David A. Fidock

David A. Fidock (born 8 December 1965), is the CS Hamish Young Professor of Microbiology and Immunology and Professor of Medical Sciences at Columbia University Irving Medical Center in Manhattan.

Education Fidock attended the University of Adelaide and earned a bachelor of mathematical sciences and an honors degree in genetics in 1985. He earned a PhD in microbiology from the Institut Pasteur in Paris in 1994. His dissertation advisor was Pierre Druilhe, and his thesis was titled "Molecular and Immuno-Epidemiological Studies of the Plasmodium falciparum STARP and LSA-1 Antigens Expressed During the Pre-Erythrocytic Stages in Humans". He underwent postdoctoral training with Anthony James at University of California, Irvine, and with Thomas Wellems at the National Institutes of Health.

Research Fidock's research focuses on the genetic and molecular mechanisms behind antimalarial drug resistance in the human parasite Plasmodium falciparum, as well as target-based drug discovery and development, and parasite metabolism and biology. He led the development of methods for genetically modifying malaria parasites and for elucidating the genetic basis of P. falciparum resistance to various first-line medicines (including artemisinin, chloroquine and piperaquine).

He has published more than 280 papers on malaria, with a current h-index of 97. His work has been cited over 34,000 times. His work has been funded by the NIH, the Bill & Melinda Gates Foundation, the Department of Defense, the Burroughs Wellcome Fund and the Medicines for Malaria Venture.

Honors 1992 "Bourse Roux" Scholarship, Pasteur Institute, Paris 2023 Elected Member, American Academy of Microbiology The Plasmodium falciparum ABC transporter ABCI3 confers parasite strain-dependent pleiotropic antimalarial drug resistance. Cell Chem Biol (in press). Plasmodium falciparum K13 mutations in Africa and Asia impact artemisinin resistance and parasite fitness. Elife 10: e66277. Inhibition of resistance-refractory P. falciparum kinase PKG delivers prophylactic, blood stage, and transmission-blocking antiplasmodial activity. Cell Chem Biol 27: 806-16. Insights into the intracellular localization, protein associations and artemisinin resistance properties of Plasmodium falciparum K13. PLoS Pathog 16: e1008482. Covalent Plasmodium falciparum-selective proteasome inhibitors exhibit a low propensity for generating resistance in vitro and synergize with multiple antimalarial agents. PLoS Pathog 15: e1007722. Plasmodium falciparum resistance to piperaquine driven by PfCRT. Lancet Infect Dis 19: 1168-9. Structure and drug resistance of the Plasmodium falciparum transporter PfCRT. Nature 576: 315-20.