Home / ATP Citrate Lyase Inhibitors / BMS 303141

BMS 303141

Catalog #: 4609
3 Citations Datasheet / COA / SDS
Catalog # Availability Size / Price Qty
4609/10
4609/50
BMS 303141 | CAS No. 943962-47-8 | ATP Citrate Lyase Inhibitors
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Description: ATP citrate lyase inhibitor; orally bioavailable

Chemical Name: 3,5-Dichloro-2-hydroxy-N-(4-methoxy[1,1'-biphenyl]-3-yl)-benzenesulfonamide

Purity: ≥98%

Product Details
Citations (3)
Reviews
Biological Activity Technical Data Background Product Datasheets Calculators

Biological Activity

BMS 303141 is an ATP citrate lyase (ACL) inhibitor (IC50 = 0.13 μM for human recombinant ACL); blocks lipid synthesis (IC50 = 8 μM in HepG2 cells). Displays no cytotoxicity up to a concentration of 50 μM. Lowers plasma glucose and triglycerides in a mouse model of hyperlipidemia. Orally bioavailable.

Technical Data

M.Wt:
424.3
Formula:
C19H15Cl2NO4S
Solubility:
Soluble to 10 mM in DMSO and to 50 mM in ethanol
Purity:
≥98%
Storage:
Store at -20°C
CAS No:
943962-47-8

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.

Background References

  1. 2-hydroxy-N-arylbenzenesulfonamides as ATP-citrate lyase inhibitors.
    Li et al.
    Bioorg.Med.Chem.Lett., 2007;17:3208
  2. A novel direct homogeneous assay for ATP citrate lyase.
    Ma et al.
    J.Lipid Res., 2009;50:2131

Product Datasheets

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Citations for BMS 303141

The citations listed below are publications that use Tocris products. Selected citations for BMS 303141 include:

3 Citations: Showing 1 - 3

  1. Tricarboxylic Acid Cycle Activity and Remodeling of Glycerophosphocholine Lipids Support Cytokine Induction in Response to Fungal Patterns.
    Authors: Márquez Et al.
    Cell Rep  2019;27:525
  2. Polarization of Human Macrophages by Interleukin-4 Does Not Require ATP-Citrate Lyase.
    Authors: Namgaladze Et al.
    Front Immunol  2018;9:2858
  3. Targeting ACLY sensitizes castration-resistant prostate cancer cells to AR antagonism by impinging on an ACLY-AMPK-AR feedback mechanism.
    Authors: Shah Et al.
    Oncotarget  2016;7:43713

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