Steve De Vos

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