A3133
Nα-Acetyl-L-arginine
≥98% (TLC), suitable for deacetylase assays
Synonym(s):
N2-acetyl-L-alanine
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About This Item
Empirical Formula (Hill Notation):
C8H16N4O3
CAS Number:
Molecular Weight:
216.24
UNSPSC Code:
12352209
eCl@ss:
32160406
PubChem Substance ID:
NACRES:
NA.26
EC Number:
205-846-6
MDL number:
Product Name
Nα-Acetyl-L-arginine,
assay
≥98% (TLC)
Quality Level
form
powder
technique(s)
deacetylase assay: suitable
color
colorless to white
storage temp.
−20°C
SMILES string
NC(NCCC[C@H](NC(C)=O)C(O)=O)=N
InChI
1S/C8H16N4O3/c1-5(13)12-6(7(14)15)3-2-4-11-8(9)10/h6H,2-4H2,1H3,(H,12,13)(H,14,15)(H4,9,10,11)/t6-/m0/s1
InChI key
SNEIUMQYRCDYCH-LURJTMIESA-N
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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T W Lo et al.
The Journal of biological chemistry, 269(51), 32299-32305 (1994-12-23)
The physiological alpha-oxoaldehyde methylglyoxal binds and modifies arginine, lysine, and cysteine residues in proteins. The kinetics and mechanism of these reactions were investigated with N alpha-acetylamino acids and bovine serum albumin at pH 7.4 and 37 degrees C. The reaction
Daniela Balz et al.
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 21(2), 75-82 (2003-03-05)
Tissue accumulation of arginine (Arg), N-acetylarginine (NA), argininic acid (AA) and homoarginine (HA) occurs in hyperargininemia, an inborn error of the urea cycle. In the present study, we investigated the in vitro effects of Arg, NA, AA and HA on
Binding of methylglyoxal to albumin and formation of fluorescent adducts. Inhibition by arginine, N-alpha-acetylarginine and aminoguanidine.
T Selwood et al.
Biochemical Society transactions, 21(2), 170S-170S (1993-05-01)
A T Wyse et al.
Brain research, 923(1-2), 50-57 (2001-12-18)
Hyperargininemia is a metabolic disorder biochemically characterized by tissue accumulation of arginine and other guanidino compounds. Convulsions, lethargy and psychomotor delay or cognitive deterioration are predominant clinical features of this disease. Although neurologic symptoms predominate in this disorder, their pathophysiology
P P De Deyn et al.
Nephron, 69(4), 411-417 (1995-01-01)
Serum levels of twelve guanidino compounds (GCs) and nerve conduction velocities were determined in a dialyzed renal insufficient pediatric population. Two dialytic groups were considered: one subjected to hemodialysis (HD, 11 patients) and one subjected to continuous cycle peritoneal dialysis
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