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MedChemExpressModel 6PPD-Q - 2754428-18-5

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6PPD-Q (6PPD-Quinone) is an environmental pollutant that can be detected in human urine and is widely present in the environment. 6PPD-Q targets and binds to CNR2, CNR1, AA2AR, LCAT, and TRPA1, with CNR2 exhibiting the highest binding affinity, potentially acting as a CNR2 receptor agonist to activate cannabinoid receptors. 6PPD-Q induces intestinal inflammation and barrier damage by disrupting mitochondrial function, reducing neuronal glycolysis metabolites and TCA cycle intermediates, and exacerbating α-synuclein (α-syn) aggregation.6PPD-Q is applicable in research on environmental toxicology, neurodegenerative diseases, and inflammation-related disorders[1].
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6PPD-Q

MCE China:6PPD-Q

Brand:MedChemExpress (MCE)

Cat. No.HY-153169

CAS:2754428-18-5

Synonyms:6PPD-Quinone

Purity:99.30%

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

Shipping:Room temperature in continental US; may vary elsewhere.

Description:6PPD-Q (6PPD-Quinone) is an environmental pollutant that can be detected in human urine and is widely present in the environment. 6PPD-Q targets and binds to CNR2, CNR1, AA2AR, LCAT, and TRPA1, with CNR2 exhibiting the highest binding affinity, potentially acting as a CNR2 receptor agonist to activate cannabinoid receptors. 6PPD-Q induces intestinal inflammation and barrier damage by disrupting mitochondrial function, reducing neuronal glycolysis metabolites and TCA cycle intermediates, and exacerbating α-synuclein (α-syn) aggregation. 6PPD-Q is applicable in research on environmental toxicology, neurodegenerative diseases, and inflammation-related disorders.

In Vitro:6PPD-Q (10 nM, 100 nM, 7 days) increases α-syn aggregation in primary dopaminergic neurons, enhances α-syn PFF-induced p-α-synSer129 expression, and promotes its accumulation in mitochondria[2].6PPD-Q (10 nM, 100 nM, 7 days) reduces mitochondrial respiration in primary dopaminergic neurons, particularly under α-syn PFF (α-synuclein preformed fibrils) treatment conditions[2].6PPD-Q (10 nM, 100 nM, 7 days) decreases glycolysis metabolites and alters TCA cycle intermediates in primary dopaminergic neurons, leading to a reduction in glycolysis metabolites (e.g., fructose-6-phosphate, pyruvate) and TCA cycle intermediates (e.g., citrate, α-ketoglutarate)[2].6PPD-Q (10 nM, 100 nM, 48 hours) does not exhibit significant cytotoxicity in primary dopaminergic neurons[2].

In Vivo:6PPD-Q (0.1, 1, 10, 100 μg/kg, p.o., once daily for 21 days) induces intestinal injury in ICR mice, characterized by increased inflammatory response in the jejunum and ileum and impaired intestinal barrier integrity[3].

IC50 & Target:CB1 CB2 ACAT-1 A2AR

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References:

[1]. Du B, et al. First report on the occurrence of N-(1, 3-dimethylbutyl)-N’-phenyl-p-phenylenediamine (6PPD) and 6PPD-quinone as pervasive pollutants in human urine from south China. Environ Sci Technol Lett, 2022, 9(12): 1056-1062.

[2]. Fang J, et al. 6PPD-quinone exposure induces neuronal mitochondrial dysfunction to exacerbate Lewy neurites formation induced by α-synuclein preformed fibrils seeding. J Hazard Mater. 2024 Mar 5;465:133312.  [Content Brief]

[3]. Yang Y, et al. Environmentally realistic dose of tire-derived metabolite 6PPD-Q exposure causes intestinal jejunum and ileum damage in mice via cannabinoid receptor-activated inflammation[J]. Science of The Total Environment, 2024, 918: 170679.  [Content Brief]

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