Mitochonic acid 5 binds mitochondria and ameliorates renal tubular and cardiac myocyte damage. Mitochonic acid 5 modulates mitochondrial ATP synthesis.

Mitochonic acid 5 (MA-5) modulates mitochondrial ATP synthesis independently of oxidative phosphorylation and the electron transport chain. Mitochondrial dysfunction causes increased oxidative stress and depletion of ATP, which are involved in the etiology of a variety of renal diseases[1]. Mitochonic acid 5 (MA-5), which is derived from the plant growth hormone indole-3-acetic acid, can protect mitochondrial function by regulating energy metabolism and reducing mitochondrial oxidative stress. To observe the protective role of Mitochonic acid 5 in microglia under inflammatory conditions, TNFα is applied. Subsequently, the MTT assay is used to evaluate cell viability. In response to the TNFα treatment, cell viability significantly decreases. However, this effect is dose-dependently inhibited by Mitochonic acid 5 treatment[2].

Administration of Mitochonic acid 5 (MA-5) to an ischemia-reperfusion injury model and a cisplatin-induced nephropathy model improved renal function. To examine the tissue-protective effect of Mitochonic acid 5, the oral bioavailability is examined. Oral administration of Mitochonic acid 5 increases the plasma concentration in a dose-response manner at the peak time of 1 hour[1].

[1]. Suzuki T, et al. Mitochonic Acid 5 Binds Mitochondria and Ameliorates Renal Tubular and Cardiac Myocyte Damage. J Am Soc Nephrol. 2016 Jul;27(7):1925-32. [2]. Lei Q, et al. Mitochonic acid 5 activates the MAPK-ERK-yap signaling pathways to protect mouse microglial BV-2 cells against TNFα-induced apoptosis via increased Bnip3-related mitophagy. Cell Mol Biol Lett. 2018 Apr 5;23:14.

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