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Digoxin is a potent inhibitor of Na+/K+-ATPase, clinically used to treat arrhythmia and heart failure.

Digoxin, a sodium-potassium ATPase inhibitor, has a negative Z score of −26.67, suggesting a function for the sodium-potassium ATPase in CHIKV infection. Relative to DMSO-treated cells, treatment of U-2 OS cells with Digoxin results in a dose-dependent decrease in CHIKV infection with a half-maximal effective concentration (EC50) of 48.8 nM. Digoxin treatment similarly decreases CHIKV infection of primary human synovial fibroblasts (HSFs) and Vero African green monkey kidney cells with EC50s of 43.9 nM and 67.3 nM, respectively. Digoxin treatment significantly diminishes CHIKV infection in these cell types, with EC50s of 16.2 µM in ST2 cells and 23.2 µM in C2C12 cells, values 330 and 475 times the EC50 of Digoxin in U-2 OS cells. Cell viability is only modestly impaired at 24 h posttreatment with 1 µM Digoxin, a dose 20 times the Digoxin EC50 for CHIKV antiviral activity in these cells[1].

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