05091
3,5-Dimethylpyrazole
produced by Wacker Chemie AG, Burghausen, Germany, ≥99.0% (GC)
Synonym(s):
3,5-Dimethyl-1H-pyrazole
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About This Item
Recommended Products
grade
produced by Wacker Chemie AG, Burghausen, Germany
Quality Level
Assay
≥99.0% (GC)
bp
218 °C (lit.)
mp
105-108 °C (lit.)
SMILES string
Cc1cc(C)[nH]n1
InChI
1S/C5H8N2/c1-4-3-5(2)7-6-4/h3H,1-2H3,(H,6,7)
InChI key
SDXAWLJRERMRKF-UHFFFAOYSA-N
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Signal Word
Warning
Hazard Statements
Precautionary Statements
Hazard Classifications
Acute Tox. 4 Oral - STOT RE 2
Target Organs
Liver
Storage Class Code
13 - Non Combustible Solids
WGK
WGK 3
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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Experimental gerontology, 38(5), 519-527 (2003-05-14)
Autophagy is a universal, highly regulated mechanism responsible for the degradation of long-lived proteins, cytomembranes and organelles during fasting and may be the cell repair mechanism that mediates the anti-ageing effects of calorie restriction (Bergamini and Gori, 1995). The function
The American journal of physiology, 266(1 Pt 1), G118-G122 (1994-01-01)
Regulation of liver macroautophagy and protein degradation by hormones and direct regulatory amino acids were studied in male 2-mo-old Sprague-Dawley albino rats with the use of the antilipolytic agent 3,5'-dimethylpyrazole (DMP; 12 mg/kg body wt ip) as a stimulatory agent.
Effects of antilipolytic agents on peroxisomal beta-oxidation of fatty acids in rat liver.
Biochemical pharmacology, 32(11), 1807-1809 (1983-06-01)
Autophagy, 3(1), 26-27 (2006-09-12)
Autophagy is a major intracellular degradation/recycling system ubiquitous in eukaryotic cells. It contributes to the turnover of cellular components by delivering portions of the cytoplasm and organelles to lysosomes, where they are digested. Starvation-induced autophagy is required for maintaining an
Metabolism: clinical and experimental, 51(1), 110-114 (2002-01-10)
This study intended to test the hypothesis that intracellular lipolysis in the pancreatic beta cells is implicated in the regulation of insulin secretion stimulated by nutrient secretagogues or cyclic adenosine monophosphate (cAMP) agonists. Indeed, although lipid signaling molecules were repeatedly
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