A mycotoxin found as food contaminants that causes mycotoxic nephropathy in livestock and Balkan nephropathy and yellow rice fever in humans induces apoptosis, blocks tubulin polymerization, and disrupts mitotic spindle assembly.
A mycotoxin found as food contaminants that causes mycotoxic nephropathy in livestock and Balkan nephropathy and yellow rice fever in humans induces apoptosis, blocks tubulin polymerization, and disrupts mitotic spindle assembly.
A corticosteroid prodrug that is converted to its active form, des-CIC, a glucocorticoid receptor agonist (Ki = 0.31 nM) used to ameliorate symptoms of airway inflammatory diseases.
A corticosteroid prodrug that is converted to its active form, des-CIC, a glucocorticoid receptor agonist (Ki = 0.31 nM) used to ameliorate symptoms of airway inflammatory diseases.
A partial receptor agonist of mGlu4, effective at 100 µM, with no activity at other mGlu receptor subtypes induces apoptosis of T cells at 300-500 µM.
A partial receptor agonist of mGlu4, effective at 100 µM, with no activity at other mGlu receptor subtypes induces apoptosis of T cells at 300-500 µM.
An essential cofactor functioning as an acyl group carrier and carbonyl-activating group for the citric acid cycle and fatty acid metabolism the pantothenate kinase step of the coenzyme A biosynthetic pathway has been identified as a target for the
An essential cofactor functioning as an acyl group carrier and carbonyl-activating group for the citric acid cycle and fatty acid metabolism the pantothenate kinase step of the coenzyme A biosynthetic pathway has been identified as a target for the
A mycotoxin found as food contaminants that causes mycotoxic nephropathy in livestock and Balkan nephropathy and yellow rice fever in humans induces apoptosis, blocks tubulin polymerization, and disrupts mitotic spindle assembly.
A mycotoxin found as food contaminants that causes mycotoxic nephropathy in livestock and Balkan nephropathy and yellow rice fever in humans induces apoptosis, blocks tubulin polymerization, and disrupts mitotic spindle assembly.
A selective inhibitor of the stress-induced PPP1R15A that does not affect the constitutive PPP1R15B 50 µM prolongs eIF2&alpha phosphorylation after ER stress, delaying translation which protects cells from misfolded protein-induced
A selective inhibitor of the stress-induced PPP1R15A that does not affect the constitutive PPP1R15B 50 µM prolongs eIF2&alpha phosphorylation after ER stress, delaying translation which protects cells from misfolded protein-induced
An activator of sGC that binds to a regulatory site, resulting in activation in an NO-independent manner (Kd = 3.2 nM) reduces hypertension, limits cardiomyocyte hypertrophy, protects against ischemia/reperfusion injury, and reduces morbidity and
An activator of sGC that binds to a regulatory site, resulting in activation in an NO-independent manner (Kd = 3.2 nM) reduces hypertension, limits cardiomyocyte hypertrophy, protects against ischemia/reperfusion injury, and reduces morbidity and
A nutlin-3 analog inhibits the growth of HCT116 cells at high concentrations (IC50 = ~8 µM) promotes the growth of HCT116 cells ~40% at concentrations between 5-100 nM.
A nutlin-3 analog inhibits the growth of HCT116 cells at high concentrations (IC50 = ~8 µM) promotes the growth of HCT116 cells ~40% at concentrations between 5-100 nM.
A nutlin-3 analog inhibits the growth of HCT116 cells at high concentrations (IC50 = ~7 µM) promotes the growth of HCT-116 cells ~20% at concentrations at or below 1 µM.
A nutlin-3 analog inhibits the growth of HCT116 cells at high concentrations (IC50 = ~7 µM) promotes the growth of HCT-116 cells ~20% at concentrations at or below 1 µM.