Steve De Vos
Head of Translational Sciences Fibrocor Therapeutics
Steve De Vos is Head of Translational Sciences at Fibrocor Therapeutics, where he leads translational strategy and biomarker development to accelerate the development of novel therapies for fibrotic diseases. He brings more than 20 years of experience spanning drug discovery, translational pharmacology, biomarker research, and preclinical-to-clinical translation, with a strong patient-centric approach. Prior to joining Fibrocor Therapeutics, Steve spent over two decades at Galapagos NV, where he held roles of increasing responsibility across drug discovery and translational research. He contributed to multiple drug discovery programs from target identification and validation through preclinical development and early proof-of-concept clinical studies in fibrosis and immune-inflammatory diseases. Throughout his career, he has focused on integrating mechanistic biology, translational biomarkers, and clinical insights to improve decision-making and increase the probability of clinical success for innovative therapeutics.
Seminars
Developing effective antifibrotic therapies demands translational strategies that extend and meaningfully complement conventional animal models. This workshop will focus on defining the translational path forward for FIB992, an oral DDR1 inhibitor, by integrating human-relevant preclinical models, patient-derived systems, translational biomarkers, and clinical insights from kidney transplantation. The discussion will highlight how these complementary approaches can strengthen target validation, support patient selection, establish proof of mechanism, and de-risk clinical development toward preserving long-term kidney allograft function.
Key Talking Points:
- Leveraging a patient-centric forward- and back-translation strategy to generate mechanistic insights and build a translational evidence package for FIB992 toward clinical proof-of-concept
- Establishing the biological rationale for DDR1 inhibition by integrating genetic KO models, human kidney allograft biopsy biobanks, and transcriptomic datasets to demonstrate that DDR1 expression and activation are associated with molecular fibrosis signatures, disease progression, and long-term graft dysfunction
- Leveraging human ex-vivo translational platforms, including precision-cut kidney slices (PCKS) and patient-derived kidney biopsies, to demonstrate FIB992-mediated reversal of profibrotic molecular programs, extracellular matrix remodeling, and immune–fibrotic interactions
- Establishing a translational pharmacodynamic strategy by developing robust target engagement assays to quantify DDR1 inhibition in preclinical studies, healthy volunteers, and kidney transplant recipients, and linking target engagement to modulation of downstream fibrotic pathways and molecular signatures
