Biography

Kihwa Kang is a program director in NCATS’ Office of Drug Development Partnership Programs, where she manages research grants, investigates innovative technology development, and oversees early clinical trials of drug-repurposing efforts.

Prior to joining NCATS, Kang served as the director of strategy planning and new business development at the CJ Research Center, a subsidiary of the South Korean company CJ CheilJedang (CJ Corporation). She was responsible for establishing partnerships among academic institutions and biotech companies after evaluating the potential of investment or licensing opportunities. She also managed the Research and Development team’s efforts to develop novel microbiome-based therapeutics. Prior to her tenure at the CJ Corporation, she worked as a scientist at Regeneron Pharmaceuticals, Inc., where she led a team that conducted target discovery and preclinical in vivo pharmacology research related to obesity and type 2 diabetes.

Kang earned her doctorate at the University of Wisconsin–Madison and completed postdoctoral training in the Department of Genetics and Complex Diseases at the Harvard School of Public Health, where she studied the role of nuclear receptor PPARδ in obesity-induced metabolic diseases and chronic inflammation.

Research Topics

Kang’s area of interest lies in chronic inflammatory diseases, particularly in the realm of cardiometabolic and central nervous system disorders. Additionally, she is intrigued by advances in technology that can streamline the process of developing effective therapeutics, which reduces costs and contributes to a more widespread impact on therapeutic development.

Selected Publications

1. Mouse Ghrelin-O-Acyltransferase (GOAT) Plays a Critical Role in Bile Acid Reabsorption
2. Physiological Role of Ghrelin as Revealed by the Ghrelin and GOAT Knockout Mice
3. Fat Mass-and Obesity-Associated (FTO) Gene Variant Is Associated With Obesity: Longitudinal Analyses in Two Cohort Studies and Functional Test
4. Adipocyte-Derived Th2 Cytokines and Myeloid PPARδ Regulate Macrophage Polarization and Insulin Sensitivity
5. Peroxisome Proliferator-Activated Receptor δ Promotes Very Low-Density Lipoprotein-Derived Fatty Acid Catabolism in the Macrophage