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Rostafuroxin potently inhibits binding of endogenous ouabain to the Na+/K+ ATPase (IC50 = 1.7 µM) through the Src-epidermal growth factor receptor (EGFR)-dependent signaling pathway.1 This blocks the ouabain-dependent increase in Na+/K+ ATPase activity. In cultured renal cells where the Na+/K+ ATPase is upregulated or has increased activity, rostafuroxin normalizes mRNA levels and Na+/K+ ATPase activity.2 At very low doses (1 and 10 µg/kg for 5-6 weeks) in Milan-hypertensive rats, it decreased the development of hypertension.3 In a Phase II clinical study, rostafuroxin did not reduce blood pressure in human patients at doses of 0.05-5.0 mg/d.4
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