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Submit ReviewZE 132 binds to programmed cell death-ligand 1 (PD-L1) with high affinity (KD = 19.36 nM); it potently and selectively inhibits the interaction between programmed cell death-1 (PD-1) and PD-L1 (IC50 = 23.49 nM). ZE 132 promotes CD8+ T cell activation and improves the in vitro cytotoxic killing activity of T-cells. ZE 132 treatment can increase Cxcl9 mRNA expression and lower Tgfb1 mRNA expression in CT26 mouse colorectal cancer model. ZE 132 shows antitumor effects, inhibiting growth of CT26 tumors in mice by 64%.
分子量 | 721.27 |
公式 | C37H41ClN4O7S |
储存 | Store at -20°C |
纯度 | ≥98% (HPLC) |
CAS Number | 2566710-63-0 |
PubChem ID | 155367962 |
InChI Key | QJSJWFVBDAPNAE-UHFFFAOYSA-N |
Smiles | CN(CCCN(CC1=C(C=C(C(Cl)=C1)OCC2=CC=CC(C3=CC=C4OCCOC4=C3)=C2C)OCC5=CN=CC(C#N)=C5)CCS(O)(=O)=O)C |
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 | 72.13 | 100 |
以下数据基于产品分子量 721.27。 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 | 1.39 mL | 6.93 mL | 13.86 mL |
5 mM | 0.28 mL | 1.39 mL | 2.77 mL |
10 mM | 0.14 mL | 0.69 mL | 1.39 mL |
50 mM | 0.03 mL | 0.14 mL | 0.28 mL |
参考文献是支持产品生物活性的出版物。
Liu et al (2021) Discovery of a novel, potent and selective small-molecule inhibitor of PD-1/PD-L1 interaction with robust in vivo anti-tumour efficacy. Br.J.Pharmacol. 178 2651 PMID: 33768523
If you know of a relevant reference for ZE 132, please let us know.
关键词: ZE 132, ZE 132 supplier, ZE132, potent, selective, inhibitor, inhibits, interaction, between, programmed, cell, death-1, PD-1, death-ligand, 1, PD-L1, promotes, CD8+, T, activation, antitumor, Immune, Checkpoints, 7533, Tocris Bioscience
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This poster summarizes the main metabolic pathways in cancer cells and highlights potential targets for cancer therapeutics. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways providing potential cancer therapeutic targets.