(-)-Huperzine A (Huperzine A) is an alkaloid isolated from a Chinese club moss, with neuroprotective activity. (-)-Huperzine A is a potent, highly specific, reversible and blood-brain barrier penetrant inhibitor of acetylcholinesterase (AChE), with an IC50 of 82 nM. (-)-Huperzine A also is non-competitive antagonist of N-methyl-D-aspartate glutamate (NMDA) receptor. (-)-Huperzine A is developed for the research of neurodegenerative diseases, including Alzheimer’s disease.
CAS Number: 102518-79-6
Molecular Weight: 242.32
Chemical Name: (1R, 9R, 13Z)-1-amino-13-ethylidene-11-methyl-6-azatricyclo[188.8.131.52, ]trideca-2(7), 3, 10-trien-5-one
Appearance: Solid Power
Purity: ≥98% (or refer to the Certificate of Analysis)
Solubility: DMSO: 0.66 mg/mL(2.72 mM).
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis
Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.
Shelf Life: ≥360 days if stored properly.
Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.
Drug Formulation: To be determined
HS Tariff Code: 382200
How to use
(-)-Huperzine A is a novel alkaloid isolated from the Chinese herb Huperzia serrata. (-)-Huperzine A preferentially inhibits tetrameric AChE (G4 form). (-)-Huperzine A is more potent than tacrine, physostigmine, galanthamine, and rivastigmine with respect to inhibition of AChE activity, whereas HupA is the least potent BuChE inhibitor among the inhibitors. (-)-Huperzine A possesses the ability to protect cells against hydrogen peroxide, Î²-amyloid protein, glutamate, ischemia and staurosporine-induced cytotoxicity and apoptosis. These protective effects are related to its ability to attenuate oxidative stress, regulate the expression of apoptotic proteins Bcl-2, Bax, P53, and caspase-3, protect mitochondria, upregulate nerve growth factor and its receptors, and interfere with amyloid precursor protein metabolism.
(-)-Huperzine A can ameliorate the learning and memory deficiency in animal models and AD patients. Its potentially beneficial actions include modification of Î²-amyloid peptide processing, reduction of oxidative stress, neuronal protection against apoptosis, and regulation of the expression and secretion of nerve growth factor (NGF) and NGF signaling. (-)-Huperzine A significantly inhibits AChE activity in the cortex, hippocampus, striatum, medial septum, medulla oblongata, cerebellum, and hypothalamus of rats that are killed 30 min following the administration of (-)-Huperzine A at several dose levels compared with the saline control.
- Wang R, et al. Acta Pharmacol Sin, 2006, 27(1), 1-26.
- Zhang HY, et al. Trends Pharmacol Sci, 2006, 27(12), 619-625.
- Zhao Q, et al. Eur J Pharmacol, 2002, 455(2-3), 101-107.
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