(3S,5R,8R,9S,10S,13R,14S,17R)-17-(3-furyl)-10,13-dimethyl-2,3,4,5,6,7, 8,9,11,12,15,16-dodecahydro-1H-cyclopenta[a]phenanthrene-3,14,17-triol

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. 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. At very low doses (1 and 10 μg/kg for 5-6 weeks) in Milan-hypertensive rats, it decreased the development of hypertension. In a Phase II clinical study, rostafuroxin did not reduce blood pressure in human patients at doses of 0.05-5.0 mg/d.

(3β,5β,14β)-21,23-Epoxy-24-Norchola-20,22-diene-3,14,17-triol is used as a receptor blocker in the treatment of hypertension.

at molecular level, in the kidney, rostafuroxin antagonizes eo by triggering of the src-epidermal growth factor receptor (egfr)-dependent signaling pathway leading to renal na+-k+ pump, and erk tyrosine phosphorylation and activation. in the vasculature, it normalizes the increased myogenic tone caused by nanomolar ouabain [1].

rostafuroxin reduces blood pressure without affecting heart rate, and restores the normal activity of the renal na+-k+-atpase in mhs rats when orally treated at doses from 1 to 100 μg/kg/day. similarly, nua rats have their blood pressure normalized by rostafuroxin [1].

2 μm for na+-k+-atpase

Store at +4°C

[1] ferrari p, ferrandi m, valentini g, bianchi g. rostafuroxin: an ouabain antagonist that corrects renal and vascular na+-k+-atpase alterations in ouabain and adducin-dependent hypertension. am j physiol regul integr comp physiol. 2006 mar;290(3):r529-35.