Ferdous1, Tesfaye Wolde1, Vijay Pandey1
1Institute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, PR China.
Abstract:
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 in vitro 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 in silico 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).
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