• In preclinical models of cornea endothelial dystrophies, a Surrozen antibody-based Wnt mimetic reduced corneal edema and stimulated endothelial cell proliferation in the cornea
  
• Surrozen's antibody based Wnt mimetic also increased detectable tear volume production in dry eye disease models

SOUTH SAN FRANCISCO, Calif., May 09, 2024 (GLOBE NEWSWIRE) -- Surrozen, Inc. ("Surrozen" or the "Company") (NASDAQ:SRZN), a company pioneering targeted therapeutics that selectively activate the Wnt pathway for tissue repair and regeneration, announced today that preclinical data highlighting the potential for Surrozen's antibody-based Wnt mimetic technologies to treat cornea endothelial damage and Dry Eye Disease (DED) were presented on May 7, 2024 at the Association for Research in Vision and Ophthalmology (ARVO) Annual Meeting in Seattle.

"We are pleased to present new data based on preclinical studies that demonstrate activation of the Wnt pathway leads to regeneration of cells in damaged eye tear gland tissue in Dry Eye Disease and proliferation of endothelial cells in Fuchs' Endothelial Cell Dystrophy, that can halt the loss of vision and blindness that develop as the diseases progress," said Yang Li, Ph.D. Executive Vice President of Research. "These early results are important as Fuchs' Endothelial Cell Dystrophy and Dry Eye Disease are severe diseases with few effective treatments available. We look forward to continuing our evaluation of this novel approach to tissue and cell regeneration utilizing our antibody based Wnt mimetic SWAP technologies."

Exploring Cornea Endothelium Regeneration with Selective Wnt Mimetics (Presentation, May 7, 2024, ARVO Annual Meeting)

Preclinical studies evaluated whether Wnt signaling activation through Surrozen's antibody-based Wnt mimetic, that utilizes the SWAP (Surrozen Wnt signal activating proteins) technologies, can induce cornea endothelial cell proliferation and restore vision in cornea endothelial dystrophies when administered locally. The company evaluated a therapeutic approach to stimulate endothelial cell proliferation as human corneal endothelial cells have a limited capacity to regenerate.

The studies profiled both human normal and Fuchs' patient cornea endothelium which determined that Frizzled (Fzd)1/2/7 was expressed in these tissues and that activating Wnt signaling via Fzd1/2/7 in human endothelial cell cultures increases proliferation.

The lead molecule, a Surrozen Fzd 1/2/7 SWAP antibody, increased proliferation of endothelial cells in vitro in human cells. In a mouse model of cryoinjury, the Surrozen's antibody demonstrated:
- activation of Wnt signaling,
- reduced corneal edema and thickness, and
- demonstrated improved corneal clarity.

In eye diseases such as Fuchs' Endothelial Cell Dystrophy (FECD), there is a loss of endothelial cells which leads to corneal swelling, haziness and vision loss. There are about 2.9 million diagnosed patients with FECD. Current therapies are limited to endothelial transplant or resection once the disease is in a late stage. There is a significant area of unmet need for therapies that could mitigate disease progression and/or improve surgical efficacy. Results presented by Surrozen demonstrate that activation of the Wnt pathway has the potential to stimulate endothelial cell proliferation, reduce central corneal thickness and improve visual clarity.