Semapimod tetrahydrochloride (CNI-1493), an inhibitor of proinflammatory cytokine production, can inhibit TNF-α , IL-1β , and IL-6. Semapimod tetrahydrochloride inhibits TLR4 signaling (IC 50 ≈0.3 μM). Semapimod tetrahydrochloride inhibits p38 MAPK and nitric oxide production in macrophages. Semapimod tetrahydrochloride has potential in a variety of inflammatory and autoimmune disorders . In Vitro Semapimod tetrahydrochloride leads to a significant decrease of p38-MAPK phosphorylation in macrophages, proinflammatory gene expression of macrophage inflammatory protein-1alpha, interleukin-6, monocyte chemoattractant protein-1, and intercellular adhesion molecule-1, and neutrophil infiltration. Semapimod tetrahydrochloride completely abrogated nitric oxide production within the tunica muscularis. ?\nSemapimod tetrahydrochloride desensitizes TLR signaling via its effect on the TLR chaperone gp96. Semapimod tetrahydrochloride inhibits ATP-binding and ATPase activities of gp96 in vitro (IC 50 ≈0.2-0.4 μM). Semapimod tetrahydrochloride desensitizes TLR signaling via its effect on the TLR chaperone gp96. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Semapimod tetrahydrochloride (5 mg/kg; i.p; daily for 2 weeks) ameliorates endothelial dysfunction in Obese Zucker (OZ) rats . ?\nSemapimod tetrahydrochloride restores AM-induced akt phosphorylation and cGMP production in OZ rats . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male OZ rats Dosage: 5 mg/kg Administration: I.p; daily for 2 weeks Result: Restored endothelium-dependent vasorelaxation in OZ rats. Form:Solid