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When treated with the glucagon-like-peptide-1 analogue exenatide, FRDA iPSC- cells upregulate frataxin expression, and show improved metabolic function and increased mitochondrial activity, demonstrating that iPSC- cells can be utilised to investigate FRDA cellular phenotypes and potentially develop novel therapeutics [35]

CD38 is a valuable antigen in MM patients, even after relapse or resistance to treatment, because its expression remained elevated in patients with relapsed refractory MM

A well-studied angiogenesis inhibitor is thrombospondin-1 (TSP1), which is a large glycoprotein present in ECM [31]

Ultimately, the autophagic vesicle membrane closes, enabling fusion with the lysosome to form an autophagic lysosome