Mediar Therapeutics Enters Antibody Collaboration with Ono Pharma for Fibro-Inflammatory Diseases

Mediar Therapeutics has entered into a collaboration and option agreement with Ono Pharmaceutical Co., Ltd. to develop novel antibody treatments for fibro-inflammatory diseases, conditions characterized by myofibroblast activation, scarring, inflammation, and tissue remodeling that can lead to organ failure.¹ Under the agreement, Ono will leverage Mediar's fibrosis-focused discovery platform and myofibroblast expertise, with an exclusive option to license worldwide rights to develop and commercialize resulting programs. Ono will make an upfront payment to Mediar and support research and development costs.¹

How does Mediar's antibody platform work?

Mediar's approach centers on directly targeting the myofibroblast, the cell type considered the central pathogenic driver of fibrosis across organ systems.¹ Myofibroblasts normally appear during wound healing and undergo programmed cell death once repair is complete, but in fibrotic disease they persist, driving excessive extracellular matrix deposition that progressively destroys normal tissue architecture and function.² The company combines novel antibody targets with detectable blood biomarkers, an approach intended to de-risk the clinical path for fibrosis therapies.¹

What is Mediar's existing pipeline?

Beyond the Ono collaboration, Mediar continues to advance three first-in-class human IgG1 antibody programs.¹ MTX-474, an EphrinB2-targeting antibody, is in phase 2 development for systemic sclerosis; Ephrin ligands and their Eph receptors are implicated in cell migration, myofibroblast activation, and tissue remodeling processes central to skin, lung, and heart fibrosis.¹ MTX-463, an anti-WISP1 antibody developed in collaboration with Eli Lilly and Company, is in phase 2 development for idiopathic pulmonary fibrosis, targeting a secreted matricellular protein whose blood levels correlate with disease severity.¹ MTX-439, an anti-SMOC2 antibody, is in phase 1 development for chronic kidney disease-mediated fibrosis, disrupting SMOC2-linked signaling that supports myofibroblast activation.¹

What did company leadership say?

Rahul Ballal, PhD, chief executive officer of Mediar Therapeutics, said, "This strategic collaboration with Ono is an important milestone for Mediar and reflects the growing recognition that directly targeting the myofibroblast can unlock new therapeutic possibilities in fibrotic diseases. By using our expertise in fibrosis discovery, we are positioned to advance new potential therapies across a broad range of diseases. We are excited to start work with Ono Pharma after longstanding support from Ono Venture Investment, Inc. (OVI), who have been investors in the company since 2021."¹ Seishi Katsumata, corporate officer and executive vice president, discovery and research at Ono, said, "Fibro-inflammatory diseases remain areas of significant unmet medical need, and we believe biologics innovation is essential to provide meaningful therapeutic advances. Mediar has established deep scientific expertise in fibrosis and antibody discovery. By combining Mediar's capabilities with Ono's experience in immunology and inflammation research area, we aim to create novel antibody therapeutics that may offer new treatment options for patients."¹

What happens next?

Financial terms of the upfront payment and specific program timelines were not disclosed in the release.¹ Mediar's existing pipeline continues to advance independently of the new collaboration, with MTX-474 currently enrolling in phase 2 (NCT07287670), MTX-463 recruiting for phase 2 (NCT06967805), and MTX-439 progressing through a phase 1 trial (NCT07473323) that includes both healthy participants and adults with diabetic kidney disease, with plans to move into a randomized phase 2 program.¹

References

1. Mediar Therapeutics enters into a collaboration and option agreement with Ono Pharma to develop novel treatments for fibro-inflammatory diseases. News release. PR Newswire; August 6, 2026. Accessed August 6, 2026.
2. McElhinney K, Irnaten M, O'Brien C. p53 and myofibroblast apoptosis in organ fibrosis. Int J Mol Sci. 2023;24(7):6737. doi:10.3390/ijms24076737