上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白,专注于信号通路和疾病研究领域。
CHIR-124 纯度: 96.57%
CHIR-124 是一种有效的,选择性的 Chk1 抑制剂,IC50 值为 0.3 nM;同时可有效抑制 PDGFR 和 FLT3,IC50 值分别为 6.6 nM 和 5.8 nM。
CHIR-124 Chemical Structure
CAS No. : 405168-58-3
规格 | 价格 | 是否有货 | 数量 |
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10 mM * 1 mL in DMSO | ¥1023 | In-stock | |
5 mg | ¥930 | In-stock | |
10 mg | ¥1581 | In-stock | |
50 mg | ¥5580 | In-stock | |
100 mg | ¥7905 | In-stock | |
200 mg | 询价 | ||
500 mg | 询价 |
* Please select Quantity before adding items.
CHIR-124 相关产品
•相关化合物库:
- Bioactive Compound Library Plus
- Apoptosis Compound Library
- Cell Cycle/DNA Damage Compound Library
- Kinase Inhibitor Library
- Protein Tyrosine Kinase Compound Library
- Anti-Cancer Compound Library
- Anti-Aging Compound Library
- Reprogramming Compound Library
- Anti-Blood Cancer Compound Library
- Angiogenesis Related Compound Library
- Anti-Liver Cancer Compound Library
生物活性 |
CHIR-124 is a potent and selective Chk1 inhibitor with IC50 of 0.3 nM, and also potently targets PDGFR and FLT3 with IC50s of 6.6 nM and 5.8 nM. |
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IC50 & Target[1] |
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体外研究 (In Vitro) |
CHIR-124 is 500- to 5,000-fold less active against other cell cycle kinases, such as cyclin-dependent kinase 2/cyclin A (0.19 μM), cdc2/cyclin B (0.51 μM), and cyclin-dependent kinase 4/cyclin D (2.1 μM). CHIR-124 (≥0.9 nM) in combination with SN-38 (≥0.42 nM) causes significant synergy or >10% deviation from additivity in human cancer cell lines expressing mutant p53, and these values overlap and fall below the IC50s for SN-38 (1.2×10-7 M) and CHIR-124 (2.2×10-7 M), respectively. Moreover, CHIR-124 (100 nM) abrogates the SN-38-induced S and G2-M phase cell cycle checkpoints. CHIR-124 (200 nM) leads to a 2.5-fold elevated level of cdc25A above that of the untreated HCT116 p53−/− cells. The down-regulation of cdc25A induced by SN-38 is completely restored by concurrent or sequential treatment with CHIR-124, proving that CHIR-124 inhibits the Chk1-mediated destruction of cdc25A in whole cells[1]. CHIR-124 occupies the ATP-binding site, inhibits Chk1 (IC50, 0.3 nM) 2,000-fold more potently than Chk2 (IC50, 0.7 μM)[2]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
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体内研究 (In Vivo) |
CHIR-124 (10 or 20 mg/kg, p.o.) does not have a significant effect on tumor growth when compared with the vehicle-treated group, but it potentiates the growth inhibitory effect of CPT-11 in a human breast carcinoma xenograft model. The potentiation of the tumor growth inhibitory effect of CPT-11 by CHIR-124 is associated with an increase in apoptosis induction in the tumors. CHIR-124 reverses the suppression of phospho-H3 staining induced by CPT-11, indicating abrogation of the G2-M checkpoint by CHIR-124[1]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
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分子量 |
419.91 |
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Formula |
C23H22ClN5O |
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CAS 号 |
405168-58-3 |
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运输条件 |
Room temperature in continental US; may vary elsewhere. |
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储存方式 |
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溶解性数据 |
In Vitro:
DMSO : 7.14 mg/mL (17.00 mM; Need ultrasonic) 配制储备液
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请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 In Vivo:
请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
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参考文献 |
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Kinase Assay [1] |
For the CHK1 assay, the kinase domain is expressed in Sf9 insect cells, and a biotinylated cdc25c peptide containing the consensus Chk1/Chk2 phosphorylation site (*)(biotin-[AHX]SGSGS*GLYRSPSMP-ENLNRPR[CONH2]) is used as the substrate. A dilution series of CHIR-124 is mixed with a kinase reaction buffer containing a final concentration of 30 mM Tris-HCl (pH 7.5), 10 mM MgCl2, 2 mM DTT, 4 mM EDTA, 25 mM β-glycerophosphate, 5 mM MnCl2, 0.01% bovine serum albumin, 1.35 nM CHK1 kinase domain, 0.5 μM peptide substrate, and 1 μM unlabeled ATP, plus 5 nM 33P γ-labeled ATP (specific activity =2,000 Ci/mmol). Reactions and detection of the phosphate transfer are carried out by a radioactive method. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
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Animal Administration [1] |
Severe combined immunodeficient mice harboring MDA-MD-435 tumor xenografts are randomized into the following treatment groups of 10: vehicle (captisol) alone, 5 mg/kg CPT-11, 10 mg/kg CHIR-124, 20 mg/kg CHIR-124, 5 mg/kg CPT-11 plus 10 mg/kg CHIR-124, or 5 mg/kg CPT-11 plus 20 mg/kg CHIR-124. Treatment is initiated on the day after randomization (day 1). CPT-11 is given i.p. daily (four times daily) ×5 on days 1 to 5, whereas CHIR-124 is given orally four times daily ×6 on days 2 to 7 in captisol. Percent tumor growth inhibition is defined as % T/C, where T = the treatment group mean, and C = the control group mean. In a similar study, tumors harvested from mice sacrificed on day 4 of treatment are examined for apoptosis by terminal deoxynucleotidyl transferase-mediated nick-end labeling staining and for mitotic index by immunofluorescence labeling with phospho-histone H3 antibody. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
参考文献 |
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