Mitochondrial-targeted peptide BP29 acetate is a mitochondria-targeted iron chelator linked to a mitochondria-homing SS-peptide. Mitochondrial-targeted peptide BP29 acetate protects human primary skin fibroblasts against ultraviolet A-induced oxidative damage to mitochondrial membranes, ATP depletion, and necrotic cell death. Mitochondrial-targeted peptide BP29 acetate prevents hydrogen peroxide-induced oxidative stress and cytotoxicity in both healthy and Friedreich's ataxia skin fibroblasts. Mitochondrial-targeted peptide BP29 acetate can be used for the research of Friedreich's ataxia [1].
In Vitro, Mitochondrial-targeted peptide BP29 (50 μM; overnight pre-treatment) acetate protects FEK4 human primary skin fibroblasts against ultraviolet A (UVA)-induced oxidative damage and necrotic cell death[1]. Mitochondrial-targeted peptide BP29 (50 μM; overnight pre-treatment) acetate protects FRDA skin fibroblasts against UVA-induced cell death[1]. Mitochondrial-targeted peptide BP29 (50 μM; overnight pre-treatment) acetate protects FRDA and healthy skin fibroblasts against H2O2-induced cytotoxicity[1].
References:
[1]. Cilibrizzi A, et al. The synthesis and properties of mitochondrial targeted iron chelators. Biometals. 2023;36(2):321-337.
In Vitro, Mitochondrial-targeted peptide BP29 (50 μM; overnight pre-treatment) acetate protects FEK4 human primary skin fibroblasts against ultraviolet A (UVA)-induced oxidative damage and necrotic cell death[1]. Mitochondrial-targeted peptide BP29 (50 μM; overnight pre-treatment) acetate protects FRDA skin fibroblasts against UVA-induced cell death[1]. Mitochondrial-targeted peptide BP29 (50 μM; overnight pre-treatment) acetate protects FRDA and healthy skin fibroblasts against H2O2-induced cytotoxicity[1].
References:
[1]. Cilibrizzi A, et al. The synthesis and properties of mitochondrial targeted iron chelators. Biometals. 2023;36(2):321-337.
















