J-113863

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

J-113863 也是人 CCR3 的有效拮抗剂（IC50 为 0.58 nM），但是小鼠 CCR3 的弱拮抗剂（IC50 为 460 nM）。 J-113863 对 CCR2、CCR4 和 CCR5 以及 LTB4 或 TNF-α 受体无活性。抗炎作用。 J-113863 是一种有效的选择性 CCR1 (CD18) 拮抗剂，IC50 值为 0.9 nM 和 5.8人和小鼠 CCR1 受体分别为 nM。

J-113863 is also a potent antagonist of the human CCR3 (IC50 of 0.58 nM) , but a weak antagonist of the mouse CCR3 (IC50 of 460 nM). J-113863 is inactive against CCR2, CCR4 and CCR5, as well as the LTB4 or TNF-α receptors. Anti-inflammatory effect. J-113863 is a potent and selective CCR1 (CD18) antagonist with IC50 values of 0.9 nM and 5.8?nM for human and mouse CCR1 receptors, respectively. The chemotaxis of the following cells were inhibited by J-113863. Modified Vaccinia virus Ankara (MVA) but not MVA and vaccinia virus (VACV) infected MH-S cells increase the expression of the CXCR2 acting chemokine CXCL2. MH-S cells constitutively produce CCL2 and CCR1 acting chemokines CCL3, CCL5 and CCL9. Consequently, supernatants of mock treated and virus infected MH-S cells induce chemotaxis of murine promyelocyte MPRO cells and human monocytic THP-1 cells at the same level. However, supernatants of MVA infected MH-S cells significantly increase chemotaxis of the CCR2 deficient human monocytic cell line U-937. J-113863 treatment improves paw inflammation and joint damage, and dramatically decreases cell infiltration into joints in arthritic mice.

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Animal Model:DBA-1 male mice (10-12 weeks) induced with Collagen Dosage:3 mg/kg, 10 mg/kg Administration:Intraperitoneal injection; once daily; for 11 days Result:Improved paw inflammation and joint damage, and dramatically decreased cell infiltration into joints.

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Autophagy

CCR

CCR1|CCR3

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353791-85-2

655.44

C30H37Cl2IN2O2

>98% (HPLC)

In Vitro:?DMSO : 50 mg/mL (76.28 mM)

[I-].CC[N+]1(C\C2=C\CCCCCC2)CCC(CC1)NC(=O)C1c2cc(Cl)ccc2Oc2ccc(Cl)cc12

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(-20℃)

With Ice Pack

≥ 2 years