Accelerating Meaningful Progress in Fibrosis
Mediar’s approach offers a critical window to tackle later-stage fibrosis, which is among the hardest-to-treat conditions with little to no available therapeutic options. We are currently advancing first-in-class antibodies in clinical studies to address fibrosis in several indications including those in lung and systemic sclerosis. Our foundational and robust science supports future expansion opportunities into other indications, which could include hepatic, renal, and cardiac fibrosis.
Our Pipeline
- Target
- Clinical Candidate
- Discovery
- Preclinical
- IND-enabling
- Phase 1
- Phase 2
WNT1-inducible signaling pathway protein-1 (WISP-1) is a secreted matricellular protein shown to have a relevant role in fibrosis progression, making the protein a compelling target for anti-fibrosis therapeutics. MTX-463 is a first-in-class human IgG1 antibody designed to neutralize the WISP-1-mediated fibrotic signaling that spans several fibrotic indications, including those in the lung and liver. A Phase 1 clinical study was initiated in April 2024 (NCT06401213) and Phase 2 studies of MTX-463 in patients with Idiopathic Pulmonary Fibrosis (IPF) are anticipated in H1-2025.
Ephrin ligands and Eph receptors mediate biological processes involved in tissue fibrosis including cell migration, myofibroblast activation, and tissue remodeling. A growing body of evidence has implicated EphrinB2 in the fibrosis of the skin, lungs, and heart. Expression of EphrinB2 and its receptors may also play a role in defining the fibrotic niche. MTX-474 is a first-in-class human IgG1 antibody designed to neutralize the EphrinB2 signaling that causes the onset and progression of fibrosis. Initiation of Phase 1 clinical studies for this program is anticipated in Q3-2024. Systemic sclerosis (SSc), a complex autoimmune disease with a high unmet medical need and large fibrosis component, is being investigated as a lead indication.
SMOC2 is a secreted matricellular protein that promotes extracellular matrix assembly, cell adhesion and fibrosis. In human studies across fibrotic indications, SMOC2 expression levels correlate with fibrotic disease severity. Murine models lacking SMOC2 are protected from fibrosis and its expression in human cellular models potentiates fibrotic markers. Mediar is conducting optimization of lead SMOC2 antibodies, which includes testing in preclinical mouse models.