27900
Creatine monohydrate
≥99.0% (NT)
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About This Item
Empirical Formula (Hill Notation):
C4H9N3O2 · H2O
CAS Number:
Molecular Weight:
149.15
Beilstein:
7942755
EC Number:
MDL number:
UNSPSC Code:
12352200
Assay
≥99.0% (NT)
ign. residue
≤0.05%
mp
~295 °C (dec.)
SMILES string
O.CN(CC(O)=O)C(N)=N
InChI
1S/C4H9N3O2.H2O/c1-7(4(5)6)2-3(8)9;/h2H2,1H3,(H3,5,6)(H,8,9);1H2
InChI key
MEJYXFHCRXAUIL-UHFFFAOYSA-N
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Biochem/physiol Actions
Creatine is a nitrogenous compound that acts as a high-energy reservoir for the rapid regeneration of ATP.
Creatine is a nitrogenous compound that acts as a high-energy reservoir for the rapid regeneration of ATP. Approximately 95% of creatine is found in skeletal muscle, primarily as phosphocreatine. Creatine can be acquired through dietary consumption or formed from L-arginine, glycine, and L-methionine in a multi-step reaction that occurs in the kidneys and liver. Creatine is then transported to muscle tissue. Creatine supplementation is used for the enhancement of sports performance, primarily by increasing muscle mass. Creatine is also being investigated as a treatment of neuromuscular diseases, where it may aid in neuroprotection and by improving the cellular bioenergetic state.
Other Notes
Identification of creatine as a cofactor of thiamine-diphosphate kinase.
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H Shikata et al.
FEBS letters, 201(1), 101-104 (1986-05-26)
Thiamin-diphosphate (TDP) kinase which catalyzes thiamin triphosphate formation from TDP requires a low-molecular-mass cofactor in addition to ATP and Mg2+. The cofactor was isolated in a crystalline form from pig skeletal muscle and identified as creatine by proton NMR, mass
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Kelsey H Fisher-Wellman et al.
Cell reports, 24(13), 3593-3606 (2018-09-27)
Chronic metabolic diseases have been linked to molecular signatures of mitochondrial dysfunction. Nonetheless, molecular remodeling of the transcriptome, proteome, and/or metabolome does not necessarily translate to functional consequences that confer physiologic phenotypes. The work here aims to bridge the gap
Ashley S Williams et al.
Cell metabolism, 31(1), 131-147 (2019-12-10)
This study sought to examine the functional significance of mitochondrial protein acetylation using a double knockout (DKO) mouse model harboring muscle-specific deficits in acetyl-CoA buffering and lysine deacetylation, due to genetic ablation of carnitine acetyltransferase and Sirtuin 3, respectively. DKO
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