推荐产品
质量水平
方案
≥98% (HPLC)
表单
powder
颜色
white to beige
溶解性
DMSO: 20 mg/mL, clear
储存温度
2-8°C
SMILES字符串
O=S(NC1=C(OC)C=CC(C2=CC=CC=C2)=C1)(C3=C(O)C(Cl)=CC(Cl)=C3)=O
InChI
1S/C19H15Cl2NO4S/c1-26-17-8-7-13(12-5-3-2-4-6-12)9-16(17)22-27(24,25)18-11-14(20)10-15(21)19(18)23/h2-11,22-23H,1H3
InChI key
SIIPNDKXZOTLEA-UHFFFAOYSA-N
应用
BMS-303141已被用于抑制乳腺癌细胞系中的ATP柠檬酸裂合酶。
生化/生理作用
BMS-303141是ATP柠檬酸裂解酶(ACL)的一种有效抑制剂。
BMS-303141是ATP柠檬酸裂解酶(ACL)的一种有效抑制剂。 BMS-303141可抑制HepG2细胞中的脂质合成,IC50值为8μM。同时,在鼠高脂血症模型中,其可降低血浆中的甘油三酸酯的含量。
危险声明
预防措施声明
危险分类
Aquatic Chronic 4
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)
Acetyl-CoA carboxylase 1-dependent protein acetylation controls breast cancer metastasis and recurrence
Cell Metabolism, 26, 842-855 (2017)
Science (New York, N.Y.), 367(6473), 45-51 (2019-12-07)
High-throughput chemical screens typically use coarse assays such as cell survival, limiting what can be learned about mechanisms of action, off-target effects, and heterogeneous responses. Here, we introduce "sci-Plex," which uses "nuclear hashing" to quantify global transcriptional responses to thousands
Cell reports, 39(9), 110870-110870 (2022-06-02)
Overcoming resistance to chemotherapies remains a major unmet need for cancers, such as triple-negative breast cancer (TNBC). Therefore, mechanistic studies to provide insight for drug development are urgently needed to overcome TNBC therapy resistance. Recently, an important role of fatty
Cell stem cell, 31(3), 359-377 (2024-03-09)
Mitochondrial fatty acid oxidation (FAO) is essential for hematopoietic stem cell (HSC) self-renewal; however, the mechanism by which mitochondrial metabolism controls HSC fate remains unknown. Here, we show that within the hematopoietic lineage, HSCs have the largest mitochondrial NADPH pools
Genome medicine, 14(1), 67-67 (2022-06-24)
The incidence of non-alcoholic fatty liver disease (NAFLD)-associated hepatocellular carcinoma (HCC) is increasing worldwide, but the steps in precancerous hepatocytes which lead to HCC driver mutations are not well understood. Here we provide evidence that metabolically driven histone hyperacetylation in
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