Name | BMS-303141 |
Synonyms | CS-887 BMS30314 BMS303141 BMS 303141 BMS-303141 3,5-dichloro-2-hydroxy-N-(4-Methoxybiphenyl-3-yl)benzenesulfonaMide 3,5-dichloro-2-hydroxy-N-(2-methoxy-5-phenylphenyl)benzenesulfonamide 3,5-Dichloro-2-hydroxy-N-(4-methoxy[1,1'-biphenyl]-3-yl)benzenesulfonamide 3,5-Dichloro-2-hydroxy-N-(4-methoxy[1,1'-biphenyl]-3-yl)-benzenesulfonamide BMS 303141 |
CAS | 943962-47-8 |
Molecular Formula | C19H15Cl2NO4S |
Molar Mass | 424.3 |
Density | 1.462±0.06 g/cm3(Predicted) |
Boling Point | 591.5±60.0 °C(Predicted) |
Solubility | soluble in DMSO |
Appearance | powder |
Color | white to beige |
pKa | 4.94±0.48(Predicted) |
Storage Condition | 2-8°C |
Stability | Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 3 months. |
Use | BMS303141 is a potent inhibitor of ATP citrate lyase (ACL). BMS-303141 inhibits lipid synthesis in HepG2 cells with an IC50 of 8 μM, and lowers plasma triglycerides in a murine hyperlipdemia model. |
Target | ACL |
In vitro study | In HepG2 cells, BMS-303141 shows inhibition of total lipid syntheses with an IC 50 of 8 μM. BMS-303141 shows no cytotoxicity up to 50 lM under a cell based Alamar Blue cytotoxicity assay, indicating the observed inhibition of lipid synthesis is not a result of compound-induced cytotoxicity. |
In vivo study | Chronic oral dosing of BMS-303141 in high-fat fed mice lowers approximate 20-30% plasma cholesterol and triglycerides, as well as 30-50% fasting plasma glucose. Chronic treatment with BMS-303141 shows a gradual inhibition of weight gain along with a reduction in adiposity without apparent changes in food intake. BMS-303141 shows an oral bioavailability of 55% but a relatively short half-life of 2.1 h. |
WGK Germany | 3 |
Reference Show more | 1: Guo Q, Kang H, Wang J, Dong Y, Peng R, Zhao H, Wu W, Guan H, Li F. Inhibition of ACLY Leads to Suppression of Osteoclast Differentiation and Function Via Regulation of Histone Acetylation. J Bone Miner Res. 2021 Jun 22. doi: 10.1002/jbmr.4399. Epub ahead of print. PMID: 34155695. 2: Zheng Y, Zhou Q, Zhao C, Li J, Yu Z, Zhu Q. ATP citrate lyase inhibitor triggers endoplasmic reticulum stress to induce hepatocellular carcinoma cell apoptosis via p-eIF2α/ATF4/CHOP axis. J Cell Mol Med. 2021 Feb;25(3):1468-1479. doi: 10.1111/jcmm.16235. Epub 2021 Jan 3. PMID: 33393219; PMCID: PMC7875901. 3: Vaughn N, Haviland DL. Acly promotes metabolic reprogramming and induction of IRF4 during early CD8+ T cell activation. Cytometry A. 2021 Aug;99(8):825-831. doi: 10.1002/cyto.a.24294. Epub 2020 Dec 29. PMID: 33325591. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.357 ml | 11.784 ml | 23.568 ml |
5 mM | 0.471 ml | 2.357 ml | 4.714 ml |
10 mM | 0.236 ml | 1.178 ml | 2.357 ml |
5 mM | 0.047 ml | 0.236 ml | 0.471 ml |
biological activity | BMS-303141 is an effective cell-permeable ATP-citrate lyase (ACL) inhibitor with an IC50 value of 0.13 μM. BMS-303141 inhibited total lipid synthesis in HepG2 cells with an IC50 value of 8 μM. |
target | TargetValue ACL (Cell-free say) 0.13 μM |
Target | Value |
ACL (Cell-free assay) | <0.13 μM |
in vitro study | in HepG2 cells, BMS-303141 shows inhibition of total lipid syntheses with an IC 50 of 8 μ m. BMS-303141 shows no cytotoxicity up to 50 lm under a cell based alamar blue cytotoxicity end, indicating the observed inhibition of lipid synthesis is not a result of compound-induced cytotoxicity. |
in vivo research | Chronic oral of BMS-303141 in high-fat fed mices approximate 20-30% plasma cholesterol and triglycerides, as well as 30-50% fasting plasma glucose. Chronic treatment with BMS-303141 shows a gradual inhibition of weight gain along with a reduction in adiposity without apparent changes in food intake. BMS-303141 shows an oral bioavailability of 55% but a relatively short half-life of 2.1 h. |