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Cyclerion Therapeutics Announces CY6463 Data Demonstrating Improved Cellular Energetics in Preclinical Models of Mitochondrial Disease
CY6463 alleviated mitochondrial dysfunction and reduced inflammation in preclinical models of mitochondrial complex 1 deficiency Data provide support for
About this update from Cyclerion Therapeutics, Inc.
[{"type":"text","content":"CY6463 alleviated mitochondrial dysfunction and reduced inflammation in preclinical models of mitochondrial complex 1 deficiency Data provide support for ongoing CY6463 clinical studies in CNS diseases associated with mitochondrial dysfunction CAMBRIDGE, Mass., June 17, 2022 (GLOBE NEWSWIRE) -- Cyclerion Therapeutics, Inc. (Nasdaq: CYCN), a clinical-stage biopharmaceutical company on a mission to develop treatments that restore cognitive function, today announced research from preclinical studies demonstrating treatment with its lead soluble guanylate cyclase (sGC) stimulator, CY6463, was associated with improved cellular energetics and reduced inflammation in preclinical models of mitochondrial disease. The data will be presented today at the 10th International Conference on cGMP, taking place June 17-19, 2022, in Augsburg, Germany. “We’re excited to share results highlighting the beneficial impact of sGC stimulation in multiple preclinical models of mitochondrial disease,” said Juli Jones, Ph.D, Head of Disease Biology at Cyclerion Therapeutics. “These results are consistent with our recent clinical data in MELAS patients demonstrating that CY6463 was associated with improvements across multiple domains of disease activity, including mitochondrial function and inflammation, and further support the therapeutic potential of CY6463 to address a broad range of diseases characterized by mitochondrial dysfunction.” Data will be presented by Emmanuel Buys, Ph.D., Head of Network Excellence at Cyclerion Therapeutics in a poster titled, “CY6463, a CNS-penetrant sGC stimulator, elicits benefits in preclinical models of mitochondrial complex 1 deficiency” during today’s poster session. The poster is made available on the Cyclerion website on the following link. Presentation highlights: CY6463 significantly increased ATP levels in lymphoblasts derived from patients with mitochondrial complex 1 deficiency (Leber hereditary optic neuropathy or Leigh syndrome)CY6463 restored mitochondrial gene expression in lymphoblasts derived from patients with mitochondrial complex 1 deficiency (Leber hereditary optic neuropathy or Leigh syndrome)CY6463 significantly decreased the astrocytic marker, GFAP, linked to inflammation in a mouse model of mitochondrial complex 1 deficiency About CY6463CY6463 is the first CNS-penetrant sGC stimulator to be develop...