| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 200mg | 电议 |
Cell lines | M2 macrophage |
Preparation Method | Macrophages (2 × 105) were sorted out from the peripheral blood of bone-cancer mice and treated with different concentrations of bindarit after IL-4 stimulation. |
Reaction Conditions | Treat macrophages with 0, 200, and 400 μM bindarit at 0, 2, and 6h after IL-4 stimulation. |
Applications | Bindarit significantly inhibited M2 macrophage polarization in vitro. Treatment of bindarit significantly decreased the level of Arg1 mRNA and functioned in a dose-dependent manner. mRNA levels of other M2 macrophage polarization markers Ym1, Mrc1, and Fizz1 were also down-regulated after bindarit treatment. Bindarit also inhibits phosphorylation of both IκBα and p65. |
Animal models | Adult male athymic nude mice, 7–8 weeks old, weighing 25–30 g |
Preparation Method | Mice received an intraperitoneal inoculation of breast sarcocarcinoma Walker 256 cells. Bone cancer was then established by inoculating Walker 256 cells (2 × 105cells, 10 μL) into the intramedullary space of the mouse femur. Control mice (n = 20) were injected with heat-killed cancer cells. |
Dosage form | 100 mg/kg |
Applications | Bindarit exhibited protective effect against bone-cancer-induced pain and inflammation. Treatment of bindarit also significantly improved the performance of the mice in spontaneous nocifensive behavior test and in mechanical hyperalgesia test, suggesting that treatment of bindarit significantly relieves the pain caused by bone cancer. Bindarit also reduced monocyte mobilization in peripheral blood. |
| 产品描述 | Bindarit (2-methyl-2-[(1-[phenylmethyl]-1H-indazol-3yl) methoxy] propanoic acid) is a small molecule that is able to prevent the chronicity of inflammation and thus decrease the cytotoxic effects of inflammation as well as inhibit the synthesis of C–C chemokines including CCL2, CCL7, and CCL8. Treatment of Bindarit has been shown to lead to a dramatic reduction of urinary CCL2 and albumin excretion.[1] In vitro study indicated that Bindarit selectively inhibited the production of the monocyte chemotactic protein subfamily of CC inflammatory chemokines (MCP-1/CCL2) at the transcriptional level. Other in vitro research also showed that Bindarit exerted a concentration-related neuroprotective activity against both Aβ25-35 and Aβ1-42 toxicity. Specifically, in cultures of mixed cortical neural cells, Bindarit reduced Aβ-related neurotoxicity in a dose-dependent manner. This effect correlated with CCL2 suppression at both mRNA and protein level.[2] In vivo study demonstrated that Bindarit limited MCP-1/CCL2 upregulation in the kidney of PCK rats and that inhibition of the chemotactic signal translated in a reduced accumulation of inflammatory cells in the kidney. In vitro studies in murine podocytes exposed to albumin overload were instrumental to establish that amelioration of podocyte structure and antiproteinuric effect by Bindarit in PCK rats could be ascribed to drug’s ability of inhibiting podocyte MCP-1/ CCL2 production.[3] References: |
m.cnreagent.com