推荐产品
质量水平
方案
≥98% (HPLC)
表单
powder
旋光性
[α]/D +80 to +90°, c = 0.3 in methanol
药品控制
regulated under CDSA - not available from Sigma-Aldrich Canada
颜色
white to beige
溶解性
DMSO: 10 mg/mL, clear
储存温度
2-8°C
SMILES字符串
CCNC(C[C@@H]1N=C(C2=CC=C(Cl)C=C2)C3=CC(OC)=CC=C3N4C1=NN=C4C)=O
InChI
1S/C22H22ClN5O2/c1-4-24-20(29)12-18-22-27-26-13(2)28(22)19-10-9-16(30-3)11-17(19)21(25-18)14-5-7-15(23)8-6-14/h5-11,18H,4,12H2,1-3H3,(H,24,29)/t18-/m0/s1
InChI key
AAAQFGUYHFJNHI-SFHVURJKSA-N
基因信息
human ... BRD2(6046) , BRD3(8019) , BRD4(23476) , BRDT(676)
生化/生理作用
I-BET762 (GSK525762) 是溴结构域和末端外 (BET) 结构域蛋白 BRD2、BRD3 和 BRD4 的选择性抑制剂，IC 50 值为 32.5–42.5 nM，与其他含溴结构域蛋白无相互作用。I-BET 模拟乙酰化组蛋白，阻止乙酰化赖氨酸和 BET reader 蛋白之间的蛋白-蛋白相互作用。这表明阻断炎症基因在活化的巨噬细胞中的表达，并对内毒素性休克和细菌性败血症具有保护作用。I-BET762 在体外和体内也显示出强效的抗骨髓瘤活性 。
I-BET762 是溴结构域和末端外 (BET) 结构域蛋白的选择性抑制剂；合成组蛋白模拟物。
I-BET762 通过控制促炎基因表达具有抗炎属性。I-BET762 在细胞模型中阻碍 MYC（原癌基因）的表达。I-BET762 的这一作用可作为治疗前列腺癌的有效疗法。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer.
Wyce A, et al.
Oncotarget, 4(12), 2419-2419 (2013)
Bromodomains: are readers right for epigenetic therapy?.
Conway S J.
ACS Medicinal Chemistry Letters, 3(9), 691?694-691?694 (2012)
Laura Helminen et al.
Nucleic acids research, 52(2), 625-642 (2023-11-28)
Treatment of prostate cancer relies predominantly on the inhibition of androgen receptor (AR) signaling. Despite the initial effectiveness of the antiandrogen therapies, the cancer often develops resistance to the AR blockade. One mechanism of the resistance is glucocorticoid receptor (GR)-mediated
Francesco Paolo Fiorentino et al.
International journal of molecular sciences, 21(24) (2020-12-20)
Small cell lung cancer (SCLC) is an aggressive type of lung cancer with high mortality that is caused by frequent relapses and acquired resistance. Despite that several target-based approaches with potential therapeutic impact on SCLC have been identified, numerous targeted
Brian Krug et al.
Cancer cell, 35(5), 782-797 (2019-05-16)
High-grade gliomas defined by histone 3 K27M driver mutations exhibit global loss of H3K27 trimethylation and reciprocal gain of H3K27 acetylation, respectively shaping repressive and active chromatin landscapes. We generated tumor-derived isogenic models bearing this mutation and show that it
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