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Longeveron® Presents Lomecel-B™ Data for Alzheimer’s Disease Indication in Late Breaking Poster Presentation at the Clinical Trials on Alzheimer’s Disease Conference (CTAD24)
Findings offer potential mechanistic and clinical insights in the development of cellular therapy Lomecel-B™ for mild Alzheimer’s disease (AD)Lomecel-B™
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[{"type":"text","content":"Findings offer potential mechanistic and clinical insights in the development of cellular therapy Lomecel-B™ for mild Alzheimer’s disease (AD)Lomecel-B™ capacity to inhibit MMP14 correlates with improved clinical and biomarker outcomes in mild ADImmunomodulatory and pro-vascular effects of Lomecel-B™ in mild AD potentially driven by ability to exert MMP14 inhibition which may protect TIE2 receptor integrity in human AD patients MIAMI, Oct. 29, 2024 (GLOBE NEWSWIRE) -- Longeveron Inc. (NASDAQ: LGVN), a clinical stage regenerative medicine biotechnology company developing cellular therapies for life-threatening and chronic aging-related conditions, today announced that its submission entitled “Lomecel-B inhibition of MMP14 activity predicts Lomecel-B bioactivity in the treatment of mild Alzheimer’s disease” was presented as a late breaking poster presentation at the 17th edition of the Clinical Trials on Alzheimer’s Disease Conference (CTAD24) taking place October 29 -November 1, 2024 in Madrid, Spain. “As a medicinal signaling cell therapy that has multiple potential mechanisms of action to address inflammatory responses in the brain, Lomecel-B™ offers the potential to address the underlying pathology of Alzheimer’s disease,” said Joshua Hare, M.D., Co-founder, Chief Science Officer, and Chairman at Longeveron. “This data adds to the positive clinical information from the Phase 2a CLEAR MIND clinical trial that showed Lomecel-B™ improved cognitive function, quality of life, and brain volume in the treatment of mild Alzheimer’s disease. We are very encouraged by the safety profile and efficacy evidence that support the differentiated therapeutic potential of Lomecel-B™ in Alzheimer’s disease.” From the Poster:Matrix metalloprotease (MMP) activity is reportedly upregulated in AD. The researchers hypothesized that excess MMP14 activity may contribute to AD pathogenesis, at least in part, by cleaving TIE2 (Tyrosine kinase with Immunoglobulin and Epidermal growth factor homology domains), a cell-surface tyrosine kinase receptor for the angiopoietins, which activates downstream signaling pathways that regulate endothelial cell health and inflammatory responses. They tested the hypothesis that Lomecel-B™ capacity to inhibit MMP14 correlates with improved clinical and biomarker outcomes in mild AD. The researchers measured MMP14 inhibito...