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Insert image: Professional clinical guidelines and administration protocols document

Regulatory and safety status: Pending FDA review

This metabolic inflexibility in Insr P1195L/ + mice could be also due to compensatory increase in fat utilization in fat and skeletal muscle during dark phase caused by impaired glucose uptake in these tissues

Mitochondrial damage can trigger mitochondrial DNA (mtDNA) release, activating the cGAS-STING1 pathway and potentially contributing to ferroptosis, as observed with inducers like zalcitabine (116)

Excessive ROS are produced in physiological functions such as mitochondrial function and phagocytic activity