Michael Oshinsky
Director, Preclinical Pain Research NIH
Dr. Michael Oshinsky is the Director of the NINDS Office of Preclinical Pain Research. As Director, Dr. Oshinsky is responsible for coordinating the research and administrative issues related to pain and headache research across NINDS’ Divisions of Neuroscience, Translational Research and Clinical Research. Dr. Oshinsky is also a co-Chair for the trans-NIH Helping to End Addiction Long-term Initiative (HEAL).
Before he joined the NIH, Dr. Oshinsky was on the faculty in the Department of Neurology at Thomas Jefferson University (TJU) from 2001-2014. At TJU, he was the Director of Preclinical Research at the Jefferson Headache Center and led an NIH funded research program aimed at developing and characterizing animal models of headache. In 2011, Dr. Oshinsky was awarded the Harold G. Wolff Award for headache research.
Seminars
This workshop will explore how human-relevant models can improve translation from preclinical discovery to clinical success by generating more predictive evidence earlier in development. Attendees will discuss how complementary in vitro, ex vivo, computational and experimental human approaches can strengthen decision-making and reduce reliance on less predictive models.
Key Questions Addressed:
- How can human iPSC-derived sensory neurons, primary human DRG and other scalable platforms improve translational relevance and enable more predictive screening?
- What can we learn from integrated model systems, from human cell-based assays through to animal validation, to better understand pain mechanisms and therapeutic requirements?
- How are New Approach Methodologies (NAMs), including 3D tissue models and computational tools, gaining acceptance and being incorporated into pain drug development?
- How can developers combine human-relevant models to strengthen go/no-go decisions, identify liabilities earlier and improve confidence before entering the clinic?
- Is pain better viewed as a collection of biologically distinct diseases?
- Which pain phenotypes are most likely to benefit from NaV1.8 inhibition?
- Where might alternative mechanisms outperform sodium channel blockade?
- Why do promising assets continue to fail despite compelling target biology?
- How should developers match mechanism, indication and patient population to improve clinical success?
