description
13C-depleted
Quality Level
isotopic purity
99.9 atom % 12C
optical activity
[α]25/D +14.5°, c = 2 in 1 M HCl
availability
available only in Japan
mp
314.5 °C (dec.) (lit.)
mass shift
depleted
SMILES string
[12CH3][12C@H](N)[12C](O)=O
InChI
1S/C3H7NO2/c1-2(4)3(5)6/h2H,4H2,1H3,(H,5,6)/t2-/m0/s1/i1+0,2+0,3+0
InChI key
QNAYBMKLOCPYGJ-BWIFZRRMSA-N
Biochem/physiol Actions
L-Alanine is a nonessential amino acid, which is highly concentrated in muscle. It is a key player in the Glucose-Alanine cycle, which enables the removal of pyruvate and glutamate from muscle to the liver. Once in the liver, glucose is regenerated from pyruvate and returned to the muscle while glutamate ultimately participates in the urea cycle to form urea. The Glucose-Alanine cycle aides to conserve ATP in muscle for muscle contraction, while the energy burden of gluconeogenesis is imposed upon the liver. Alanine inhibits pyruvate kinase to regulate gluconeogenesis and glycolysis in order to maintain glucose homeostasis during starvation. Alanine prevents hepatic autophagy. Alanine formation is a result of transamination of glutamate and pyruvate.
Packaging
This product may be available from bulk stock and can be packaged on demand. For information on pricing, availability and packaging, please contact Stable Isotopes Customer Service.
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
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Alanine and glutamine synthesis and release from skeletal muscle. II. The precursor role of amino acids in alanine and glutamine synthesis.
Garber A J, et al.
The Journal of Biological Chemistry, 251(3), 836-843 (1976)
Muscle alanine synthesis and hepatic gluconeogenesis
Snell K
Biochemical Society Transactions, 8(2), 205-213 (1980)
Lillian L Siu et al.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 31(19), 2477-2484 (2013-05-22)
The antiepidermal growth factor receptor monoclonal antibody cetuximab has improved survival in patients with metastatic, chemotherapy-refractory, wild-type K-RAS colorectal cancer. The addition of brivanib, a tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor and fibroblast growth factor receptor, to