Alexei Kharitonenkov
Russian biochemist
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Alexei Kharitonenkov (Russian: Алексей Игоревич Харитоненков) is a Russian-American researcher best known for his discoveries of endocrine functions of Fibroblast Growth Factor 21 (FGF21) and its prospects in developing novel therapies for metabolic diseases.[1][2][3] He is also known for his landmark identification of the signal-regulatory family of proteins (SIRPs),[4] and their corresponding protein-tyrosine phosphatases,[5] which helped unveil the molecular machinery of immune self-recognition ("do-not-eat me" signal) and their potential for the development of drugs to fight cancer.[6][7][8][9][10]
Education
In 1985, Kharitonenkov graduated with an MS in Physics from Moscow State University (MSU), Moscow, Russia.[11] In 1990, he received a Ph.D. degree in biochemistry from MSU,[12] followed by post-doctoral fellowship trainings in molecular biology and signal transduction at the Max Planck Institute of Biochemistry (1992-1994).[13]
Career
From 1986 to 1992, Kharitonenkov was a research fellow at Biochemistry Department, Biology Faculty, Moscow State University, Moscow, Russia.[11][12][14] Between 1994 and 1998 he was a staff scientist at the Molecular Biology department of the Max Planck Institute of Biochemistry.[4][13][15][16][17] Next, he joined Eli Lilly and Company and worked there until 2014.[18] He then moved to Calibrium, LLC.[19] Upon acquisition of this company,[20] he pursued his research at Novo Nordisk USA in 2016.[21][22] More recently, Kharitonenkov has been an executive and/or founder of startups within the biopharmaceutical field,[23][24] where he has also been an inventor.[25]
He has authored more than 100 peer-reviewed papers, most of them studying aspects of signal transduction, molecular biology, pharmacology, drug discovery and development in the areas of cancer and metabolic diseases.[26] He is also a contributing author to chapters of review books on endocrine FGFs and metabolism[27] and FGF21 as a therapeutic agent.[28] In 1997 and 2005, he contributed to priming articles describing the structures and functions of SIRPs[4] and FGF21.[29] He is named as an inventor on multiple patents.[30]
Works
Kharitonenkov's research papers have been cited over 14,500 times.[31]
According to Google Scholar,[26] his most cited papers are:
- Kharitonenkov A, Chen Z, Sures I, Wang H, Schilling J, and Ullrich A. A family of proteins that inhibit signaling through tyrosine kinase receptors. Nature 386:181-6 (1997) doi:10.1038/386181a0. PMID 9062191 Cited 726 times.[26]
- Kharitonenkov, Alexei; Shiyanova, Tatiyana L.; Koester, Anja; Ford, Amy M.; Micanovic, Radmila; Galbreath, Elizabeth J.; Sandusky, George E.; Hammond, Lisa J.; Moyers, Julie S.; Owens, Rebecca A.; Gromada, Jesper; Brozinick, Joseph T.; Hawkins, Eric D.; Wroblewski, Victor J.; Li, De-Shan (2005–06). "FGF-21 as a novel metabolic regulator". The Journal of Clinical Investigation. 115 (6): 1627–1635. doi:10.1172/JCI23606. ISSN 0021-9738. PMC 1088017. PMID 15902306. Cited 2241 times.[26]
- Coskun T, Bina HA, Schneider MA, Dunbar JD, Hu CC, Chen Y, Moller DE, and Kharitonenkov A. Fibroblast growth factor 21 corrects obesity in mice, Endocrinology 149:6018-27 (2008) doi:10.1210/en.2008-0816. PMID 18687777 Cited 1104 times.[26]
- Fisher, Ffolliott M.; Kleiner, Sandra; Douris, Nicholas; Fox, Elliott C.; Mepani, Rina J.; Verdeguer, Francisco; Wu, Jun; Kharitonenkov, Alexei; Flier, Jeffrey S.; Maratos-Flier, Eleftheria; Spiegelman, Bruce M. "FGF21 regulates PGC-1 and browning of white adipose tissues in adaptive thermogenesis". Genes & Development. 26 (3): 271-281 (2012). doi:10.1101/gad.177857.111. PMID 22302939. Cited 1449 times.[26]
Significance
The discovery of FGF21's metabolic action by Kharitonenkov el. al. in 2005,[29] and 2012,[32] represents an important breakthrough in the search for pharmacological alternatives to current treatments of diabetes and other metabolic diseases,[33] as acknowledged in prominent subject reviews[1][2][3][34][35][36] and reference books.[37] Kharitonenkov's and others' research on FGF21 mostly advocates for an adipocentric mode of action;[38][39][40][41] however, recent reports are suggestive of the brain being a primary target where this hormone would first produce its effects.[42][43] This poses some uncertainty on peripheral vs. centrally-driven mechanism of acton of this novel metabolic regulator.