BMS-303141 | ATP citrate lyase (ACL) inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $70.00 | ||
| 25 mg | $280.00 |
BMS-303141 (943963-47-8) is a potent and selective ATP citrate lyase (ACL) inhibitor, IC50=0.13 μM. Inhibits lipid biosynthesis, IC50=8 μM in HepG2 cells.1,2 Reduces weight gain, lowers plasma cholesterol, triglycerides and glucose in high-fat-fed mice.2 A novel tool compound for exploring the potential of ACL inhibition as a target for metabolic disorders such as obesity and dyslipidemia.2 Impairs proliferation or induces death in androgen-depleted castration resistant prostate cancer cells.3 Reduces cell cycle progression in iBN cells.4
References/Citations:
1) Li et al. (2007), 2-hydroxy-N-arylbenzenesulfonamides as ATP-citrate lyase inhibitors; Bioorg. Med. Chem., 17 3208
2) Ma et al. (2009), A novel direct homogeneous assay for ATP citrate lyase; J. Lipid Res., 50 2131
3) Shah et al. (2016), Targeting ACLY sensitizes castration-resistant prostate cancer cells to AR antagonism by impinging on an ACLY-AMPK-AR feedback mechanism; Oncotarget, 7 43713
4) Rhee and Dekoter (2017), Regulation of Lipid Metabolism and Cell Cycle Progression by PU.1 in Myeloid Progenitor Cells; Blood, 130 2433
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
BMS-303141 (943963-47-8) is a potent and selective ATP citrate lyase (ACL) inhibitor, IC50=0.13 μM. Inhibits lipid biosynthesis, IC50=8 μM in HepG2 cells.1,2 Reduces weight gain, lowers plasma cholesterol, triglycerides and glucose in high-fat-fed mice.2 A novel tool compound for exploring the potential of ACL inhibition as a target for metabolic disorders such as obesity and dyslipidemia.2 Impairs proliferation or induces death in androgen-depleted castration resistant prostate cancer cells.3 Reduces cell cycle progression in iBN cells.4
References/Citations:
1) Li et al. (2007), 2-hydroxy-N-arylbenzenesulfonamides as ATP-citrate lyase inhibitors; Bioorg. Med. Chem., 17 3208
2) Ma et al. (2009), A novel direct homogeneous assay for ATP citrate lyase; J. Lipid Res., 50 2131
3) Shah et al. (2016), Targeting ACLY sensitizes castration-resistant prostate cancer cells to AR antagonism by impinging on an ACLY-AMPK-AR feedback mechanism; Oncotarget, 7 43713
4) Rhee and Dekoter (2017), Regulation of Lipid Metabolism and Cell Cycle Progression by PU.1 in Myeloid Progenitor Cells; Blood, 130 2433
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