David Lagares
Chief Executive Officer, President & Founder Zenon Biotech
David Lagares, Ph.D, MBA is a serial scientist-entrepreneur, company builder, and operator with +18 years of experience translating breakthrough science into therapeutic innovation. His former laboratory at Harvard Medical School and Massachusetts General Hospital pioneered first-in-class “mechano-therapeutics” and “senolytics,” uncovering novel mechanisms involved in fibro-inflammation, aging, fibrosis, and cancer and identifying new therapeutic approaches to regenerate chronically damaged organs. These discoveries, published in leading journals including Nature and Science, led to patented therapeutic platforms and the creation of two Boston-based biotech companies, Zenon Biotech and Mediar Therapeutics. His innovative research and strategic vision about the future treatment of human diseases have been supported with multi-million dollar investment from VCs, federal funding, industry-sponsored research, and non-profit Foundation grants. These innovations have advanced programs from target discovery to Phase 2 clinical trials. Today, Dr. Lagares serves as Founder, CEO, and President of Zenon Biotech, where he leads the development of first-in-class therapeutics targeting mechanobiology-driven diseases. His career sits at the intersection of scientific discovery and entrepreneurship: translating pioneering science into medicines for patients.
Seminars
- Understanding how matrix stiffness and mechanical signaling create self-sustaining fibrotic pathways across organs, independent of the initiating injury or inflammation
- Identifying and validating druggable nodes across the mechanotransduction pathway, from focal-adhesion mechanosensors to downstream transcriptional effectors
- Applying emerging discovery platforms and translational models to develop selective mechanobiology-targeted therapies that disrupt fibrotic tissue while preserving normal homeostasis and repair
- Reflecting on the discoveries that have enabled antifibrotic therapies to slow disease progression, and debating whether these same insights are sufficient to guide therapies that stop or reverse fibrosis
- Defining what true fibrosis regression means, including ECM remodeling, fibrinolysis, fibroblast deactivation, restored tissue architecture and functional recovery
- Determining whether different cell types, molecular mechanisms, datasets, biomarkers, and clinical trial designs are needed to distinguish therapies that slow progression from those that actively reverse fibrotic disease
