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    Latrepirdine (Dimebolin) HCl
    Latrepirdine (Dimebolin) HCl

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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 #: V0966
    CAS #: 97657-92-6Purity ≥98%

    Description: Latrepirdine HCl (Dimebon; Dimebolin; Dimeboline; Preparation 84), the hydrochloride salt of Latrepirdine, is an orally bioactive, neuroactive and non-selective antihistamine drug  with the potential to be used for Alzheimer's disease and Huntington's disease. It is also an antagonist of multiple other targets including GluR, and 5-HT receptors, used as an antihistamine drug. Latrepirdine has been shown to inhibit brain cell death in animal models of Alzheimer's disease and Huntington's disease. Research suggests it may also have cognition-enhancing effects in healthy individual. Latrepirdine has been used clinically in Russia and other countries, However, a Phase III clinical trial for Alzheimer's disease treatment failed to show any benefit.

    References: J Alzheimers Dis. 2010;21(2):389-402; Mol Psychiatry. 2013 Aug;18(8):889-97.

    Related CAS #: 3613-73-8 (free base)  

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    Molecular Weight (MW)392.37
    CAS No.97657-92-6
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 24 mg/mL (61.2 mM)
    Water: <1 mg/mL
    Ethanol: 13 mg/mL (33.1 mM)
    SMILES CodeCC1=CC=C(CCN2C3=C(CN(C)CC3)C4=C2C=CC(C)=C4)C=N1
    SynonymsDimebon; Dimeboline; Dimebolin; Latrepirdine; Preparation 84;

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    In Vitro

    In vitro activity: Latrepirdine increases succinate dehydrogenase activity (MTT-assay), mitochondrial membrane potential (DeltaPsim), and cellular ATP levels in primary mouse cortical neurons and human neuroblastoma cells (SH-SY5Y). Latrepirdine enhances mitochondrial function both in the absence and presence of stress and Dimebon-treated cells are partially protected to maintain cell viability. Latrepirdine leads to enhanced mTOR- and Atg5-dependent autophagy in cultured mammalian cells. latrepirdine stimulates MTOR- and ATG5-dependent autophagy, leading to the reduction of intracellular levels of APP metabolites, including Aβ in cultured cells. Latrepirdine stimulates the degradation of α-syn in differentiated SH-SY5Y neurons, and in mouse brain following chronic administration, in parallel with elevation of the levels of markers of autophagic activity. Latrepirdine increases intracellular ATP levels and glucose transporter 3 translocation to the plasma membrane in primary neuron.

    Cell Assay: N2a cells, stable human cervical carcinoma (HeLa) cells expressing EGFP-LC3, and mouse embryonic fibroblasts (MEFs) derived from wildtype mice or ATG5-/- mice are maintained in “growth medium” (high glucose Dulbecco's modified Eagle's medium supplemented with 10% FBS and 100 units/mL Penicillin/Streptomycin) at 37°C, 5% CO2. N2a cells stably transfected with APPK670N, M671L are maintained in growth medium supplemented with 0.2 mg/mL G418. Cells are washed 1× with ice cold PBS (pH 7.4) then incubated with either Latrepirdine (5 nM, 500 nM or 50 μM) or vehicle (growth medium). Following 3-, 6-, or 24-hour of treatment, cells are washed 1x with ice cold PBS, and collected in lysis buffer (50 mM Tris-HCl, 150 mM NaCl, 1 mM Pepstatin, 1 mM PMSF, 1% Triton X-100, EDTA-free mini-complete protease inhibitor cocktail tablet) then centrifuged (14,000 RPM) for 15 minutes at 4°C. For time-course experiments, cells are washed 2× with ice-cold PBS (pH 7.4) and incubated for the indicated time in serum-free DMEM containing 50 μg/mL CHX or 50 μg/mL Cycloheximide (CHX)+50 μg/mL Chloroquine (CQ). Baseline (T0) samples are collected immediately prior to treatment

    In VivoLatrepirdine treatment of TgCRND8 transgenic mice is associated with improved learning behavior and with a reduction in accumulation of Aβ42 and α-synuclein. Latrepirdine administration results in increased levels of the biomarkers thought to correlate with autophagy activation in the brains of TgCRND8 (APP K670M, N671L, V717F) or wild-type mice, and that treatment is associated with abrogation of behavioral deficit, reduction in Aβ neuropathology, and prevention of autophagic failure among TgCRND8 mice.
    Animal modelMice:Male 53-55-day-old TgCRND8 mice (N=25) are randomly distributed into either of the two treatment groups: Latrepirdine (n=13 TgCRND8) or vehicle (n=12 TgCRND8). Animals receive 21 consecutive once daily intraperitoneal injections of either 3.5 mg/kg Latrepirdine or 0.9% saline (vehicle). 90-day-old male TgCRND8 mice (N=28) or their wild-type littermates (N=56) are randomly distributed into either of two treatment groups: Latrepirdine (n=13 TgCRND8; n=21 nTg) or vehicle (n=15 TgCRND8; n=25 nTg). Following treatment, animals are sacrificed and transcardially perfused with ice-cold PBS (pH 7.4). Male 90-day-old (n=5 per genotype) or 120-day-old (n=6 per genotype) TgCRND8 mice or their non-transgenic littermates are sacrificed and transcardially perfused with ice-cold PBS (pH 7.4). One hemisphere from each mouse is post-fixed in 4% paraformaldeyhde in PBS (pH 7.4) for histological analysis and the other hemisphere is dissected and snap-frozen for biochemical analysis.
    Formulation & Dosage3.5 mg/kg; i.p.

    J Alzheimers Dis. 2010;21(2):389-402; Mol Psychiatry. 2013 Aug;18(8):889-97.

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

    Latrepirdine activates autophagy via mTOR-pathway following 3- and 6-hour treatment. Mol Psychiatry. 2013 Aug;18(8):889-97.
    24-hour incubation with 50μM latrepirdine potentiates Atg5-independent accumulation of APP metabolites and p62. Mol Psychiatry. 2013 Aug;18(8):889-97.
    Chronic latrepirdine therapy enhanced autophagy and arrested progression of behavioral impairment and neuropathology among TgCRND8 mice. Mol Psychiatry. 2013 Aug;18(8):889-97.


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