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Kriya Therapeutics announces preclinical data for KRIYA-825, gene therapy injection for the treatment of GA

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Key Takeaways

  • KRIYA-825, a gene therapy for GA, uses a CR2-CR1 fusion protein to inhibit complement C3 and C5 activity.
  • Preclinical study data showed dose-dependent efficacy in preserving retinal thickness and reducing retinal degeneration.
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(Image Credit: AdobeStock/Aonprom Photo)

(Image Credit: AdobeStock/Aonprom Photo)

Kriya Therapeutics recently announced preclinical data on its gene therapy candidate KRIYA-825, a one-time gene therapy delivered by suprachoroidal injection, for the treatment of geographic atrophy (GA).1

Kriya is a biopharmaceutical company focused on developing gene therapies for the treatment of chronic diseases affecting millions of people around the world. An adeno-associated virus (AAV)–based gene therapy, KRIYA-825 expresses a complement CR2-CR1 fusion protein––designed to inhibit the activity of complement C3 and C5––for the treatment of GA.

“We are excited about the tremendous potential of KRIYA-825 for the treatment of geographic atrophy,” said Shankar Ramaswamy, MD, cofounder and CEO of Kriya. “We are proud of the data that the team has generated to date, and we look forward to continuing to share further updates as we advance KRIYA-825 through clinical development for patients with geographic atrophy.”

The data were presented by Kriya in a presentation titled “A Novel AAV Gene Therapy Complement Inhibitor: KRIYA-825 Exhibits Dose-Dependent Murine Efficacy and NHP Biodistribution” at the 2025 Association for Research and Ophthalmology (ARVO) annual meeting held May 4 to 8 in Salt Lake City, Utah.

Utilizing a mouse model of severe retinal damage by sodium iodate (NaIO3), the authors “demonstrated the potential of KRIYA-825 to ameliorate inflammatory-driven retinal degeneration, a key feature of geographic atrophy,” a press release said.

Key takeaways from the data include the following1:

  • KRIYA-825–treated mice demonstrated dose-dependent preservation of retinal thickness.
  • Retinal damage caused by NaIO3 increased C3b fragment levels relative to iC3b, and KRIYA-825 treatment helped to suppress C3b to iC3b protein levels.

Through a dose range–finding study in nonhuman primates, the ability of a novel device to deliver KRIYA-825 to the suprachoroidal space and achieve target biodistribution in ocular tissues was demonstrated, according to the press release.

Key takeaways from this data include the following1:

  • Suprachoroidal delivery of KRIYA-825 using the Everads Suprachoroidal Injector was well tolerated.
  • Robust transgene mRNA levels were detected in relevant ocular tissues, including the choroid and retinal pigment epithelium cell layers of the retina, with minimal detectable transgene mRNA in tissues collected outside of the eye.

Kriya’s KRIYA-825 was designed with the following goals in mind1:

  • Robust complement inhibition: a CR2-CR1 fusion protein, where the CR1 domain is designed to block the activity of both complement C3 and C5, while the CR2 domain is designed to bind to the surfaces of cells where complement fragments deposit and cause damage.
  • Multiyear durability: AAV-medicated continuous expression of CR2-CR1 fusion protein following a 1-time injection to eliminate the need for frequent intravitreal injections that currently available therapies for GA require.
  • Targeted delivery: A one-time suprachoroidal injection to achieve the transduction and delivery of therapeutic protein to retinal cells while minimizing inflammation and overall patient burden.

According to the press release, KRIYA-825 has not yet been approved for use by the FDA, and the clinical safety and efficacy of KRIYA-825 for the treatment of GA have not yet been established.

Reference
  1. Kriya presents data at the 2025 Association for Research in Vision and Ophthalmology (ARVO) Annual Meeting. Kriya Therapeutics, Inc. May 8, 2025. Accessed May 15, 2025. https://finance.yahoo.com/news/kriya-presents-data-2025-association-154500461.html

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