May 6, 2021: Sanofi has entered into a three-year research collaboration with Stanford University School of Medicine.
Together, the two organizations and their scientists will work to advance the understanding of immunology and inflammation through open scientific exchange.
Additionally, Sanofi will provide funding and scientific inputs into projects of mutual interest, crossing multiple therapeutic areas including autoimmune diseases and inflammatory conditions.
“We look forward to working with some of the most innovative scientists in the human immunology community.
Together we will explore groundbreaking concepts and obtain deeper insights into underlying inflammatory disease mechanisms,” said Frank Nestle, Global Head of Research and Chief Scientific Officer, Sanofi.
“Sanofi’s collaboration with Stanford University aims to transform how autoimmune disorders and inflammatory conditions are understood and treated.
It will help accelerate our ambitious immunoscience programs as we advance a rich pipeline of first- and best-in-class medicines across key therapeutic areas to address unmet patient needs.”
Sanofi and Stanford Medicine will create a Joint Steering Committee to fund up to three programs a year.
Sanofi will host an annual research forum for researchers from both organizations to further exchange ideas, share knowledge and perspectives on relevant scientific matters, and discuss collaborative research projects.
“Stanford Medicine is dedicated to advancing knowledge and discovery with the goal of improving our ability to predict, prevent and cure disease with the most precise approaches,” said Lloyd Minor, MD, Dean of the Stanford School of Medicine.
“The opportunity for long-term collaboration with our colleagues at Sanofi will allow us to explore together new frontiers in autoimmune diseases and inflammatory conditions.”
The collaboration will begin with three “deep-dive” research projects:
- Exploring cytokine crosstalk in type 2 inflammation, specifically examining the impact of Sanofi’s investigational molecules on excessive type 2 inflammation.
- Decoding molecular drivers of effector and suppressor T cells in autoimmunity, to better understand the specific antigens that may cause type 1 diabetes.
- Defining the mechanisms of immune-related adverse events with immune checkpoint inhibitor therapy – with a focus on pneumonitis and inflammatory arthritis – to explore the role of genomics and pathogenic cell identification.”