16012-55-8
16012-55-8
Chemical Structure
β-N-methylamino-L-alanine hydrochloride
Synonym(s): BMAA hydrochloride
- CAS No.: 16012-55-8
- Formula:C4H11ClN2O2
- Molecular Weight:154.60
IUPAC Name: (S)-2-amino-3-(methylamino)propanoic acid hydrochloride
InChIKey: VDXYGASOGLSIDM-DFWYDOINSA-N
SMILES: N[C@@H](CNC)C(O)=O.[H]Cl
Biological Activity: β-N-methylamino-L-alanine hydrochloride (BMAA hydrochloride) is a neurotoxin produced by cyanobacteria. β-N-methylamino-L-alanine hydrochloride activates mGluR3 and inhibits PKC. β-N-methylamino-L-alanine hydrochloride can be used in the research of neurodegenerative diseases and immune diseases[1][2][3][4][5][6][7][8][9][10][11][12][13].
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β-N-methylamino-L-alanine hydrochloride | 98.0% | β-N-methylamino-L-alanine hydrochloride (BMAA hydrochloride) is a neurotoxin produced by cyanobacteria. β-N-methylamino-L-alanine hydrochloride activates mGluR3 and inhibits PKC. β-N-methylamino-L-alanine hydrochloride can be used in the research of neurodegenerative diseases and immune diseases. | ||||||||||||||||||||
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β-N-methylamino-L-alanine hydrochloride (Standard) | ≥98% | 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. 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. | ||||||||||||||||||||
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References
- [1]. Caller T, et, al. The Potential Role of BMAA in Neurodegeneration. Neurotox Res. 2018 Jan; 33(1): 222-226. [Content Brief]
- [2]. Cox PA, et, al. BMAA and Neurodegenerative Illness. Neurotox Res. 2018 Jan; 33(1): 178-183. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [8]. Santucci S, et al. beta-N-methylamino-L-alanine induced in vivo retinal cell death. J Neurochem. 2009 May;109(3):819-25. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
