Biologically Active Small Molecules

An irreversible inhibitor of I&kappaB&alpha phosphorylation, preventing activation of NF-&kappaB by cytokines and lipopolysaccharide (IC₅₀ = 10 &muM) blocks gene expression that is regulated through the classical pathway of

An activator of sGC, stimulating activity at concentrations as low as 10-100 nM inhibits platelet aggregation (IC50 = 36 nM), induces relaxation of preconstricted aorta rings (IC50 = 304 nM) effective in vivo, decreasing mean arterial blood

An activator of sGC, stimulating activity at concentrations as low as 10-100 nM inhibits platelet aggregation (IC50 = 36 nM), induces relaxation of preconstricted aorta rings (IC50 = 304 nM) effective in vivo, decreasing mean arterial blood

An activator of sGC, stimulating activity at concentrations as low as 10-100 nM inhibits platelet aggregation (IC50 = 36 nM), induces relaxation of preconstricted aorta rings (IC50 = 304 nM) effective in vivo, decreasing mean arterial blood

An activator of sGC, stimulating activity at concentrations as low as 10-100 nM inhibits platelet aggregation (IC50 = 36 nM), induces relaxation of preconstricted aorta rings (IC50 = 304 nM) effective in vivo, decreasing mean arterial blood

A stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 &muM, up to 92-fold in vitro, relaxes vessels and inhibits platelet aggregation at nM concentrations in vivo, decreases blood pressure

A stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 &muM, up to 92-fold in vitro, relaxes vessels and inhibits platelet aggregation at nM concentrations in vivo, decreases blood pressure

A stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 &muM, up to 92-fold in vitro, relaxes vessels and inhibits platelet aggregation at nM concentrations in vivo, decreases blood pressure

A stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 &muM, up to 92-fold in vitro, relaxes vessels and inhibits platelet aggregation at nM concentrations in vivo, decreases blood pressure

An inhibitor of Raf-1 and B-Raf (IC50 = 6 and 22 nM, respectively), as well as several receptor tyrosine kinases, including VEGFR2, VEGFR3, PDGFR&beta, FLT3, and c-Kit (IC50 = 90, 15, 20, 57, and 58 nM, respectively) inhibits tumor angiogenesis

An inhibitor of Raf-1 and B-Raf (IC50 = 6 and 22 nM, respectively), as well as several receptor tyrosine kinases, including VEGFR2, VEGFR3, PDGFR&beta, FLT3, and c-Kit (IC50 = 90, 15, 20, 57, and 58 nM, respectively) inhibits tumor angiogenesis

An inhibitor of Raf-1 and B-Raf (IC50 = 6 and 22 nM, respectively), as well as several receptor tyrosine kinases, including VEGFR2, VEGFR3, PDGFR&beta, FLT3, and c-Kit (IC50 = 90, 15, 20, 57, and 58 nM, respectively) inhibits tumor angiogenesis