Kent Gordon, PhD, is a Senior Medical Science Liaison with Vertex Pharmaceuticals in their Pain business unit. Dr. Gordon has worked in the pain therapeutic industry for the past nine years, primarily in Medical Affairs. Prior to joining Vertex Pharmaceuticals, he held roles at Averitas Pharma, which commercializes treatments for chronic pain associated with neuropathy, and Bioventus Inc., which focuses on treatments for pain related to osteoarthritis. Dr. Gordon earned his PhD in Biomedical Engineering from the University of North Carolina at Chapel Hill, where his research centered on the development of microfluidic devices for neuroscience applications.

Kara Margolis, MD, is a Professor of Pediatrics and Cell Biology at the NYU Grossman School of Medicine, and a Professor of Molecular Pathobiology at the NYU College of Dentistry, where she also serves as Director of the NYU Pain Research Center. Dr. Margolis is a pediatric gastroenterologist and physician-scientist with clinical and scientific expertise in disorders affecting both the gut and the brain, including abdominal pain-related disorders of gut-brain interactions (DGBIs). In the laboratory, Dr. Margolis leads clinical, translational, and basic science research programs focused on discovering novel mediators that link abdominal pain-related disorders to mental health conditions such as anxiety and depression. Her work is funded by the NIH, the Department of Defense, and various foundations.

Luda Diatchenko, MD, PhD, is a Canada Research Chair in Human Pain Genetics, a Fellow of the Royal Society of Canada, and a Professor in the Faculties of Dentistry and Medicine at McGill University. Dr. Diatchenko earned her MD and PhD in Molecular Biology from the Russian State Medical University.

She began her career in industry, serving as Leader of the RNA Expression Group at Clontech, Inc., and later as Director of Gene Discovery at Attagene, Inc. Her academic career commenced in 2000 at the Center for Neurosensory Disorders at the University of North Carolina.

Since then, Dr. Diatchenko’s research has focused on uncovering the genetic mechanisms that influence human pain perception and the risk of developing chronic pain conditions. Her work enables new approaches to identifying drug targets, predicting treatment responses to analgesics, and improving diagnostics.

Javier Lopez Soto, PhD, earned his doctorate in Neuroscience from the National University of La Plata in Argentina, where he investigated G-protein–coupled receptor (GPCR) signaling pathways that modulate voltage-gated calcium channels—key regulators of neurotransmitter release in neurons. His research uncovered novel mechanisms by which GPCRs influence synaptic transmission through direct modulation of calcium channels.

Dr. Lopez Soto then joined Dr. Diane Lipscombe’s lab at Brown University as a postdoctoral associate, where he studied the expression, regulation, and function of calcium channels in nociceptors. There, he discovered an epigenetic mechanism that controls cell-specific RNA processing of a calcium channel gene, enhancing opioid sensitivity and morphine analgesia. This work provided key insights into the reduced effectiveness of pain relief following peripheral injury.

Building on these experiences, Dr. Lopez Soto launched his independent research program at the College of Veterinary Medicine at NC State. The Lopez Soto Lab focuses on how alternative pre-mRNA splicing—a critical step in gene expression—shapes the activity of ion channels and synaptic proteins in sensory neurons. Alternative splicing generates protein isoform diversity that underlies neuronal identity and function. Because it is often disrupted by nerve injury or inflammation and contributes to chronic pain, his lab integrates genomics, molecular biology, electrophysiology, and behavior to link cell-specific splicing to neural function and disease.

Emerging findings from his lab suggest that alternative splicing in nociceptors fine-tunes synaptic protein interactions, impacting vesicle release and neurogenic inflammation. His research lays the groundwork for developing cell-specific splicing mechanisms as therapeutic targets, establishing a paradigm in which manipulating alternative splicing at functionally relevant loci may attenuate pathological pain.

Christopher Peters, PhD, is an Associate Professor in the Department of Anesthesiology at Wake Forest University School of Medicine. He has an extensive research background investigating the cellular and neurobiological mechanisms that contribute to persistent postsurgical, neuropathic, cancer-related, and musculoskeletal pain.

Dr. Peters earned his PhD at the University of Minnesota under the mentorship of Dr. Patrick Mantyh. His research focused on mechanistic and interventional studies to better understand cancer-related pain resulting from bone metastasis and chemotherapy-induced neuropathy. His early work helped establish that tumor-derived factors, inflammation, and injury to primary afferent neurons innervating bone can simultaneously drive chronic pain. He tested several therapies targeting these mechanisms, including gabapentin, an endothelin A receptor antagonist, and an anti–nerve growth factor–sequestering antibody—findings that informed multiple clinical trials aimed at reducing cancer-related bone pain. This foundational experience in neuroscience, behavioral pharmacology, and animal model development was instrumental in his growth as an independent investigator in translational pain research.

In 2007, Dr. Peters pursued a postdoctoral fellowship under the mentorship of Dr. Jim Eisenach at Wake Forest University. There, he conducted preclinical studies examining supraspinal mechanisms contributing to pain chronicity. His research established a critical role for the descending noradrenergic system in modulating spinal neuroinflammation and resolving postsurgical pain. Through these studies and interactions with pain clinicians, he recognized the substantial individual variability in the development of chronic pain after surgery. This insight motivated him to focus on identifying biological, environmental, and individual factors that influence postoperative pain resolution and recovery, leading to his first independent R01 grant and faculty appointment in the Department of Anesthesiology in 2011.

Since joining the faculty, Dr. Peters has received multiple NIH and DOD grant awards and has served as a project leader and animal core director on two multi-investigator Program Project Grants.

His current research focuses on identifying key neural circuits and sensory neuronal subsets that drive both ongoing and movement-related pain behaviors in mouse models of inflammatory and postsurgical knee osteoarthritis (OA). His lab also investigates the role of sensory neuron–derived neuropeptides in pain and disease progression—including cartilage degeneration, synovial inflammation, and bone remodeling—in OA models. The ultimate goal of his research is to develop more effective non-opioid analgesics and treatment strategies to relieve pain and limit disease severity in knee OA and related musculoskeletal conditions, with the potential for clinical translation.

Seok-Yong Lee, PhD, is the George Barth Geller Professor of Molecular Biology and Professor of Biochemistry at Duke University School of Medicine. He earned his PhD from the University of California, Berkeley, and completed postdoctoral training with Dr. Rod MacKinnon at The Rockefeller University before launching his independent research career at Duke in 2009.

Dr. Lee’s research focuses on the structural and mechanistic understanding of membrane transport proteins, with the broader goal of informing therapeutic development. His lab investigates how nociceptors detect and integrate thermal and chemical stimuli, with particular emphasis on transient receptor potential (TRP) channels that mediate pain and temperature sensation. His multidisciplinary approach—combining structural biology, electrophysiology, pharmacology, and chemical biology—aims to elucidate the molecular basis of somatosensation and its dysregulation in disease.

His group also explores the role of adenosine in pain signaling, demonstrating how inhibition of the equilibrative nucleoside transporter subtype 1 (ENT1)—responsible for adenosine uptake—can modulate pain perception.

Dr. Lee’s work has provided fundamental insights into how ion channels and transporters govern sensory perception. These discoveries have advanced the development of novel, non-opioid approaches to pain treatment. He is widely recognized for his contributions to the structural biology and pharmacology of ion channels and transporters, as well as to molecular sensory neuroscience.