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MedChemExpress - Model ß-N-methylamino-L-alanine hydrochloride -16012-55-8
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].MCE products for research use only. We do not sell to patients.
β-N-methylamino-L-alanine hydrochloride
MCE China:β-N-methylamino-L-alanine hydrochloride
Brand:MedChemExpress (MCE)
Cat. No.HY-W015546
CAS:16012-55-8
Synonyms:BMAA hydrochloride
Purity:98.0%
Storage:-20°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Shipping:Room temperature in continental US; may vary elsewhere.
Description: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.
In Vitro:β-N-methylamino-L-alanine hydrochloride (0.05-3 mM, 24 h) inhibits melatonin synthesis by mGluR3 activation and PKC inhibitions in primary pinealocytes[4]. β-N-Methylamino-L-Alanine (500 μM, 21 days) hydrochloride shows toxicity in PC12 cells[7]. β-N-methylamino-L-alanine (1-3 mM, 48 h) hydrochloride suppresses cell cycle progression at the G1/S checkpoint and proliferation in non-neuronal cells NIH3T3[9]. β-N-methylamino-L-alanine (50-1000 µM, 24 h) hydrochloride perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells[10]. β-N-methylamino-L-alanine (1.5-2.0 mM, 24 h) hydrochloride alters morphology, ATP levels and reduces proliferation of fish immune cells (CLC)[11].
In Vivo:β-N-methylamino-L-alanine (460 mg/kg, s.c., daily, 2 weeks) hydrochloride inhibits melatonin synthesis in a Wistar rat model[4]. β-N-methylamino-L-alanine (BMAA-HCl, 400 mg kg, s.c.) hydrochloride induces developmental neurotoxicity in a rat model[5]. β-N-methylamino-L-alanine (100-350 mg/kg, i.p., 5 consecutive days) hydrochloride causes neurological and pathological phenotypes mimicking Amyotrophic Lateral Sclerosis (ALS) in male rats[6]. β-N-methylamino-L-alanine (5-10 nmol, intravitreal injections) hydrochloride induces in vivo retinal cell death in mice[8]. β-N-methylamino-L-alanine (250 mg/kg, i.p., 5 consecutive days) hydrochloride produces oxidative damage in liver and kidney of rats, with the significant increase of lipid peroxidation and high catalase activity[12]. β-N-methylamino-L-alanine (40-460 mg/kg, s.c., 2 days) hydrochloride perturbs the intermediary metabolism in neonatal rats, with impairments in learning and memory function[13].
IC50 & Target:mGluR3
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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]
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