Ted Price
Co-Founder 4E Therapeutics
Theodore (Ted) Price is Ashbel Smith Professor in the Department of Neuroscience at University of Texas at Dallas where is the Director of the Center for Advanced Pain Studies. Ted did his PhD with Ken Hargreaves at UT Health San Antonio and his postdoc with Fernando Cervero at McGill. Ted started his independent lab in 2007 at University of Arizona and moved to UT Dallas in 2014. Ted’s lab’s goal is to identify molecular mechanisms causing chronic pain with emphasis on developing new drugs to treat pain. His lab’s focus is on human molecular neuroscience with specialization on dorsal root ganglion and spinal dorsal horn. Ted has published more than 250 peer reviewed studies, and has been continuously funded by NIH for more than 15 years. He is co-founder of many companies, including 4E Therapeutics.
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?
