RPR107393 free base

Name: RPR107393 free base
Brand: MedChemExpress
SKU: HY-100299
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Cat. No.: HY-100299: Ficha de datos Instrucciones de manejo
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RPR107393 free base is an orally active potent selective squalene synthase (SQS) inhibitor. RPR107393 free base inhibits rat liver microsomal squalene synthase with an IC₅₀ value of 0.8 nM. RPR107393 free base reduces triglyceride biosynthesis by suppressing fatty acid biosynthesis via an increase in intracellular farnesol and its derivatives. RPR107393 free base reduces plasma cholesterol in rats and marmosets. RPR107393 free base can be used for metabolic disease research, such as hypercholesterolemia, hypertriglyceridemia and atherosclerosis^[1][2].

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RPR107393 free base Estructura química

No. CAS : 197576-78-6

Tamaño	Stock	Cantidad
1 mg	Obtener un presupuesto 2 - 3 weeks 1 - 2 weeks 3 - 4 weeks 2 - 3 weeks	Estimated Time of Arrival: December 31
5 mg	Obtener un presupuesto 2 - 3 weeks 1 - 2 weeks 3 - 4 weeks 2 - 3 weeks	Estimated Time of Arrival: December 31
10 mg	Obtener un presupuesto 2 - 3 weeks 1 - 2 weeks 3 - 4 weeks 2 - 3 weeks	Estimated Time of Arrival: December 31
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100 mg	Obtener un presupuesto

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Descripciòn

IC₅₀ & Target

IC50: 0.8±0.2 nM (rat liver microsomal squalene synthase)^[1]

In Vitro

RPR107393 free base (10 min) is a potent inhibitor of rat liver microsomal squalene synthase, with IC₅₀ values of 0.6 to 0.9 nM, and is inactive (3 % inhibition at 1 mM) against HMG-CoA reductase from rat liver microsomes^[1].
RPR107393 free base (6 h) concentration-dependently inhibits cholesterol biosynthesis (IC₅₀ = 880 nM) and triglyceride biosynthesis (IC₅₀ = 410 nM) in rat hepatocytes^[2].
RPR107393 free base (10 μM, 2-24 h) decreases the incorporation of [1-¹⁴C]acetic acid into lipids in rat hepatocytes in a time-dependent manner, with maximal inhibition of cholesterol and triglyceride biosynthesis occurring at 2 h and 24 h, respectively^[2].
RPR107393 free base (1 μM, 4 h) inhibits cholesterol and triglyceride biosynthesis by 82.4 % and 70.0 % in rat hepatocytes, respectively, with the latter effect potentiated by MVL supplementation, suggesting a mechanism involving increased FPP derivatives^[2].
RPR107393 free base (1-10 μM, 4 h) increases carnitine-dependent mitochondrial β-oxidation (by 26.5 % at 1 μM and 39.5 % at 10 μM), it reduces overall triglyceride biosynthesis through a β-oxidation-independent pathway^[2].
RPR107393 free base (10 μM, 4 h) suppresses triglyceride biosynthesis in rat hepatocytes, reducing fatty acid and triglyceride synthesis by 67.7 % and 68.5 %, respectively, through inhibiting fatty acid synthesis rather than later metabolic stages^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

RPR107393 free base (10, 25 and 30 mg/kg, p.o., sigle dose, b.i.d. for 2-4 days, or q.d. for 7 days) exerts potent hypolipidemic effects after oral administration in rats^[1].
RPR107393 free base (20 mg/kg, p.o., b.i.d. or q.d. for 7 days) selectively lowers LDL cholesterol while maintaining a favorable HDL profile in marmosets^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Sprague-Dawley rats (130-150 g)^[1]
Dosage:	10 and 25 mg/kg
Administration:	p.o., sigle dose
Result:	Reduced cholesterol biosynthesis by 92 % at 10 mg/kg, with an approximate ED50 value of 5 mg/kg. Reduced cholesterol biosynthesis by 74 % after 6 h, and the time for 50 % inhibition was ~7 hr at 10 mg/kg. Inhibited hepatic cholesterol biosynthesis with an inhibition of 82 % at 25 mg/kg after 10 h, but the effect was no longer apparent at 21 h. Inhibited cholesterol biosynthesis associated with an accumulation of radiolabeled diacid products in the liver.

Animal Model:	Sprague-Dawley rats (130-150 g)^[1]
Dosage:	30 mg/kg
Administration:	p.o., b.i.d. for 2-4 days
Result:	Lowered serum cholesterol by 35 % after 2 days and by nearly 50 % after 3 days. The reduction in cholesterol was greater in the very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) fractions (66-88 %) than in the high-density lipoprotein (HDL) fraction (maximum, 35 %). Reduced serum triglycerides by up to 70 %. Induced hepatic microsomal HMG-CoA reductase activity by 12 to 34-fold.

Animal Model:	Sprague-Dawley rats (130-150 g) given a chow diet or the same diet supplemented with 2 % cholestyramine (HY-104081)^[1]
Dosage:	30 mg/kg
Administration:	p.o., q.d. for 7 days
Result:	The R and S enantiomers reduced serum cholesterol by 9 % and 24 %, and triglycerides by 46 % and 57 %, respectively. Coadministration with 2 % cholestyramine in the diet reduced serum cholesterol by 49 %. The R enantiomer administered alone did not lower serum LDL cholesterol, whereas coadministration with cholestyramine resulted in a 30 % reduction. The reductions in LDL cholesterol with the S enantiomer in the absence and the presence of cholestyramine were 33 % and 61 %, respectively. The reduction was greater in the VLDL and LDL fractions than in the HDL fraction.

Animal Model:	Male common marmosets (Callithrix jacchus)^[1]
Dosage:	20 mg/kg
Administration:	p.o., b.i.d. for 7 days
Result:	Reduced plasma cholesterol by 50 %. The reduction in plasma cholesterol was selectively in the LDL fraction (≤50 %), whereas cholesterol in the HDL fraction was unchanged. Produced a greater reduction in plasma cholesterol than Lovastatin (HY-N0504) or Pravastatin (HY-B0165) (which produced ≤31 % reduction at 50 mg/kg, b.i.d.).

Animal Model:	Male common marmosets (Callithrix jacchus)^[1]
Dosage:	20 mg/kg
Administration:	p.o. q.d. for 7 days
Result:	Both enantiomers reduced total plasma cholesterol by approximately 27 %. The R and S enantiomers reduced LDL cholesterol by 50 % and 43 %, respectively. Showed no significant changed in HDL cholesterol levels.

Peso molecular

330.42

Fòrmula

C₂₂H₂₂N₂O

No. CAS

197576-78-6

SMILES

OC1(C2=CC=C(C3=CC=C4N=CC=CC4=C3)C=C2)CN5CCC1CC5

Envío

Room temperature in continental US; may vary elsewhere.

Almacenamiento

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureza y Documentación

Instrucciones de manejo (2659 KB)

Referencias

[1]. Amin D, et al. RPR107393, a potent squalene synthase inhibitor and orally effective Cholesterol-lowering agent: comparison with inhibitors of HMG-CoA reductase. J Pharmacol Exp Ther. 1997 May;281(2):746-52. [Content Brief]

[2]. Hiyoshi H, et al. Squalene synthase inhibitors suppress triglyceride biosynthesis through the farnesol pathway in rat hepatocytes. J Lipid Res. 2003 Jan;44(1):128-35. [Content Brief]