Molecular Formula | C19H20N2O3
|
Molar Mass | 324.37 |
Density | 1.18±0.1 g/cm3 (20 ºC 760 Torr) |
Boling Point | 542.9±40.0 °C(Predicted) |
pKa | 3.59±0.10(Predicted) |
Storage Condition | 2-8°C |
In vitro study | Bindarit treatment inhibited the production of monocyte chemoattractant protein -1(MCP-1) by human monocytes in response to bacterial LPS or C. Albicans, with IC50 of 172 µm and 403 µm respectively. Bindarit inhibited LP-induced MCP-1 production and was associated with reduced levels of MCP-1 mRNA transcripts with an IC50 of 75 µm. Bindarit inhibited MCP-1 production in LPS-stimulated MM6 cells with an IC50 of 425 μm and did not affect IL-8 or IL-6 release. Bindarit treatment, inhibits MCP-1 release from IL-1 stimulated osteoblast cell line Saos-2. Bindarit is not toxic to human IIB-MEL-J melanomas or ECs in vitro even at maximum concentrations, although it inhibits MCP-1 expression. Bindarit(10-300 μm) reduces rat vascular smooth muscle cell (VSMC) proliferation, migration, and invasion. Bindarit induces down-regulation of the traditional NF-κB pathway. Bindarit specifically inhibited p65 and p65/p50-induced MCP-1 promoter activation, but had no effect on other activated promoters tested, indicating that Bindarit acts as a specific subset of NF-κB subtypes, and select its target in all NF-κB inflammatory pathways. Bindarit regulates cancer cell proliferation and migration, mainly through the negative regulation of TGF-β and AKT signaling. |
In vivo study | Oral administration of Bindarit to NZB/W mice at a dose of 50 mg/kg delayed the onset of proteinuria, significantly protected against renal impairment and prolonged the life of NZB/W mice or lupus mice. Bindarit treatment completely inhibited MCP-1 upregulation in the progression of nephritis. Bindarit treats human melanoma, inhibits MCP-1, and also reduces tumor growth and macrophage infiltration, causing tumor necrosis. Bindarit effectively reduces neointimal formation by acting directly on VSMC proliferation and migration in animal models of non-hyperlipidemic and hyperlipidemic vascular injury, and by reducing macrophage content in the neointima. Bindarit acts on mice bearing prostate cancer PC-3M-Luc2 xenografts, resulting in invasive tumor metastatic disease, and on Balb/c mice containing breast cancer 4T1-Luc cells, local tumor formation is impaired. In addition, Bindarit treatment of 4T1-Luc primary tumors significantly reduced tumor-associated macrophage infiltration, and myeloid-derived suppressor cell infiltration. |