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While STARD1-dependent BA synthesis stimulates carcinogenesis through the induction of transcription factors involved in the stemness, self-renewal, and inflammation, the enrichment of mitochondria in cholesterol and subsequent impact on mitochondrial membrane fluidity impairs chemotherapy that targets the mitochondrial apoptotic pathway by restraining the mitochondrial outer membrane permeabilization and subsequent engagement of the apoptosome [135]

FOXO4-DRIs D-retro-inverso configuration provides exceptional proteolytic stability compared to equivalent L-amino acid senolytic peptides a critical property for cell-based and pre-clinical research where intracellular peptidase activity would rapidly degrade unstable L-amino acid sequences