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Acyl-CoA: cholesterol acyltransferase (ACAT) inhibitor. Decreases cholesterol levels in the plasma and liver of diabetic-hypercholesterolemic rats.
|Storage||Store at +4°C|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 449.57. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.22 mL||11.12 mL||22.24 mL|
|5 mM||0.44 mL||2.22 mL||4.45 mL|
|10 mM||0.22 mL||1.11 mL||2.22 mL|
|50 mM||0.04 mL||0.22 mL||0.44 mL|
References are publications that support the biological activity of the product.
Adameova et al (2006) Protective effect of SimV. and VULM 1457 in ischaemic-reperfused myocardium of the diabetic-hypercholesterolemic rats. Pharmazie 61 807 PMID: 17020164
Adameova et al (2007) The myocardial infarct size-limiting and antiarrhythmic effects of acyl-CoA: cholesterol acyltransferase inhibitor VULM 1457 protect the hearts of diabetic-hypercholesterolaemic rats against ischaemia/reperfusion injury both in vitro and in v Eur.J.Pharmacol. 576 114 PMID: 17764671
Vojtassakova et al (2007) Effect of VULM 1457, an ACAT inhibitor, on serum lipid levels and on real time red blood cell flow in diabetic and non-diabetic hamsters fed high cholesterol-lipid diet. Gen.Physiol.Biophys. 26 254 PMID: 18281742
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Keywords: VULM 1457, VULM 1457 supplier, Acyl-CoA, cholesterol, acyltransferase, ACAT, inhibitors, inhibits, Transferases, VULM1457, Acyl-CoA:Cholesterol, Acyltransferase, 2988, Tocris Bioscience
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Literature in this Area
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.