Drug intelligence / Profile preview

beta-N-methylamino-L-alanine

Development stage
Preclinical
Modality
Small Molecules
Administration
Oral
01

Overview

beta-N-methylamino-L-alanine (BMAA) is a non-proteinogenic amino acid produced by cyanobacteria and some other microorganisms. It is a neurotoxin implicated in the etiology of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and Parkinsonism-dementia complex (ALS-PDC), particularly in populations with dietary exposure to BMAA through cycad seeds or contaminated aquatic food sources. Mechanistically, BMAA acts as an agonist at multiple glutamate receptors—including NMDA-type and AMPA/kainate receptors—leading to excitotoxicity. It can also induce oxidative stress via effects on the cystine/glutamate antiporter system xc(-), increasing extracellular glutamate levels. Additionally, BMAA disrupts mitochondrial function and calcium homeostasis in neurons, contributing to neuronal injury[1][2][4][5][6]. Its role as a causative agent in human disease remains under investigation.

Other names
β-Methylamino-L-alaninebeta-N-methylamino-L-alanine hydrochloride
02

Targets

NeuraminidaseiGluR (Ionotropic receptor 76b (Ir76b))SLC7A11 (Cystine-Glutamate Antiporter)NMDAR (Glutamate receptor ionotropic, NMDA)aaRS (Aminoacyl-tRNA synthetase family)mGluR (Metabotropic glutamate receptors)

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