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


CAS No. : 16012-55-8

(Synonyms: BMAA (hydrochloride))

16012-55-8
Price and Availability of CAS No. : 16012-55-8
Size Price Stock
100mg $150 In-stock
250mg $180 In-stock
1g $400 In-stock
5 g Get quote
10 g Get quote
We match the lowest price on market.

We offer a substantial discount on larger orders, please inquire via [email protected]

or Fax: (86)21-58955996

Inquiry for price and availability only. Please place your order via our email or fax.

Cat. No. : HY-W015546
M.Wt: 154.60
Formula: C4H11ClN2O2
Purity: >98 %
Solubility: H2O : 31.25 mg/mL (ultrasonic;warming;heat to 60°C)
Introduction of 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]. 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].

Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

β-N-methylamino-L-alanine hydrochloride can be used to induce amyotrophic lateral sclerosis (ALS) models[6].

1. Induction of amyotrophic lateral sclerosis[6]
Background
β-N-methylamino-L-alanine hydrochloride activates NMDA receptors and metabolite glutamate receptors (mGluR1/5) by mimicking glutamate, leading to intracellular calcium overload, inducing oxidative stress, damaging organelles such as the endoplasmic reticulum and mitochondria, and ultimately causing neuronal degeneration and excitatory necrosis.
Specific Modeling Methods
1. Rats: Male Wistar rats
Administration: 200-350 mg/kg • i.p. • once a day for 5 days
Note
(1) Should begin from weaning/21 days after birth to avoid interference during the critical period of newborn rats brain development
Modeling Indicators
Neurological Function Score: 0 points: The entire sole of the hind limbs touches the ground when walking. When the tail is suspended, the hind limbs are in a T-shape with coordinated kicking movements, and there is a resistant response to stimulation from the tail; 1-3 points: When the tail is suspended, it cannot make a T-shaped movement with its hind legs, resulting in uncoordinated kicking; 4 points: When walking, they do not place the entire sole of their hind feet on the ground; they walk on their toes; 5 points: When the tail is suspended, the hind legs will extend backward. When pulled from the tail, the hind legs will often separate from the body and gradually lose their resistance; 6 points: When turning, the hind legs remain under the body, the posture adjustment is slow, and there are uncoordinated kicks when the tail is suspended; 7 points: Begin to walk sideways, the resistance disappears, and their hind limbs separate from their body. 8 points: When walking, the hind legs slip; when the tail is suspended, the hind legs are brought together, and the hind legs are clearly separated from the body; 9 points: Loss of coordination while walking, with a noticeable tendency to walk sideways; 10 points: Complete loss of hind limb motor function, muscle spasms, and whole-body tremors. The scores increased significantly after modeling, manifested as hind limb coordination disorder, irregular kicking, decreased muscle strength, and in severe cases, loss of hind limb control (score ≥ 7 points).
Histological Analysis: The endoplasmic reticulum of lumbar spinal cord motor neurons is fragmented, ribosomes dissociate, and mitochondria swell, vacuolate, or even degenerate; oligodendrocytes exhibit apoptosis-characteristic nuclear morphology.
Molecular changes: Increased caspase-3 expression in the perinuclear region of motor neurons; elevated total protein and phosphorylated form (P-Ser9-GSK3β) of GSK3β in the lumbar spinal cord and motor cortex, and increased content of high molecular weight TDP-43 aggregates; decreased NAA content, and significantly reduced NAA/Cr, NAA/Cho, and NAA/(Cho+Cr) ratios.

Your information is safe with us.

Our product is for R&D purpose only.