![CCR2-RA-[R]图片](http://www.cnreagent.com/data/daily/2022/12/07/165359_318362_umcs_1047296.png)
| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
CCR2-RA -[R] can inhibit CCR2 in a non-competitive binding manner, mainly by blocking activation-related conformational changes and the formation of G-protein binding interfaces.
Preparation Method | For dissociation experiments, the membranes were first incubated with 3 nM CCR2-RA-[R]CCR2-RA-[R] for 90 minutes. Dissociation was initiated by the addition of 10 mM of JNJ-27141491 at different time points. |
Reaction Conditions | 3 nM [3H]CCR2-RA-[R] for 90 minutes |
Applications | CCR2-RA-[R] had IC50 values of 103 + 18. Saturation binding experiments yielded a Kp of 5.8 + 0.2 nM with a Bmax of 9.7 + 0.2 pmol/mg. |
Cell lines | U2OS-CCR2 cells |
Preparation Method | For the antagonist assays, cells were first preincubated for 30 minutes with increasing concentrations of antagonist(including CCR2-RA-[R]) or vehicle control that was added in 5 ul of compound solution (final concentration of 0.25% dimethylsulfoxide).Subsequently, cells were stimulated with an ECso concentration (3 nM) of CCL2. |
Reaction Conditions | Increasing concentrations of the antagonists(including CCR2-RA-[R] were added 30 minutes before agonist stimulation to determine their IC 50 value.( No specific concentration) |
Applications | INCB3344 competitively inhibited CCL2-induced G protein activation, whereas CCR2-RA-[R] showed a noncompetitive or allosteric mode of inhibition. |
Animal models | Adult female Sprague-Dawley rats (150-200 g) |
Preparation Method | CCR2-RA-[R] were given a one-time intraperitoneal (i.p.) injection one hour prior to behavioral testing. |
Dosage form | 10 mg/kg CCR2-RA-[R] for 1 time |
Applications | CCR2-RA-[R] treatment of nerve-injured rats produced stereospecific bilateral reversal of tactile hyperalgesia |
| 产品描述 | CCR2-RA -[R] can inhibit CCR2 in a non-competitive binding manner, mainly by blocking activation-related conformational changes and the formation of G-protein binding interfaces[1,2]. For CCR2-RA-[R] the most important residues for binding were found to be the highly conserved tyrosine Y(7.53) and phenylalanine F(8.50) of the NPxxYx(5,6)F motif, as well as V(6.36) at the bottom of TM-VI and K(8.49) in helix-VIII[3]. CCR2-RA-[R] had IC50 values of 103 nM.Saturation binding experiments yielded a Kp of 5.8 + 0.2 nM with a Bmax of 9.7 + 0.2 pmol/mg.CCR2-RA-[R] clearly showed noncompetitive antagonism for CCR2 with respect to CCL2, as indicated by a decrease in CCL2's efficacy in the presence of increasing concentrations of CCR2RA-[R][1]. Focal nerve demyelination increased behavioral reflex responsiveness to mechanical stimuli between postoperative day (POD) 3 and POD28 in both the hindpaw ipsilateral and contralateral to the nerve injury. CCR2 RA-[R] treatment of nerve-injured rats produced stereospecific bilateral reversal of tactile hyperalgesia[4]. CCR2i CCR2-RA-[R] (MCP-1 receptor inhibitor) were administered via intraperitoneal injection. With or without PDX, treatment with CCR2-RA-[R] reduced the number of neutrophils and recruited macrophages, indicating that the basic function of PDX was disappeared after using CCR2 inhibitors(CCR2-RA-[R])[5]. CCR2 RA-[R] enhances the response to ¨>>PD-1 by promoting the counts of progenitor Tex[6]. Compared to the model group, the fluorescence intensity of spleen was markedly decreased by Pirfenidone and CCR2-RA-[R] Moreover, Compared to the model group, the fluorescence intensity of liver metastasis foci was dramatically reduced by Pirfenidone and CCR2-RA-[R][7]. References: |
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