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L-BMAA hydrochloride

Neurotoxic amino acid CAS# 16012-55-8

L-BMAA hydrochloride

2D Structure

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3D structure

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L-BMAA hydrochloride

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Chemical Properties of L-BMAA hydrochloride

Cas No. 16012-55-8 SDF Download SDF
PubChem ID 51358333 Appearance Powder
Formula C4H11ClN2O2 M.Wt 154.6
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 60 mM in water
Chemical Name (2S)-2-amino-3-(methylamino)propanoic acid;hydrochloride
SMILES CNCC(C(=O)O)N.Cl
Standard InChIKey VDXYGASOGLSIDM-DFWYDOINSA-N
Standard InChI InChI=1S/C4H10N2O2.ClH/c1-6-2-3(5)4(7)8;/h3,6H,2,5H2,1H3,(H,7,8);1H/t3-;/m0./s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of L-BMAA hydrochloride

DescriptionNeurotoxic glutamate agonist originally isolated from Cycas circinalis. Implicated in the pathogenesis of amyotrophic lateral sclerosis-Parkinsonism-dementia complex of Guam (Guam ALS-PD).

L-BMAA hydrochloride Dilution Calculator

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L-BMAA hydrochloride Molarity Calculator

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Preparing Stock Solutions of L-BMAA hydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 6.4683 mL 32.3415 mL 64.6831 mL 129.3661 mL 161.7076 mL
5 mM 1.2937 mL 6.4683 mL 12.9366 mL 25.8732 mL 32.3415 mL
10 mM 0.6468 mL 3.2342 mL 6.4683 mL 12.9366 mL 16.1708 mL
50 mM 0.1294 mL 0.6468 mL 1.2937 mL 2.5873 mL 3.2342 mL
100 mM 0.0647 mL 0.3234 mL 0.6468 mL 1.2937 mL 1.6171 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on L-BMAA hydrochloride

Neurotoxicity of beta-N-methylamino-L-alanine (BMAA) and beta-N-oxalylamino-L-alanine (BOAA) on cultured cortical neurons.[Pubmed:2551452]

Brain Res. 1989 Sep 11;497(1):64-71.

Recent studies have implicated the ingestion of the structurally related plant excitotoxins, beta-N-methylamino-L-alanine (BMAA), and beta-N-oxalylamino-L-alanine (BOAA), in the pathogenesis of two human motor system diseases, the amyotrophic lateral sclerosis-Parkinsonism-dementia complex of Guam (Guam ALS-PD), and lathyrism, respectively. We have investigated the toxicity of these amino acids on cultured mouse cortical neurons in the presence of physiological concentrations of bicarbonate (a required toxic cofactor for BMAA neurotoxicity). A 24 h exposure to 10 microM - 3 mM BMAA, or to 300 nM - 100 microM BOAA, induced, concentration-dependent neuronal degeneration without glial damage; the neurotoxic EC50 for BMAA was about 1 mM, and the EC50 for BOAA was about 20 microM. At high concentrations, both compounds destroyed essentially the entire neuronal population. Neurotoxicity also depended on exposure duration, with reduced injury at an exposure time of 1 h, and increased injury at an exposure time of 3 days. Despite the fact that ingestion of BMAA and BOAA both lead to motor system damage, previous studies have suggested that the two excitotoxins act primarily on different glutamate receptor subtypes: BMAA on N-methyl-D-aspartate (NMDA) receptors, and BOAA on non-NMDA receptors. Consistent with these studies, the neurotoxicity of high concentrations of BMAA was substantially attenuated by 1 mM D-amino-5-phosphonovalerate (D-APV), whereas BOAA neurotoxicity was less sensitive to D-APV but was attenuated by 2 mM kynurenate.(ABSTRACT TRUNCATED AT 250 WORDS)

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