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    Lamotrigine (BW430C; LTG)
    Lamotrigine (BW430C; LTG)

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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 #: V0998
    CAS #: 84057-84-1Purity ≥98%

    Description: Lamotrigine (Lamictal, BW 430C; BW430C; Crisomet, Lamictin, Lamitor), an approved anti-convulsant drug used in the treatment of epilepsy and bipolar disorder, is an inhibitor of 5-HT with IC50 of 240 μM and 474 μM in human platelets and rat brain synaptosomes. Lamotrigine is also a sodium channel blocker. 

    References: Drugs. 1993 Jul;46(1):152-76; Epilepsia. 1986 Sep-Oct;27(5):483-9.

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    Molecular Weight (MW)256.09 
    CAS No.84057-84-1 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 10 mg/mL (39.0 mM)
    Water: <1 mg/mL
    Ethanol: 3 mg/mL (11.7 mM) 
    Solubility (In vivo)0.5% methylcellulose: 30 mg/mL  
    SynonymsBW-430C; Lamotrigine, Lamictal, BW 430C; BW430C; Crisomet, Lamictin, Lamitor

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    In Vitro

    In vitro activity: Lamotrigine stabilises presynaptic neuronal membranes by blockade of voltage-dependent sodium channels, thus preventing the release of excitatory neurotransmitters, particularly glutamate and aspartate. In rat cerebral cortex tissue incubated with veratrine 10 mg/L, lamotrigine is twice as potent in inhibiting the release of glutamate and aspartate (ED 50 = 5.38 mg/L for each) than the release of GABA (ED50 = 11.2 mg/L), and is much less potent in inhibiting acetylcholine release (ED50 = 25.6 mg/L) when cortical slices is exposed to veratrine 75 mg/L. Basal glutamate release is unaffected. Lamotrigine inhibits high-frequency sustained repetitive firing of sodium-dependent action potentials, indicating a direct effect on voltage-activated sodium channels. Lamotrigine does not induce PCP-like central nervous system (CNS) effects, does not act by direct inhibition at the NMDA receptor, and would be expected to be devoid of the undesirable effects associated with NMDA blockade.

    In VivoIn mice and rats, lamotrigine prevents MES- and pentetrazol-induced hindlimb extension, suggesting an antiepileptic profile in animals. These effects peak 1 hour after lamotrigine administration and persist for more than 24 hours. Lamotrigine is active in the electrically evoked EEG after-discharge test, which is thought to indicate activity against both simple and complex partial seizures. After-discharge duration is reduced dose-dependently by lamotrigine in rats at intravenous doses >5 mg/kg. 
    Animal modelDog/Rat 
    Formulation & DosageDissolved in 0.25% methylcellulose solution; 4.5 (dogs) and 11.7 (rats) mg /kg; i.v. injection

    Drugs. 1993 Jul;46(1):152-76; Epilepsia. 1986 Sep-Oct;27(5):483-9. 

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

    Concentration-dependent inhibition of lamotrigine on the 5-HT3 receptor currents. Korean J Physiol Pharmacol. 2017 Mar; 21(2): 169–177.
    Competitive inhibition of lamotrigine on the 5-HT3 receptor currents. Korean J Physiol Pharmacol. 2017 Mar; 21(2): 169–177.
    Effects of lamotrigine on 5-HT3 receptor deactivation and desensitization. Korean J Physiol Pharmacol. 2017 Mar; 21(2): 169–177.


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