Series B Co-led by New Investors Amplitude Ventures and ICG

MTX-474 Global Phase 2a study Initiated in Systemic Sclerosis (SSc)

MTX-463 Global Phase 2a Study in Idiopathic Pulmonary Fibrosis (IPF) Enrolling & Partnered with Lilly

MTX-439 Advancing to Phase 1 studies for Fibrosis Associated with Chronic Kidney Disease (CKD)

BOSTON, Jan. 7, 2026 /PRNewswire/ — Mediar Therapeutics, Inc., a clinical-stage biotechnology company advancing first-in-class therapies designed to halt fibrosis, today announced an oversubscribed $76 million Series B financing co-led by Amplitude Ventures and ICG, with participation from new investors Longwood Fund, Asahi Kasei Pharma Ventures, Alexandria Real Estate Trust (ARE), and existing Series A investors. Joining the Mediar board from Amplitude Ventures is Bharat Srinivasa, PhD, and from ICG is Allan Marchington, PhD. Proceeds from the financing will further support advancement of Mediar’s wholly owned assets, including MTX-474, an antagonist of EphrinB2, being studied in a Phase 2a study in patients with systemic sclerosis (SSc), and MTX-439, a SMOC2 antagonist, proceeding to Phase 1 studies for the treatment of chronic kidney disease (CKD) associated fibrosis.

“It has been a transformative 12 months for Mediar, from our deal with Eli Lilly and Company on MTX-463, to this oversubscribed Series B financing with leading biotech investors,” said Rahul Ballal, PhD, Chief Executive Officer of Mediar Therapeutics. “With $175 million raised through these transactions, we can advance our novel anti-fibrotics through clinical studies and potentially bring life-changing therapies to patients suffering from fibrosing diseases of the skin, lung, and kidney. I would like to take this moment to thank our entire Mediar team for their dedication and demonstration that direct targeting of the myofibroblast holds promise to halt fibrosis.”

The company has initiated the EncompaSSc trial, a randomized, double-blinded, placebo-controlled 24-week Phase 2a study designed to evaluate the efficacy, safety, and tolerability of MTX-474 in approximately 90 patients living with SSc, using the validated mRSS (Modified Rodnan Skin Score) tool, as the primary endpoint.

“The EncompaSSc study marks an important milestone in our effort to bring new treatment options to patients living with SSc,” said Lorinda Chung, MD, MS, Global Principal Investigator of the trial and professor of Medicine and Dermatology at Stanford Medicine. “Emerging research shows that EphrinB2 signaling may contribute to the progression of fibrosis in multiple organ systems impacted by systemic sclerosis. These patients have a large unmet need, and this Phase 2a trial will allow us to evaluate MTX-474’s potential to treat patients suffering with this disease.”

“By addressing the fundamental causes of fibrosis, Mediar is paving the way for transformative clinical advances in the field,” said Allan Marchington, PhD, Head of Life Sciences at ICG. “We are proud to co-lead this financing to accelerate these vital therapies.”

“We are excited about Mediar’s unique approach to targeting fibrosis across multiple organ systems,” added Bharat Srinivasa, PhD, Principal at Amplitude Ventures. “Together, we aim to translate this deep scientific understanding into novel therapies that positively impact patient lives.”

The company is also finalizing an IND-enabling package for MTX-439, a SMOC2 antagonist, for the treatment of fibrosis associated with chronic kidney disease (CKD), with plans to initiate Phase 1 studies in the first half of 2026.

About MTX-474

MTX-474 is a first-in-class human IgG1 antibody designed to neutralize the EphrinB2 signaling that causes the onset and progression of fibrosis. 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 are measurable in human blood and correlates with disease severity. A Phase 1 study was recently completed and a Phase 2 clinical study in patients with SSc is now open (NCT07287670). More information can be found at www.encompassctrial.com

About MTX-463

MTX-463 is a first-in-class human IgG1 antibody developed against WNT1-inducible signaling pathway protein-1 (WISP1). WISP1 is a secreted matricellular protein shown to have a relevant role in fibrosis progression, is measurable in human blood, and correlates with disease severity. Data indicates that MTX-463 neutralizes WISP1-mediated fibrotic signaling and significantly reduced fibrosis in vitro and in various preclinical models. A Phase 1 study was recently completed and a Phase 2 study in patients with IPF is now open (NCT06967805). More information can be found at: www.wispertrial.com

About MTX-439

MTX-439 is a first-in-class human IgG1 antibody engineered to inhibit the activity of SPARC-related modular calcium-binding protein 2 (SMOC2). SMOC2 has been shown to promote extracellular matrix assembly and cell adhesiveness. SMOC2 is a driver of renal fibrosis and SMOC2 levels are elevated in patients with chronic kidney disease, both in the tissue and in circulation. MTX-439 selectively binds to SMOC2 and neutralizes its activity significantly reducing fibrosis in multiple preclinical models. MTX-439 is anticipated to enter Phase 1 studies in the first half of 2026.

About Mediar Therapeutics

Mediar Therapeutics is pioneering a new approach to fibrosis treatment that aims to halt the disease at a different source – the myofibroblast, the key pathogenic cell in fibrosis that drives scarring, disease progression, and ultimately organ failure. Mediar was founded based on a deep understanding of the complex science underlying fibrosis progression. By combining novel targets with reliable, easily detectable blood biomarkers and familiar modalities, Mediar’s goal is to bring forward novel anti-fibrotic therapies that potentially have a precision medicine approach. For more information, contact info@mediartx.com or follow us on LinkedIn.

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