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Submit ReviewAZD 2098 is a potent and selective CCR4 antagonist (pIC50 = 7.8). Exhibits no activity at CXCR1 and CXCR2, CCR1, CCR2b, CCR5, CCR7, and CCR8 at 10 μM, and no significant activity when screened against a panel of 120 receptors and enzymes. Inhibits CCL22 Ca2+ response and Th2 cell CCL17/22 driven chemotaxis in vitro. Inhibits lung inflammation following antigen challenge in ovalbumin- sensitized rats.
AZD 2098 is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Antiviral Library. 了解 Tocris 化合物库的更多信息。
分子量 | 334.18 |
公式 | C11H9Cl2N3O3S |
储存 | Store at +4°C |
纯度 | ≥98% (HPLC) |
CAS Number | 566203-88-1 |
PubChem ID | 10308720 |
InChI Key | FLSMVCMSUNISFK-UHFFFAOYSA-N |
Smiles | COC1=NC=CN=C1NS(=O)(C2=C(Cl)C(Cl)=CC=C2)=O |
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 | 33.42 | 100 | |
ethanol | 3.34 | 10 |
以下数据基于产品分子量 334.18。 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 | 2.99 mL | 14.96 mL | 29.92 mL |
5 mM | 0.6 mL | 2.99 mL | 5.98 mL |
10 mM | 0.3 mL | 1.5 mL | 2.99 mL |
50 mM | 0.06 mL | 0.3 mL | 0.6 mL |
参考文献是支持产品生物活性的出版物。
Toogood et al (2017) Small molecule immuno-oncology therapeutic agents. Bioorg.Med.Chem.Lett. S0960 31218 PMID: 29326017
Kindon et al (2017) Discovery of AZD-2098 and AZD-1678, two potent and bioavailable CCR4 receptor antagonists. ACS Med.Chem.Lett. 8 981 PMID: 28947948
Mullard et al (2014) Cancer charity sees success re-prioritizing industry's shelved compounds. Nat.Rev.Drug Discov. 13 319 PMID: 24781536
If you know of a relevant reference for AZD 2098, please let us know.
关键词: AZD 2098, AZD 2098 supplier, AZD2098, potent, selective, CCR4, chemokines, receptors, antagonists, antagonism, chemotaxis, Chemokine, CC, Receptors, 6541, 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.