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Submit ReviewSB 297006 is a potent and selective CCR3 antagonist (IC50 = 39 nM). Displays 250-fold selectivity for CCR3 over other chemokine receptors, including CXCR1, CXCR2, CCR1 and CCR7 (IC50 >27 μM). Inhibits calcium mobilization induced by MCP-4, eotaxin-2 and eotaxin in RBL-2H3 cells transfected with CCR3 (IC50 values are 80, 90 and 210 nM respectively).
SB 297006 is also offered as part of the Tocriscreen Antiviral Library. 了解 Tocris 化合物库的更多信息。
分子量 | 342.35 |
公式 | C18H18N2O5 |
储存 | Store at RT |
纯度 | ≥99% (HPLC) |
CAS Number | 58816-69-6 |
PubChem ID | 9840971 |
InChI Key | BEZXGSZPWXRHIN-INIZCTEOSA-N |
Smiles | O=C(C2=CC=CC=C2)N[C@H](C(OCC)=O)CC1=CC=C([N+]([O-])=O)C=C1 |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
溶剂 | 最高浓度 mg/mL | 最高浓度 mM | |
---|---|---|---|
溶解性 | |||
DMSO | 34.23 | 100 | |
ethanol | 6.85 | 20 |
以下数据基于产品分子量 342.35。 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
浓度/溶剂体积/质量 | 1 mg | 5 mg | 10 mg |
---|---|---|---|
1 mM | 2.92 mL | 14.6 mL | 29.21 mL |
5 mM | 0.58 mL | 2.92 mL | 5.84 mL |
10 mM | 0.29 mL | 1.46 mL | 2.92 mL |
50 mM | 0.06 mL | 0.29 mL | 0.58 mL |
参考文献是支持产品生物活性的出版物。
Yoshimoto and Hansch (1976) Quantitative structure-activity relationships of D- and L-N-actyl-alpha-aminoamide ligands binding to chymotrypsin. On the problem of combined treatment of stereoisomers. J.Org.Chem. 41 2269 PMID: 932854
White et al (2000) Identification of a potent, selective non-peptide CC chemokine receptor-3 antagonist that inhibits eotaxin-, eotaxin-2-, and monocyte chemotactic protein-4-induced eosinophil migration. J.Biol.Chem. 275 36626 PMID: 10969084
If you know of a relevant reference for SB 297006, please let us know.
关键词: SB 297006, SB 297006 supplier, SB297006, ccr3, chemokines, receptors, antagonists, selective, potent, Rantes, Chemokine, CC, Receptors, 4213, Tocris Bioscience
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Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.