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Atossa Therapeutics Announces Acceptance of Manuscript Highlighting Utrophin-Modulation Potential of (Z)-Endoxifen in Duchenne Muscular Dystrophy
Atossa Therapeutics Announces Acceptance of Manuscript Highlighting Utrophin-Modulation Potential of (Z)-Endoxifen in Duchenne Muscular Dystrophy
About this update from Atossa Therapeutics, Inc.
[{"type":"text","content":"Review article accepted for publication in Degenerative Neurological and Neuromuscular Disease and builds on Atossa's previously published Duchenne Muscular Dystrophy (DMD) researchSEATTLE, May 20, 2026 /PRNewswire/ -- Atossa Therapeutics, Inc. (NASDAQ: ATOS) (Atossa or the Company), a clinical-stage biopharmaceutical company developing novel therapies in oncology and other areas of significant unmet clinical need, today announced that the manuscript titled, \"(Z)-Endoxifen as a Potential Modulator of Utrophin Pathways in Duchenne Muscular Dystrophy: A Mechanistic and Transcriptomic Perspective,\" has been accepted for publication in Degenerative Neurological and Neuromuscular Disease.\n \n \n \n \n \n \n \nThe review centers on utrophin, a structural and functional homolog of dystrophin. Utrophin may partially compensate for dystrophin deficiency by supporting sarcolemmal and muscle-cell membrane stability when dystrophin is absent or deficient. The manuscript describes how (Z)-endoxifen, the primary active metabolite of tamoxifen, could create a cellular environment that favors utrophin expression, localization, and function, which could potentially influence disease-relevant processes, such as protein kinase C beta-1 signaling, estrogen receptor signaling, calcium homeostasis, inflammation, fibrosis, mitochondrial function, and muscle regeneration. The authors describe (Z)-endoxifen as a compelling mechanistic candidate in treating DMD and identified next steps including preclinical evaluation in dystrophin-deficient models and biomarker development focused on utrophin expression and localization, calcium handling, PKC activity, developmental myosin, transcriptomic signatures, and muscle composition imaging.\"This publication advances our scientific rationale for studying (Z)-endoxifen through the lens of utrophin biology, one of the most compelling mutation-agnostic strategies in DMD,\" said Dr. Steven C. Quay, M.D., Ph.D., President and Chief Executive Officer of Atossa Therapeutics. \"DMD remains a devastating disease with significant unmet need, and we are encouraged by the mechanistic and transcriptomic evidence suggesting that (Z)-endoxifen may help support pathways involved in utrophin-mediated muscle stabilization and repair.\"The new article builds on Atossa's previously published DMD manuscript in Degenerative Neuro...