NG-amino-L-Arginine (hydrochloride)
mRNA synthesis
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Inhibitor Cocktails
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
NG-amino-L-arginine, a novel structural analog of L-arginine, is an inhibitor of nitric oxide synthase (NOS) [1,2]. Nitric oxide synthases (NOSs) have been involved in catalyzing the production of nitric oxide (NO) from L-arginine. As an important cellular signaling molecule, NO has been implicated in modulating vascular tone, airway tone, insulinsecretion, and peristalsis. It has also been shown that NO is involved in angiogenesis and neural development and can function as a retrograde neurotransmitter [3].
In vitro: NG-amino-L-arginine potently and stereoselectively induced endothelium-dependent contraction. NG-amino-L-arginine caused concentration-dependent, competitive, and stereoselective antagonism of acetylcholine-elicited relaxation and cyclic GMP accumulation. NG-Amino-L-arginine was 100- to 300- fold more potent than NG-methyl-L-arginine [1]. NG-amino-L-arginine (100 μM) almost abolished endothelium-dependent relaxation induced by acetylcholine, but was rapidly restored by addition of 300 μM L-arginine. The maximal response to acetylcholine was inhibited by NG-amino-L-arginine in excess of 1 μM and was abolished by concentrations in the range of l0-30 μM [1]. NG-Amino-L-arginine inactivated the citrulline-forming activity of the nNOS, iNOS, and eNOS isoforms with the maximal inactivation rates of 0.35, 0.26, and 0.53 min-1 and Ki values of 0.3, 3, and 2.5 μM, respectively [2].
In vivo: In awake animal models of sepsis, treatment with NG-amino-L-arginine showed higher systemic and pulmonary vascular resistance indices and decreased heart rates, cardiac indices, oxygen delivery indices, and oxygen consumption indices when compared with controls [4]. NG-amino-L-arginine increased mortality rates after endotoxin challenge [4].
References:
[1] Fukuto J M, Wood K S, Byrns R E, et al. NG-amino-L-arginine: a new potent antagonist of L-arginine-mediated endothelium-dependent relaxation[J]. Biochemical and biophysical research communications, 1990, 168(2): 458-465.
[2] Wolff D J, Lubeskie A. Inactivation of Nitric Oxide Synthase Isoforms by Diaminoguanidine andN G-Amino-L-arginine[J]. Archives of biochemistry and biophysics, 1996, 325(2): 227-234.
[3] Frstermann U, Closs E I, Pollock J S, et al. Nitric oxide synthase isozymes. Characterization, purification, molecular cloning, and functions[J]. Hypertension, 1994, 23(6 Pt 2): 1121-1131.
[4] Cobb J P, Natanson C, Hoffman W D, et al. N omega-amino-L-arginine, an inhibitor of nitric oxide synthase, raises vascular resistance but increases mortality rates in awake canines challenged with endotoxin[J]. Journal of Experimental Medicine, 1992, 176(4): 1175-1182.
Physical Appearance | A crystalline solid |
Storage | Store at -20°C |
M.Wt | 225.7 |
Cas No. | 1031799-40-2 |
Formula | C6H15N5O2·HCl |
Solubility | ≤10mg/ml in PBS(pH7.2) |
Chemical Name | N5-(hydrazinyliminomethyl)-L-ornithine, monohydrochloride |
SDF | Download SDF |
Canonical SMILES | NNC(NCCC[C@H](N)C(O)=O)=N.Cl |
运输条件 | 蓝冰运输或根据您的需求运输。 |
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