β-N-methylamino-L-alanine (hydrochloride) (Standard)

Clenbuterol (Standard) is the analytical standard of Clenbuterol. This product is intended for research and analytical applications. Clenbuterol (NAB-365) is a β2-adrenergic receptor agonist with an EC50 of 31.9 nM[1]. Clenbuterol is a very potent inhibitor of the lipopolysaccharide (LPS) -induced release of TNF-α and IL-1β. Clenbuterol can inhibit the inflammatory process. Clenbuterol is a bronchodilator[2].

Product Specifications

CAS Number

[16012-55-8]

Product Name Alternative

BMAA (hydrochloride) (Standard)

UNSPSC

12352211

Target

Bacterial; mGluR; PKC; Reference Standards

Related Pathways

Anti-infection; Epigenetics; GPCR/G Protein; Neuronal Signaling; Others; TGF-beta/Smad

Field of Research

Inflammation/Immunology; Neurological Disease

Smiles

N[C@@H](CNC)C(O)=O.[H]Cl

Molecular Formula

C4H11ClN2O2

Molecular Weight

154.60

References & Citations

[1]Caller T, et, al. The Potential Role of BMAA in Neurodegeneration. Neurotox Res. 2018 Jan; 33 (1) : 222-226.|[2]Cox PA, et, al. BMAA and Neurodegenerative Illness. Neurotox Res. 2018 Jan; 33 (1) : 178-183.|[3]Okamoto S, et, al. β-N-methylamino-L-alanine (BMAA) suppresses cell cycle progression of non-neuronal cells. Sci Rep. 2018 Dec 20; 8 (1) : 17995.|[4]Pierozan P, et al. The environmental neurotoxin β-N-methylamino-L-alanine inhibits melatonin synthesis in primary pinealocytes and a rat model. J Pineal Res. 2018 Aug;65 (1) :e12488. |[5]van Onselen R, et al. Evaluating amino acids as protectants against β-N-methylamino-l-alanine-induced developmental neurotoxicity in a rat model. Toxicol Appl Pharmacol. 2020 Sep 15;403:115140.|[6]de Munck E, et al. β-N-methylamino-l-alanine causes neurological and pathological phenotypes mimicking Amyotrophic Lateral Sclerosis (ALS) : the first step towards an experimental model for sporadic ALS. Environ Toxicol Pharmacol. 2013 Sep;36 (2) :243-255.|[7]van Onselen R, et al. β-N-Methylamino-L-Alanine Toxicity in PC12: Excitotoxicity vs. Misincorporation. Neurotox Res. 2018 Jan;33 (1) :15-23.|[8]Santucci S, et al. beta-N-methylamino-L-alanine induced in vivo retinal cell death. J Neurochem. 2009 May;109 (3) :819-25.|[9]Okamoto S, et al. β-N-methylamino-L-alanine (BMAA) suppresses cell cycle progression of non-neuronal cells. Sci Rep. 2018 Dec 20;8 (1) :17995.|[10]Engskog MK, et al. β-N-Methylamino-L-alanine (BMAA) perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells as determined by metabolic profiling. Amino Acids. 2017 May;49 (5) :905-919. |[11]Sieroslawska A, et al. Assessment of the cytotoxic impact of cyanotoxin beta-N-methylamino-L-alanine on a fish immune cell line. Aquat Toxicol. 2019 Jul;212:214-221.|[12]de Munck E, et al. Effect of β-N-methylamino-L-alanine on oxidative stress of liver and kidney in rat. Environ Toxicol Pharmacol. 2013 Mar;35 (2) :193-9. |[13]Engskog MK, et al. The cyanobacterial amino acid β-N-methylamino-l-alanine perturbs the intermediary metabolism in neonatal rats. Toxicology. 2013 Oct 4;312:6-11.