1. Metabolic Enzyme/Protease
  2. Oxidative Phosphorylation
  3. XN methyl pyrazole

XN methyl pyrazole (XP) is an orally active, blood-brain barrier permeable uncoupler/proton carrier. XN methyl pyrazole uncouples oxidative phosphorylation, depolarizes mitochondrial transmembrane potential, increases energy expenditure, spontaneous activity levels, and cortical inosine monophosphate levels. XN methyl pyrazole reduces plasma purine and energy metabolite levels, improves glucose tolerance, and decreases weight gain, while avoiding potential estrogenic side effects. XN methyl pyrazole can be used in studies related to diet-induced obesity and insulin resistance.

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XN methyl pyrazole

XN methyl pyrazole Chemical Structure

CAS No. : 2820169-36-4

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Description

XN methyl pyrazole (XP) is an orally active, blood-brain barrier permeable uncoupler/proton carrier. XN methyl pyrazole uncouples oxidative phosphorylation, depolarizes mitochondrial transmembrane potential, increases energy expenditure, spontaneous activity levels, and cortical inosine monophosphate levels. XN methyl pyrazole reduces plasma purine and energy metabolite levels, improves glucose tolerance, and decreases weight gain, while avoiding potential estrogenic side effects. XN methyl pyrazole can be used in studies related to diet-induced obesity and insulin resistance[1].

In Vitro

XN methyl pyrazole (0-50 μM; 24 h) does not reduce the viability of HepG2 or C2C12 cells at concentrations below 50 μM after 24 h incubation[1].
XN methyl pyrazole (1-15 μM; 1 h) acts as a protonophore to depolarize the mitochondrial transmembrane potential in C2C12 cells at concentrations from 1 to 15 μM after 1 h incubation, uncoupling oxidative phosphorylation[1].

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

In Vivo

XN methyl pyrazole (30 mg/kg; p.o.; once daily; 11 weeks) improves diet-induced obesity and insulin resistance in male C57BL/6J mice by increasing energy expenditure by up to 27% and locomotor activity, while reducing weight gain and HOMA-IR by 77.9%[1].

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

Animal Model: C57BL/6J (9-week-old male, diet-induced obesity via 12-week high-fat diet)[1]
Dosage: 30 mg/kg
Administration: p.o.; once daily; 11 weeks
Result: Reduced final body weight to 37.87 g compared to 40.42 g in controls.
Improved glucose tolerance compared to controls.
Reduced homeostatic model assessment of insulin resistance (HOMA-IR) by 77.9% to 10.94.
Increased mean energy expenditure by 20−27% compared to controls.
Increased respiratory exchange ratio compared to controls.
Increased total movement compared to controls.
Increased locomotor movement by 75-135% compared to controls.
Increased percent ambulatory time compared to controls.
Decreased plasma concentrations of purine metabolites (adenosine monophosphate, inosine monophosphate, inosine, hypoxanthine, xanthine) and creatine relative to controls.
Increased cortical inosine monophosphate abundance by 76% compared to controls.
Caused no significant changes in plasma triglycerides, total cholesterol, inflammatory cytokines (MCP-1, IL-6), or liver enzyme (AST, ALT) activities relative to controls.
Clinical Trial
Molecular Weight

380.44

Formula

C22H24N2O4

CAS No.
SMILES

OC1=CC(OC)=C(C2=NN(C)C(C3=CC=C(O)C=C3)=C2)C(O)=C1C/C=C(C)\C

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Purity & Documentation
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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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XN methyl pyrazole
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HY-139994
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