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    Gabapentin
    Gabapentin

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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 #: V1286
    CAS #: 60142-96-3Purity ≥98%

    Description: Gabapentin HCl (Neurontin; Aclonium; Convalis; Gabapentin Stada), the hydrochloride salt of gabapentin which is a GABA analog, is an orally bioavailable medication that was approved for use in the treatment of seizures and neuropathic pain. Gabapentin is structurally similar to GABA and is reported in various research studies to be able to increase GABA concentrations in the brain. 

    References: J Pharmacol Exp Ther. 1999 Mar;288(3):1026-30; Br J Pharmacol. 2002 Jan;135(1):257-65.

    Related CAS #: 60142-95-2 (HCl)   60142-96-3 (free base)

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    Molecular Weight (MW)171.24
    FormulaC9H17NO2
    CAS No.60142-96-3
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 34 mg/mL (198.6 mM)
    Water:<1 mg/mL
    Ethanol: <1 mg/mL
    Other info

    Chemical Name: 2-[1-(aminomethyl)cyclohexyl]acetic acid

    SMILES Code: NCC1(CCCCC1)CC(=O)O           

    Synonyms

    Neurontin; Gabapentin; Neurontin; Gabapentine; Gabapentin HCl; Gabapentin hydrochloride; Aclonium; Convalis; gabapentin; Gabapentin Hexal; Gabapentin Stada


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    In Vitro

    In vitro activity: Gabapentin produces concentration-dependent inhibitions of the K(+)-induced [Ca(2+)](i) increase in fura-2-loaded human neocortical synaptosomes with IC50 of 17 mM and maximal inhibition of 37%. Gabapentin may bind to the Ca(2+) channel alpha 2 delta subunit to selectively attenuate depolarization-induced Ca(2+) influx of presynaptic P/Q-type Ca(2+) channels; this results in decreased glutamate/aspartate release from excitatory amino acid nerve terminals leading to a reduced activation of AMPA heteroreceptors on noradrenergic nerve terminals. Gabapentin produces alterations in the cytosolic and extracellular concentrations of several amino acids, including L-leucine, L-valine and L-phenylalanine, in rat cortical astrocytes and synaptosomes, effects that are postulated to be of pharmacological significance. Gabapentin reduces potassium-evoked calcium influx via voltage-gated calcium channels in a mouse pituitary cell line that constitutively expresses GABAB receptors comprising the functional gb1a–gb2 subunit heterodimer. Gabapentin can increase N-methyl-d-aspartate (NMDA)-evoked currents in GABA-positive rat dorsal horn neurones in the presence of protein kinase C, possibly by increasing the glycine sensitivity of the NMDA receptor complex. Gabapentin produces a delayed allosteric enhancement of an unspecified voltage-activated potassium current in rat dorsal root ganglion neurons.

    In VivoGabapentin dose-dependently (10-100 mg/kg, p.o.) blocks both static and dynamic allodynia in the rats.
    Animal modelRats
    Formulation & Dosage10-100 mg/kg; p.o.
    References

    Neuropharmacology. 2002 Feb;42(2):229-36; Curr Opin Pharmacol. 2006 Feb;6(1):108-13.


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

    Gabapentin HCI

    (a) Time-course showing gabapentin inhibition of peak IBa. (b) Whole-cell current trace of peak HVA IBa activated under control conditions (con) and following a 10 min application of gabapentin (GBP). (c) Dose-response of GBP-mediated inhibition of peak HVA IBa. Br J Pharmacol. 2002 Jan;135(1):257-65.


    Gabapentin HCI

    Gabapentin inhibited Ca2+ influx into cultured DRG as measured using fura-2 fluorescence imaging. Br J Pharmacol. 2002 Jan;135(1):257-65.

    Gabapentin HCI

    (a) Trace showing changes in fluorescence ratio produced by changes in KCl in imaging experiments. (b) Graph showing linear correlation between change in fluorescence ratio and membrane potential at varying concentrations of K+.



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