AP39 free base is a mitochondrial-targeted H(2)S donor that can improve the survival rate of porcine islets in culture. AP39 free base regulates mitophagy through the AMPK-ULK1-FUNDC1 pathway, inhibits cell pyroptosis, and improves doxorubicin-induced myocardial fibrosis.

AP39 inhibits excessive mitochondrial autophagy through the PINK1/Parkin pathway in cardiomyocytes. The results showed that CSE protein expression levels were significantly decreased in the CoCl2 group, while the intervention with AP39 significantly upregulated CSE protein expression levels. This effect of AP39 was reversed by the endogenous H2S synthesis inhibitor PAG. [1]

In the AP39 +ISO group, the deposition of collagen fibers mentioned above was reduced compared to the ISO group. In comparison to the AP39 +ISO group, the AP39 +ISO+PAG group showed a significant increase in collagen fiber deposition. There was no significant difference in myocardial collagen deposition between the AP39 +ISO+PAG group and the ISO group. Moreover, no significant difference in myocardial collagen fiber deposition was observed between the AP39 group and the Control group. [1]