On May 8, 2024 Carisma Therapeutics Inc. (Nasdaq: CARM) ("Carisma" or the "Company"), a clinical-stage biopharmaceutical company focused on discovering and developing innovative immunotherapies, reported new data demonstrating preclinical proof of concept using engineered anti-fibrotic macrophages for the treatment of liver fibrosis (Press release, Carisma Therapeutics, MAY 8, 2024, View Source [SID1234642907]). The data was presented in a poster session at the American Society of Gene and Cell Therapy (ASGCT) (Free ASGCT Whitepaper) 2024 Annual Meeting on May 8, 2024, in Baltimore, MD.
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"We are pleased to unveil preclinical proof of concept data for our liver fibrosis program, which highlight the potential of engineered macrophages to combat a prevalent disease that is associated with late-stage metabolic dysfunction-associated steatohepatitis (MASH) and represents a significant unmet need," said Michael Klichinsky, PharmD, PhD, Co-founder and Chief Scientific Officer of Carisma. "The data, from two independent models, demonstrate that engineered macrophages trafficked to fibrotic tissues, expressed genetically encoded disease-modifying payloads, and significantly reduced fibrosis in the liver. Given these encouraging data, we look forward to further progressing the liver fibrosis program, which is our first expansion outside of oncology."
In the presentation titled "Genetically Engineered Macrophage Cell Therapy Reverses Liver and Lung Fibrosis in Preclinical Models," Carisma presented preclinical proof-of-concept data for engineered macrophage cell therapy in liver fibrosis. In liver models, the data showed that a single dose of macrophages co-expressing the anti-fibrotic factor relaxin and the anti-inflammatory cytokine IL10 significantly improved established fibrosis in a CCl4-induced liver fibrosis model, with a 116% reduction in fibrosis relative to untreated control. Also, systemic administration of engineered macrophages co-expressing relaxin and IL10 significantly reduced liver fibrosis in a high fat diet MASH model, with a 45% reduction in fibrosis relative to untreated control. In both models, the relaxin-IL10 macrophage treatment also resulted in a greater reduction in liver fibrosis compared to non-engineered macrophages.
The presentation also included initial data for the use of engineered macrophages in pulmonary fibrosis. The data showed that a single dose of macrophages expressing a dominant negative TGFβ receptor, which nullified pro-fibrotic TGFβ signaling in the lung, prevented fibrosis in a bleomycin mouse model of pulmonary fibrosis, with a 90% reduction in fibrosis relative to untreated control.
Carisma expects to nominate a development candidate for its liver fibrosis program in the first quarter of 2025.
The poster presented at ASGCT (Free ASGCT Whitepaper) 2024 is now available online in the "Publications" section of Carisma’s website at View Source