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    (-)-Huperzine A (HupA)
    (-)-Huperzine A (HupA)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1082
    CAS #: 102518-79-6Purity ≥98%

    Description: (-)-Huperzine A (Hup A; Selagine; (-)-Selagine) is a naturally occurring, highly specific and reversible inhibitor of acetylcholinesterase (AChE) with neuroprotective activity. It inhibits AChE with Ki of 7 nM, and exhibits 200-fold more selectivity for G4 AChE over G1 AChE. Chemically, (-)-Huperzine A is an active Lycopodium alkaloid isolated from traditional Chinese herb. It also acts as an NMDA receptor antagonist. (-)-Huperzine A has been investigated as a possible treatment for diseases characterized by neurodegeneration-particularly Alzheimer's disease. Huperzine A is also marketed as a dietary supplement with claims made for its ability to improve memory and mental function.

    References: Eur J Pharmacol. 2002 Nov 29;455(2-3):101-7; Trends Pharmacol Sci. 2006 Dec;27(12):619-25.

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    Molecular Weight (MW)242.32
    CAS No.102518-79-6
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO:<1 mg/mL
    Water: <1 mg/mL
    Ethanol:<1 mg/mL
    Solubility (In vivo)30% propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL
    SynonymsHup A; Huperzine A; Selagine; (-)-huperzine A; (-)-Selagine.

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    In Vitro

    In vitro activity: (-)-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, β-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.

    In Vivo(-)-Huperzine A can ameliorate the learning and memory deficiency in animal models and AD patients. Its potentially beneficial actions include modification of β-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.
    Animal modelMale Sprague-Dawley rats
    Formulation & DosageDissolved in saline; 0.1mg/kg; oral gavage

    Eur J Pharmacol. 2002 Nov 29;455(2-3):101-7; Trends Pharmacol Sci. 2006 Dec;27(12):619-25; Acta Pharmacol Sin. 2006 Jan;27(1):1-26.

    These protocols are for reference only. InvivoChem does not independently validate these methods.

    (-)-Huperzine A (HupA)

    Effects of the co-administration of huperzine A (0.2, 0.3 and 0.4 mg/kg) and morphine on locomotor activity in the development phase of behavioral sensitization. Exp Ther Med. 2017 Apr; 13(4): 1584–1591.

    (-)-Huperzine A (HupA)

    Examination of the state-dependency hypothesis. Exp Ther Med. 2017 Apr; 13(4): 1584–1591.
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    Effects of huperzine A on the expression of morphine sensitization in the Sal+Mor group. Exp Ther Med. 2017 Apr; 13(4): 1584–1591.


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