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Merck

373210

BLT-1

≥95% (HPLC), solid, HDL receptor SR-BI inhibitor, Calbiochem®

Synonyme(s) :

HDL Receptor SR-BI Inhibitor, BLT-1, Block Lipid Transport-1, 2-Hexyl-1-cyclopentanone thiosemicarbazone, 33M20

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A propos de cet article

Formule empirique (notation de Hill) :
C12H23N3S
Numéro CAS:
321673-30-7
Poids moléculaire :
241.40
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
MFCD00571007

Principaux documents

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Nom du produit

HDL Receptor SR-BI Inhibitor, BLT-1, The HDL Receptor SR-BI Inhibitor, BLT-1, also referenced under CAS 321673-30-7, controls the biological activity of HDL Receptor SR-B. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

InChI

1S/C12H23N3S/c1-2-3-4-5-7-10-8-6-9-11(10)14-15-12(13)16/h10H,2-9H2,1H3,(H3,13,15,16)/b14-11+

InChI key

OWGUSBISUVLUJF-SDNWHVSQSA-N

assay

≥95% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze, protect from light

color

white

solubility

DMSO: 100 mg/mL

shipped in

ambient

Quality Level

100

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Catégories apparentées

General description

A cell-permeable thiosemicarbazone copper chelator that potently blocks the HDL receptor SR-BI- (scavenger receptor, class B, type I) mediated lipid uptake (IC50 = 21 and 57 nM against DiI and CE uptake, respectively, from DiI-HDL and CE-HDL using hamster ldlA-7 cells expressing murine SR-BI) in a reversible manner, while exerting little effect toward intracellular membrane trafficking or cytoskeletal organization. BLT-1 chelates Cu+2 in a 2:1 stoichiometric ratio and a half molar equivalent of CuCl2 is shown to fully prevent zebrafish embryos from BLT-1-induced development defects, while BLT-1 can likewise be used to chelate excess amount of copper (>4 µM) and rescue embryos from copper toxicity.

Packaging

Packaged under inert gas

Preparation Note

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

Other Notes

Nieland, T.J.F., et al. 2008. Biochemistry47, 460.
Raldua, D., and Babin, P.J. 2007. Toxicol. Lett.175, 1.
Nieland, T.J.F., et al. 2002. Proc. Natl. Acad. Sci. USA99, 15422.
Peterson, R.T., et al. 2000. Proc. Natl. Acad. Sci. USA97, 12965.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Toxicity: Standard Handling (A)

Classe de stockage

11 - Combustible Solids

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificats d'analyse (COA)

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Thomas J F Nieland et al.
Biochemistry, 47(1), 460-472 (2007-12-11)
Scavenger receptor, class B, type I (SR-BI), controls high-density lipoprotein (HDL) metabolism by mediating cellular selective uptake of lipids from HDL without the concomitant degradation of the lipoprotein particle. We previously identified in a high-throughput chemical screen of intact cells
Demetrio Raldúa et al.
Toxicology letters, 175(1-3), 1-7 (2007-09-25)
Block lipid transport-1 (BLT-1) is a small chemical widely used to inhibit the transfer of lipids between high-density lipoproteins (HDL) and cells mediated by scavenger receptor B, type 1 (SR-BI). This study demonstrated that BLT-1 induced in zebrafish (Danio rerio)
Resveratrol intervention attenuates chylomicron secretion via repressing intestinal FXR-induced expression of scavenger receptor SR-B1.
Pang, et al.
Nature Communications, 14, 2656-2656 (2023)
Thomas J F Nieland et al.
Proceedings of the National Academy of Sciences of the United States of America, 99(24), 15422-15427 (2002-11-20)
The high-density lipoprotein (HDL) receptor, scavenger receptor, class B, type I (SR-BI), mediates both the selective uptake of lipids, mainly cholesterol esters, from HDL to cells and the efflux of cholesterol from cells to lipoproteins. The mechanism underlying these lipid
R T Peterson et al.
Proceedings of the National Academy of Sciences of the United States of America, 97(24), 12965-12969 (2000-11-23)
Much has been learned about vertebrate development by random mutagenesis followed by phenotypic screening and by targeted gene disruption followed by phenotypic analysis in model organisms. Because the timing of many developmental events is critical, it would be useful to

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