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Progression from simple steatosis to MASH involves cellular stress pathways triggered by lipotoxicity, endoplasmic reticulum stress, mitochondrial dysfunction, and oxidative injury

It is intended to be administered by intramuscular injection

e , Schematic illustrating the potential role of INTS12 and its coordinated Pol II removal in TC-DPC repair

Administration of GSH precursors like cysteine/N-acetylcysteine, glycine and/or glutamic acid will facilitate the synthesis of GSH within each cell of the body including the atherosclerotic plaque, reducing ROS and LDL oxidation, enhancing NO production, and mitigating atherosclerosis and its complications (221229)