A synthetic analog of Joro spider toxin
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NASPM (hydrochloride)

Item No. 18453

Product Insert (PDF)Safety Data Sheet (SDS) (PDF)
Technical Information
Formal Name
N-(3-((4-((3-aminopropyl)amino)butyl)amino)propyl)-2-(naphthalen-1-yl)acetamide, trihydrochloride
CAS Number
1049731-36-3
Synonyms
  • 1-Naphthylacetyl spermine
Molecular Formula
C22H34N4O • 3HCl
Formula Weight
479.9
Purity
≥95%
Formulation
A crystalline solid
Solubility(Learn about Variance in Solubility)
DMSO: 1.7 mg/mLPBS (pH 7.2): 10 mg/mL
λmax
224, 280 nm
SMILES
O=C(NCCCNCCCCNCCCN)CC1=CC=CC2=C1C=CC=C2.Cl.Cl.Cl
InChi Code
InChI=1S/C22H34N4O.3ClH/c23-12-6-15-24-13-3-4-14-25-16-7-17-26-22(27)18-20-10-5-9-19-8-1-2-11-21(19)20;;;/h1-2,5,8-11,24-25H,3-4,6-7,12-18,23H2,(H,26,27);3*1H
InChi Key
JNEOJAUJWOPWJS-UHFFFAOYSA-N
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    1 mg

    $28

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    5 mg

    $104

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    10 mg

    $149

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    25 mg

    $203

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    Product Description

    NASPM is a synthetic analog of Joro spider toxin that blocks GluR2-lacking, Ca2+-permeable AMPA receptors. The blocking effect of NASPM on these receptors is use and voltage-dependent. At -60 mV, NASPM can suppress current responses in kainate-induced type II neurons (which are typified by strong inward rectification and high permeability to Ca2+) with an IC50 value of 0.33 µM.1 However, at +40 mV, NASPM does not affect Ca2+-permeable AMPA receptors.1 NASPM has been shown to protect against ischemia-induced neuronal cell death by preventing influx of toxic levels of Ca2+ into injured neurons.2 This compound can be used to study the role of GluR2 subunits in calcium permeability of AMPA receptors.3,2

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Koike, M., Iino, M., and Ozawa, S. Blocking effect of 1-naphthyl acetyl spermine on Ca(2+)-permeable AMPA receptors in cultured rat hippocampal neurons. Neurosci. Res. 29(1), 27-36 (1997).

    2. Oguro, K., Oguro, N., Kojima, T., et al. Knockdown of AMPA receptor GluR2 expression causes delayed neurodegeneration and increases damage by sublethal ischemia in hippocampal CA1 and CA3 neurons. J. Neurosci. 19(21), 9218-9227 (1999).

    3. Dong, L.D., Gao, F., Wang, X.H., et al. GluA2 trafficking is involved in apoptosis of retinal ganglion cells induced by activation of EphB/EphrinB reverse signaling in a rat chronic ocular hypertension model. J. Neurosci. 35(13), 5409-5421 (2015).