Staff Profile: Sandeep Rana

Sandeep Rana, Ph.D.

Research Scientist (Chemistry)

Division of Pre-Clinical Innovation
Early Translation Branch (Contractor)

National Center for Advancing Translational Sciences

National Institutes of Health

Email Sandeep Rana

Biography

Sandeep Rana joined NCATS in 2019 as a research chemist on the Adenine Team in the Early Translation Branch. The Adenine Team’s research focuses on developing novel and selective probes to investigate biological processes and optimizing them to become potential drug candidates to treat rare and neglected targets. These probes will be used to explore and understand the role of disease-relevant proteins.

Before joining NCATS, Rana worked as a research assistant professor at the Eppley Institute for Research in Cancer and Allied Diseases at the University of Nebraska Medical Center in Omaha, Nebraska. His research primarily focused on the discovery and development of reversible and irreversible small-molecule inhibitors to perturb disease-relevant biomolecules. In parallel, Rana reported the first selective degrader of CDK9 by utilizing a proteolysis targeting chimera (PROTAC)-based degradation strategy.

Rana received his Ph.D. training in organic and medicinal chemistry at Kansas State University, under the supervision of Professor Duy H. Hua, working on the development of small-molecule probes against Alzheimer’s disease. After receiving his doctorate, Rana joined the Mayo Clinic as a research fellow in the Department of Molecular Pharmacology and Experimental Therapeutics. He has authored more than 25 peer-reviewed scientific publications.

Research Topics

Rana’s research is focused on the design, synthesis and development of modulating proteins that are often dysregulated across multiple diseases, such as cancer (breast, ovarian, colorectal and pancreatic) and neurodegeneration (Alzheimer’s and Huntington’s).

Selected Publications

  1. CDK5 Inhibitor Downregulates Mcl-1 and Sensitizes Pancreatic Cancer Cell Lines to Navitoclax.
  2. Selective degradation of CDK6 by a palbociclib based PROTAC.
  3. Synthesis of aminopyrazole analogs and their evaluation as CDK inhibitors for cancer therapy.
  4. Chemically induced degradation of CDK9 by a proteolysis targeting chimera (PROTAC).
  5. Isatin Derived Spirocyclic Analogues with α-Methylene-γ-butyrolactone as Anticancer Agents: A Structure-Activity Relationship Study.