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Staff Profile: Samarjit Patnaik

Samarjit Patnaik, Ph.D.
Samarjit Patnaik, Ph.D.

Research Scientist, Chemistry (Contractor)

Division of Pre-Clinical Innovation

National Center for Advancing Translational Sciences

National Institutes of Health

E-mail Samarjit Patnaik


Samarjit Patnaik joined NIH in early 2009 and now works at NCATS on a chemistry team led by Juan J. Marugan, Ph.D. Patnaik focuses primarily on developing drug-like small molecule probes, mostly derived from high-throughput screening hits, to interrogate novel targets and pathways in cellular and animal disease models with a focus on rare and neglected diseases. He also devises chemical tools that facilitate target deconvolution from phenotypic assays. His work has led to the out-licensing of a class of noninhibitory chaperones for glucocerbrosidase as a prospective therapy for Gaucher disease and the initiation of a collaboration with the National Cancer Institute’s Experimental Therapeutics program for the pre-clinical development of perinucleolar compartment inhibitors as agents against cancer metastasis.

Before joining NCATS, Patnaik worked in the Oncology Medicinal Chemistry Division at GlaxoSmithKline, where his team developed the pre-clinical candidate GSK1838705A as a dual insulin growth factor-1 receptor/anaplastic lymphoma kinase inhibitor.

Patnaik received his B.Sc. in chemistry from St. Stephen’s College in Delhi, India, and a B.A. in natural sciences from Cambridge University. He received a Ph.D. in organic chemistry at Indiana University.

Research Topics

  • Lysosomal storage disorders (Gaucher, Niemann-Pick type C, mucolipidosis type IV)
  • Cancer (Eya2/Six1, perinucleolar compartment)
  • Ion channels: TRPV1 (pain), TRPML1 (lysosomal storage disorder ML4)
  • G-protein coupled receptor (neuropeptide S receptor, addiction)

Selected Publications

  1. Inhibition of PIP4Kγ ameliorates the pathological effects of mutant huntingtin protein.
  2. Identification of 4-phenylquinolin-2(1H)-one as a specific allosteric inhibitor of Akt.
  3. Gastric Acid Secretion from Parietal Cells Is Mediated by a Ca(2+) Efflux Channel in the Tubulovesicle.
  4. Orphan GPR110 (ADGRF1) targeted by N-docosahexaenoylethanolamine in development of neurons and cognitive function.
  5. Activation of β-Glucocerebrosidase Reduces Pathological α-Synuclein and Restores Lysosomal Function in Parkinson's Patient Midbrain Neurons.