Bindarit

324, 37

NZB/W F1 female mice with a spontaneous autoimmune disease

ca.50 mg/kg/day

Bindarit treatment causes a dose-dependent inhibition of the capacity of human monocytes to produce monocyte chemotactic protein-1 (MCP-1) in response to bacterial LPS or C. albicans with IC50 of 172 uM and 403 uM, respectively. The inhibition of LP-induced MCP-1 production by Bindarit is associated with reduced levels of MCP-1 mRNA transcripts with IC50 of 75 uM. Bindarit inhibits the production of MCP-1 by LPS-stimulated MM6 cells with IC50 of 425 uM, without affecting the release of IL-8 or IL-6. [2] Bindarit treatment inhibits the release of MCP-1 from IL-1 stimulated osteoblast cell line Saos-2. [3] Bindarit, even at the maximal concentration, does not exhibit a direct in vitro cytotoxic effect on human IIB-MEL-J melanoma or ECs, although it inhibits MCP-1 expression. [4] Bindarit (10-300 uM) reduces rat vascular smooth muscle cell (VSMC) proliferation, migration, and invasion. [5] Bindarit induces the downregulation of the classical NF-kappaB pathway. Bindarit displays a specific inhibitory effect on the p65 and p65/p50 induced MCP-1 promoter activation, with no effect on other tested activated promoters, indicating that Bindarit acts on a specific subpopulation of NF-kappaB isoforms and selects its targets within the whole NF-kappaB inflammatory pathway. [6] Bindarit modulates cancer-cell proliferation and migration, mainly through negative regulation of TGF-beta and AKT signaling. [7]

DMSO 65 mg/mL, Water <1 mg/mL, Ethanol 65 mg/mL

2-((1-benzyl-1H-indazol-3-yl)methoxy)-2-methylpropanoic acid