Kevin Dines
Scientific Executive Director Bristol Myers Squibb
Kevin Dines, PhD, is Scientific Executive Director at Bristol Myers Squibb, where he leads preclinical neuroscience efforts across small- and large-molecule modalities. With more than 25 years of experience in neuroinflammation, neurodegeneration, and in vivo pharmacology, he guides programs from early discovery through IND and early clinical translation. Prior to BMS, Dr. Dines held senior roles at Receptos/Celgene, BioTox Sciences, and Tanabe Research Laboratories. He earned his PhD in Physiology from the University of Aberdeen.
Seminars
As neuroimmunology drug development pushes toward greater translational efficiency, in vitro systems, especially patient-derived and cell-based models are gaining traction as alternatives to traditional animal studies. This workshop will examine how in vitro data can be used more strategically to justify clinical entry, where current models fall short, and how evolving regulatory perspectives are reshaping preclinical expectations.
Key Topics to Be Explored:
- Can cell-based efficacy data replace animal models as a viable route to early proof of concept in neuroimmune drug development?
- How can in vitro systems be optimized to model specific features or symptoms of complex CNS disorders, rather than entire disease pathologies?
- What role do patient-derived cells, co-culture systems, and human-relevant endpoints play in bridging preclinical and clinical evidence?
- How are regulatory agencies interpreting mechanistic in vitro data in the absence of strong in vivo correlation or validated biomarkers?
- When does strong human genetic evidence outweigh the need for extensive model validation and how can earlystage companies tailor their strategy accordingly?
- What lessons can be drawn from recent FDA or EMA submissions where in vitro results played a central role in moving programs forward?
Despite decades of reliance on rodent models in neuroinflammation and neurodegeneration, there is growing consensus that animal systems often fail to capture key human disease mechanisms. This panel will debate whether we are entering a postanimal-model era or simply shifting expectations and redefining how in vivo studies are used.
- What have we truly learned from animal models and where have they fallen short in reflecting the complexity of human neuroimmune diseases?
- How do chimeric and humanized mouse models help bridge the translational gap, and what are their limitations?
- When is reliance on animal models necessary, and when can strong human genetic or phenotypic data support a “modellight” approach?
- How should we balance phenotypic versus target-driven strategies in preclinical testing, especially given the artificial nature of many models (e.g., amyloid beta overexpression)?
- Are current in vitro models a step backward or an important complement in understanding multifactorial diseases where secondary mechanisms matter?
- How do different companies weigh model necessity depending on target confidence and therapeutic strategy, and what does the future hold for smarter, more selective use of in vivo models?
