Biologically Active Small Molecules

A reversible, competitive antagonist of GPR35, blocking activation by the synthetic agonist pamoic acid with a Ki of 12.8 nM less potently blocks activation of GPR35 by zaprinast (IC50 = 160 nM) shows ~57-fold selectivity for GPR35 over the

A reversible, competitive antagonist of GPR35, blocking activation by the synthetic agonist pamoic acid with a Ki of 12.8 nM less potently blocks activation of GPR35 by zaprinast (IC50 = 160 nM) shows ~57-fold selectivity for GPR35 over the

A reversible, competitive antagonist of GPR35, blocking activation by the synthetic agonist pamoic acid with a Ki of 12.8 nM less potently blocks activation of GPR35 by zaprinast (IC50 = 160 nM) shows ~57-fold selectivity for GPR35 over the

A selective inhibitor of PKC-induced NF-&kappaB pathway activation (IC₅₀ = 0.07 &muM) inhibits IL-8 production in HEK293 cells (IC₅₀ &le 0.

A selective inhibitor of PKC-induced NF-&kappaB pathway activation (IC₅₀ = 0.07 &muM) inhibits IL-8 production in HEK293 cells (IC₅₀ &le 0.

A selective inhibitor of PKC-induced NF-&kappaB pathway activation (IC₅₀ = 0.07 &muM) inhibits IL-8 production in HEK293 cells (IC₅₀ &le 0.

A selective inhibitor of PKC-induced NF-&kappaB pathway activation (IC₅₀ = 0.07 &muM) inhibits IL-8 production in HEK293 cells (IC₅₀ &le 0.

A selective GPR55 inverse agonist that antagonizes GPR55 constitutive activity (IC₅₀ = 15 &muM) blocks GPR55-mediated endothelial wound healing and reverses LPI-inhibited platelet aggregation.

A selective GPR55 inverse agonist that antagonizes GPR55 constitutive activity (IC₅₀ = 15 &muM) blocks GPR55-mediated endothelial wound healing and reverses LPI-inhibited platelet aggregation.

A selective GPR55 inverse agonist that antagonizes GPR55 constitutive activity (IC₅₀ = 15 &muM) blocks GPR55-mediated endothelial wound healing and reverses LPI-inhibited platelet aggregation.

A selective GPR55 inverse agonist that antagonizes GPR55 constitutive activity (IC₅₀ = 15 &muM) blocks GPR55-mediated endothelial wound healing and reverses LPI-inhibited platelet aggregation.

A selective small molecule inhibitor of PKD (IC₅₀s = 182, 280, 227 nM for PKD1, 2, and 3, respectively) 25 &microM has been shown to inhibit prostate cancer cell proliferation, cell migration, and invasion.