BLT-1 is a specific inhibitor of the SR-BI (Scavenger receptor, class B, type I) mediated lipid transfer. The compound inhibits both cellular selective lipid uptake of HDL cholesteryl ether and efflux of cellular cholesterol to HDL.
CAS Number: 321673-30-7
Molecular Weight: 241.40
Block lipid transport-1
Chemical Name: 2-Hexyl-1-cyclopentanone thiosemicarbazone
Appearance: Solid Power
Purity: ≥98% (or refer to the Certificate of Analysis)
Solubility: DMSO : 41.67 mg/mL (172.62 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble)
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis
Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.
Shelf Life: ≥360 days if stored properly.
Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.
Drug Formulation: To be determined
HS Tariff Code: 382200
How to use
BLT-1 has IC50s of 60 and 110 nM for cellular DiI-HDL and [3H]CE-HDL uptake in ldlA[mSR-BI] cells. BLT-1 has an IC50 of 0.96 μM for the HCV entry in Huh 7.5.1 cells. BLT-1 (50 μM; 3 hours) does not induce general defects in clathrin-dependent and -independent intracellular membrane trafficking in HeLa, BSC-1 cells. BLT-1 can inhibit SR-BI-dependent selective uptake of [3H]CE from [3H]CE-HDL by mSR-BI-t1-containing liposomes in cells (IC50=0.057 µM) and liposomes (IC50=0.098 µM).
- Nieland TJ, et al. Discovery of chemical inhibitors of the selective transfer of lipids mediated by the HDL receptorSR-BI. Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15422-7.
- Nieland TJ, et al. Identification of the molecular target of small molecule inhibitors of HDL receptor SR-BI activity. Biochemistry. 2008 Jan 8;47(1):460-72.
- Raldúa D, et al. BLT-1, a specific inhibitor of the HDL receptor SR-BI, induces a copper-dependent phenotype during zebrafish development. Toxicol Lett. 2007 Dec 10;175(1-3):1-7. Epub 2007 Aug 22.
- Hirofumi Ohashi, et al. Reply to Padmanabhan and Dixit: Hepatitis C virus entry inhibitors for optimally boosting direct-acting antiviral-based treatments. Proc Natl Acad Sci U S A. 2017 Jun 6;114(23):E4527-E4529.
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