Didrovaltrate

Didrovaltrate (Didrovaltratum) is an L-type calcium channel blocker, ROS scavenger, autophagy enhancer, and lipid accumulation inhibitor. Didrovaltrate blocks L-type calcium currents in a concentration-dependent manner, shifts the current-voltage curve upward, modulates steady-state inactivation kinetics, and inhibits the nuclear translocation of glucocorticoid receptors. Didrovaltrate reduces ROS levels, downregulates the expression of muscle atrophy-related genes, enhances autophagy via lipophagy, and decreases Oleic acid-induced lipid accumulation. Didrovaltrate exhibits cytotoxic activity against cancer cells. Didrovaltrate can be used in research related to skeletal muscle atrophy, non-alcoholic fatty liver disease, breast cancer, lung cancer, gastric cancer, and prostate cancer^[1][2][3][4]. In Vitro:Didrovaltrate (30-100 μg/L) reduces the peak L-type calcium current (maximum L-type calcium current), decreasing it from 6.01 pA/pF to 3.45 pA/pF and 2.16 pA/pF, with inhibition rates of 42.6% and 64.1%, respectively^[1].
Didrovaltrate (2.5-5 μM; 24 h) significantly downregulates the expression of muscle atrophy marker genes *Atrogin-1*, *Murf1* and *Mstn* in atrophic C2C12 myotubes induced by Dexamethasone (DEX) (HY-14648), restores the fusion index and myotube diameter, reverses C2C12 myotube atrophy, reduces ROS production, and inhibits the nuclear translocation of glucocorticoid receptor and FOXO3a^[2].
Didrovaltrate (2.5-25 μM; 24 h) reduces the viability of Huh7 hepatocytes at concentrations of 10 μM and higher^[3].
Didrovaltrate (10 μM; 24 h) reduces oleic acid (HY-N1446)-induced lipid accumulation in Huh7 hepatocytes in an Atg5-dependent manner^[3].
Didrovaltrate (10 μM; 0-24 h) enhances autophagic flux in Huh7 hepatocytes and increases the formation of LC3 puncta in cells^[3].
Didrovaltrate (1-100 μM; 48 h) potently inhibits the viability of MCF7 human breast adenocarcinoma cells, with an IC₅₀ of 3.9 μM; after 48 h of treatment, this compound exhibits moderate to weak cytotoxic activity against the A549, HGC27, PC3, and HUVEC cell lines^[4].