MPTP hydrochloride

Catalog No.S4732 Batch:S473202

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Technical Data

Formula

C12H15N·HCl
Molecular Weight 209.72 CAS No. 23007-85-4
Solubility (25°C)* In vitro Water 41 mg/mL (195.49 mM)
Ethanol 41 mg/mL (195.49 mM)
DMSO 26 mg/mL (123.97 mM)
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description MPTP hydrochloride is a dopaminergic neurotoxin and cause selective destruction of dopaminergic neurons in animal models of parkinsonism. MPTP hydrochloride induces apoptosis.MPTP hydrochloride can be used to induce animal models of Parkinson’s disease.
In vitro The morphology of N2AB-1 and glioma cells was unaltered when these cells were exposed to all doses of MPTP. And, C6 glioma cell proliferation was also unaffected by MPTP treatment[3]. MPTP Promotes Apoptosis and Tau Phosphorylation in Human Neuroblastoma M17 Cells. MPTP significantly promotes Tau phosphorylation at Ser262 in human neuroblastoma M17 cells. MPTP caused a dose-dependent increase in the intracellular α-synuclein level in our M17 human neuroblastoma cells. MPTP appears to promote Tau phosphorylation in the brain by activating both PKA and GSK3β[4].
In vivo The number of tyrosine hydroxylase-positive neurons was decreased in the substantia nigra pars compacta of MPTP-treated mice. MPTP decreased thioredoxin reductase 1 expression and thioredoxin reductase activity in the mouse midbrain, reduced the number of thioredoxin reductase 1-positive cells in the substantia nigra pars compacta of mice. Administration of the toxin MPTP can cause neurochemical, behavioral and histopathological alterations in human and nonhuman primates that are similar to those observed in Parkinsonian patients. Compared with primates, rodents are insensitive to MPTP. MPTP can be administered by various routes, such as gavage and stereotactic injection, but the most common and reproducible route is systemic administration, including subcutaneous, intravenous, intraperitoneal and intramuscular injection. MPTP is a lipophilic protoxin that can rapidly cross the blood-brain barrier following systemic injection. Once it enters the brain, MPTP is converted to 1-methyl-4-phenylpyridine by monoamine oxidase B[1]. MPTP has been shown to be toxic to dopaminergic neurons of the nigrostriatal system in humans, monkeys, and mice and to produce long-lasting depletion of DA and its metabolites in the striatum[2].

Protocol (from reference)

Cell Assay:

[3]
  • Cell lines

    N2AB-1 neural cell line and the C6 glioma cell line

  • Concentrations

    47.7, 4.77 and 0.477 μM

  • Incubation Time

    1, 2, 3 days

  • Method

    N2AB-1 and C6 glioma cells were plated in 24-well costar dishes (16 mm diameter) at 50,000 cells per well with the culture medium described above. After 24 h medium was removed and medium with varying concentrations of MPTP or MPP+ was added in duplicate. Control and treated cells were then trypsinized and counted with a hemocytometer every day for 3 days following treatment.
Animal Study:

[1]
  • Animal Models

    C57BL/6 mice

  • Dosages

    20 mg/kg

  • Administration

    i.p.

Selleck's MPTP hydrochloride has been cited by 23 publications

Disulfide bridge-targeted metabolome mining unravels an antiparkinsonian peptide [ Acta Pharm Sin B, 2024, 14(2):881-892] PubMed: 38322339
Echinacoside exerts neuroprotection via suppressing microglial α-synuclein/TLR2/NF-κB/NLRP3 axis in parkinsonian models [ Phytomedicine, 2024, 123:155230] PubMed: 38000105
Intravitreal MPTP drives retinal ganglion cell loss with oral nicotinamide treatment providing robust neuroprotection [ Acta Neuropathol Commun, 2024, 12(1):79] PubMed: 38773545
Phosphorylated α-synuclein deposited in Schwann cells interacting with TLR2 mediates cell damage and induces Parkinson's disease autonomic dysfunction [ Cell Death Discov, 2024, 10(1):52] PubMed: 38278799
CDK5-USP30 signaling pathway regulates MAVS-mediated inflammation via suppressing mitophagy in MPTP/MPP+ PD model [ Ecotoxicol Environ Saf, 2024, 279:116446] PubMed: 38772138
GSK-3β inhibitor amplifies autophagy-lysosomal pathways by regulating TFEB in Parkinson's disease models [ Exp Neurol, 2024, S0014-4886(24)00359-5] PubMed: 39490621
Advancing the early detection of canine cognitive dysfunction syndrome with machine learning-enhanced blood-based biomarkers [ Front Vet Sci, 2024, 11:1390296] PubMed: 39170638
Impeding the combination of astrocytic ASCT2 and NLRP3 by talniflumate alleviates neuroinflammation in experimental models of Parkinson's disease [ Acta Pharm Sin B, 2023, 13(2):662-677] PubMed: 36873178
NOX4 as a critical effector mediating neuroinflammatory cytokines, myeloperoxidase and osteopontin, specifically in astrocytes in the hippocampus in Parkinson's disease [ Redox Biol, 2023, 62:102698] PubMed: 37058998
Fucoidan from Fucus vesiculosus prevents the loss of dopaminergic neurons by alleviating mitochondrial dysfunction through targeting ATP5F1a [ Carbohydr Polym, 2023, 303:120470] PubMed: 36657849

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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