
My long-term research interest and goal is to establish an active, externally-funded research program at Widener University with the motto of "Better health through discovery, de novo design, and effective delivery of novel drugs." Despite tremendous medical advances, we still face many health challenges for which there is no effective cure. The age-associated disorders like cancer and Alzheimer's disease are two of the most notorious examples of such devastating diseases.
Cancer is still the second leading cause of death in the U.S. Similarly, there are currently 5.2 million Alzheimer's disease patients in the U.S., and the numbers are expected to rise significantly owing to the aging population of baby boomers and lack of any effective cure. In this context, the primary aim of my research work is to unravel the molecular mechanisms underlying these diseases and use these novel mechanistic understandings to discover and design effective therapeutics against these traditionally-challenging diseases:
Alzheimer's Disease – Apolipoprotein E (ApoE) is one of the most significant risk factors for late-onset or sporadic Alzheimer's disease. ApoE has been shown to be critical in clearing the harmful ApoE deposits from the brain and its ability to do that depends upon its lipidation status. Therefore, there is a growing interest in understanding the underlying mechanisms involved in ApoE lipidation and using these mechanistic understandings to discover drugs to enhance ApoE lipidation status.
My laboratory is investigating potential involvement of abnormal glucose metabolism in poor ApoE lipidation.
Cancer – The p53 protein plays a central role in protecting cells against carcinogenesis. It is inhibited in 50% of human tumors, however, by interaction with the oncogenic MDM2 protein. Therefore, blocking the p53-binding pocket on MDM2 protein by small-molecule drugs, leading to activation of the tumor suppressor p53 protein presents a fundamentally novel strategy against several types of cancers. In this regard, my laboratory is involved in discovery and design of novel molecules that can mimic the p53 structural features involved in binding to the MDM2 pocket with the ultimate aim of blocking p53-MDM2 interaction.