1. Neuronal Signaling
    Immunology/Inflammation
    GPCR/G Protein
    Autophagy
  2. Amyloid-β
    Histamine Receptor
    Adrenergic Receptor
    5-HT Receptor
    Autophagy
  3. Latrepirdine dihydrochloride

Latrepirdine dihydrochloride (Synonyms: Dimebolin dihydrochloride)

Cat. No.: HY-14537 Purity: 99.75%
Handling Instructions

Latrepirdine dihydrochloride is a neuroactive compound with antagonist activity at histaminergic, α-adrenergic, and serotonergic receptors. Latrepirdine stimulates amyloid precursor protein (APP) catabolism and amyloid-β () secretion.

For research use only. We do not sell to patients.

Latrepirdine dihydrochloride Chemical Structure

Latrepirdine dihydrochloride Chemical Structure

CAS No. : 97657-92-6

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10 mM * 1 mL in DMSO USD 55 In-stock
Estimated Time of Arrival: December 31
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ready for reconstitution
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10 mg USD 90 In-stock
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25 mg USD 180 In-stock
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50 mg USD 310 In-stock
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100 mg USD 520 In-stock
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200 mg USD 720 In-stock
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Customer Review

Based on 1 publication(s) in Google Scholar

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  • Biological Activity

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Description

Latrepirdine dihydrochloride is a neuroactive compound with antagonist activity at histaminergic, α-adrenergic, and serotonergic receptors. Latrepirdine stimulates amyloid precursor protein (APP) catabolism and amyloid-β () secretion.

IC50 & Target

Amyloid-β (Aβ), Histaminergic receptor, α-adrenergic receptor, Serotonergic receptor[1]

In Vitro

Latrepirdine has been reported to possess several properties that are potentially relevant to the treatment of neurodegenerative diseases: (1) protection of cultured cells from the cytotoxicity of amyloid-β (Aβ) peptide; (2) stabilization of mitochondrial function and calcium homeostasis; (3) modulation of Aβ release from cultured cells, isolated intact nerve terminals, and from hippocampal neurons in living mouse brain; and (4) promotion of neurogenesis in the murine hippocampus. Treatment of cultured mammalian cells with Latrepirdine leads to enhanced mTOR- and Atg5-dependent autophagy. Latrepirdine modulates Atg5-dependent autophagic activity in a dose-dependent manner and via the mTOR-signaling pathway. HeLa cells stably expressing LC3 fused are treated with EGFP (eGFP-LC3) for 3 or 6 hours in the absence or presence of 50 μM Latrepirdine. Treatment with Latrepirdine for 3 or 6 hours markedly enhances the number of eGFP-LC3 punctae, indicating that Latrepirdine induces formation of autophagosomes. Next, mouse N2a neuroblastoma cells are treated in the absence (vehicle) or presence of 5 nM, 500 nM or 50 μM Latrepirdine for 3 or 6 hours in order to determine the effects of acute drug treatment on the regulation of autophagy. A significant and dose-dependent increase is observed in LC3-II levels in N2a cells following 3- or 6-hour treatment with either 500 nM or 50 μM Latrepirdine. A significant decrease of p-mTOR and p-S6K from N2a cells treated with 50 μM Latrepirdine for 3 hours is observed, whereas the total mTOR and p70S6K levels remain relatively constant[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Latrepirdine treatment of TgCRND8 transgenic mice is associated with improved learning behavior and with a reduction in accumulation of Aβ42 and α-synuclein. Male, 90-day-old TgCRND8 mice or their wild-type littermates (nTg) receive 31 consecutive once daily i.p. injections of either 3.5 mg/kg Latrepirdine or 0.9% saline (vehicle). At the culmination of treatment, mice are tested for cued and contextual fear conditioning using a paradigm that has been widely accepted for evaluating learning and memory deficits in APP transgenic mice. A significant increase in cued memory only among Latrepirdine-versus vehicle-treated TgCRND8 mice (p=0.01) is observed. A weak, non-significant trend toward an improvement in contextual memory among Latrepirdine-versus vehicle-treated mice (p=0.099) is also observed[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Clinical Trial
Molecular Weight

392.37

Formula

C₂₁H₂₇Cl₂N₃

CAS No.
SMILES

CN(C1)CCC2=C1C3=CC(C)=CC=C3N2CCC4=CN=C(C)C=C4.Cl.Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 6.4 mg/mL (16.31 mM; Need warming)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.5486 mL 12.7431 mL 25.4861 mL
5 mM 0.5097 mL 2.5486 mL 5.0972 mL
10 mM 0.2549 mL 1.2743 mL 2.5486 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 0.5 mg/mL (1.27 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 0.5 mg/mL (1.27 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 0.5 mg/mL (1.27 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
Cell Assay
[1]

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[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration
[1]

Mice[1]
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.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

References

Purity: 99.75%

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Keywords:

LatrepirdineDimebolinAmyloid-βHistamine ReceptorAdrenergic Receptor5-HT ReceptorAutophagyβ-amyloid peptideAbetaBeta ReceptorSerotonin Receptor5-hydroxytryptamine ReceptorInhibitorinhibitorinhibit

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Latrepirdine dihydrochloride
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