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Pyrroloquinoline quinone

$512

  • Brand : BIOFRON

  • Catalogue Number : BN-O1792

  • Specification : 98%(HPLC)

  • CAS number : 72909-34-3

  • Formula : C14H6N2O8

  • Molecular Weight : 330.21

  • PUBCHEM ID : 1024

  • Volume : 1mg

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Catalogue Number

BN-O1792

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

330.21

Appearance

Botanical Source

Structure Type

Category

SMILES

C1=C(C2=C(C(=O)C(=O)C3=C2NC(=C3)C(=O)O)N=C1C(=O)O)C(=O)O

Synonyms

coenzyme PQQ/2,7,9-Tricarboxy-1H-pyrrolo(2,3-f)quinoline-4,5-dione/PQQ Cofactor/Pyrroloquinoline-quinone/4,5-dioxo-1H-pyrrolo[2,3-f]quinoline-2,7,9-tricarboxylic acid/4,5-dihydro-4,5-dioxo-1H-pyrrolo-[2,3-f]quinoline-2,7,9-tricarboxylic acid/1H-Pyrrolo[2,3-f]quinoline-2,7,9-tricarboxylic acid, 4,5-dihydro-4,5-dioxo-/methoxanthin/4,5-Dioxo-4,5-dihydro-1H-pyrrolo[2,3-f]quinoline-2,7,9-tricarboxylic acid/PQQ/Pyrroloquinoline quinone/2,7,9-Tricarboxy-4,5-dihydro-4,5-dioxo-1H-pyrrolo[2,3-f]quinoline/Methoxatin/1H-Pyrrolo[2,3-f]quinolin-2,7,9-tricarboxylic acid, 4,5-dihydro-4,5-dioxo-/1H-pyrrolo(2,3-f)quinoline-2,7,9-tricarboxylic acid, 4,5-dihydro-4,5-dioxo-

IUPAC Name

4,5-dioxo-1H-pyrrolo[2,3-f]quinoline-2,7,9-tricarboxylic acid

Density

2.0±0.1 g/cm3

Solubility

Flash Point

569.8±34.3 °C

Boiling Point

1018.6±65.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

MMXZSJMASHPLLR-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:72909-34-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

26168402

Abstract

Pyrroloquinoline quinone (PQQ), an aromatic tricyclic o-quinone, was identified initially as a redox cofactor for bacterial dehydrogenases. Although PQQ is not biosynthesized in mammals, trace amounts of PQQ have been found in human and rat tissues because of its wide distribution in dietary sources. Importantly, nutritional studies in rodents have revealed that PQQ deficiency exhibits diverse systemic responses, including growth impairment, immune dysfunction, and abnormal reproductive performance. Although PQQ is not currently classified as a vitamin, PQQ has been implicated as an important nutrient in mammals. In recent years, PQQ has been receiving much attention owing to its physiological importance and pharmacological effects. In this article, we review the potential health benefits of PQQ with a focus on its growth-promoting activity, anti-diabetic effect, anti-oxidative action, and neuroprotective function. Additionally, we provide an update of its basic pharmacokinetics and safety information in oral ingestion.

KEYWORDS

anti-diabetes; anti-oxidant; neuroprotection; pyrroloquinoline quinone (PQQ); redox cofactor

Title

Recent progress in studies on the health benefits of pyrroloquinoline quinone.

Author

Akagawa M1, Nakano M2, Ikemoto K2.

Publish date

2016

PMID

30240821

Abstract

Pyrroloquinoline quinone (PQQ), a redox cofactor in the mitochondrial respiratory chain, has been reported to protect SH-SY5Y cells from cytotoxicity induced by rotenone, a mitochondrial complex I inhibitor. In this study, we aimed to investigate the mitochondrial mechanisms involved in the neuroprotection of PQQ both in vitro and in vivo. The cultured human SH-SY5Y neuroblastoma cells were exposed to different concentrations of PQQ after which the cells were treated with rotenone. Electron microscopy images showed that PQQ could prevent the mitochondrial morphology damage. The down-regulation of mitochondrial biogenesis related genes (PGC-1alpha and TFAM) and mitochondrial fission and fusion related genes (Drp1and Mfn2) in rotenone-injured SH-SY5Y cells could be inhibited by PQQ. PQQ could also promote the transposition of Drp1 and Mfn2 from cytosol to mitochondria. In addition, rotenone was injected into the left medial forebrain bundle of SD rats to establish a Parkinson’s disease (PD) model in vivo, after which different doses of PQQ or Edaravone were given intraperitoneally once daily for 8 weeks. PQQ could up-regulate the mRNA levels of PGC-1alpha, TFAM, Drp-1 and Mfn2 in the midbrain of PD rats. Our findings indicated that PQQ could prevent mitochondrial dysfunction by promoting mitochondrial biogenesis and regulating mitochondrial fission and fusion, which might contribute to its neuroprotective effect in PD models.

Copyright © 2018 Elsevier B.V. All rights reserved.

KEYWORDS

Mitochondria; Neuroprotection; Parkinson’s disease; Pyrroloquinoline quinone; Rotenone

Title

Mitochondrial regulation by pyrroloquinoline quinone prevents rotenone-induced neurotoxicity in Parkinson's disease models.

Author

Lu J1, Chen S1, Shen M2, He Q2, Zhang Y3, Shi Y3, Ding F2, Zhang Q4.

Publish date

2018 Nov 20

PMID

29185343

Abstract

Pyrroloquinoline quinone (PQQ), a redox-active o-quinone found in various foods and mammalian tissues, has received an increasing amount of attention because of a number of health benefits that can be attributed to its ability to enhance mitochondrial biogenesis. However, its underlying molecular mechanism remains incompletely understood. We have now established that the exposure of mouse NIH/3T3 fibroblasts to a physiologically relevant concentration of PQQ significantly stimulates mitochondrial biogenesis. The exposure of NIH/3T3 cells to 10-100 nM PQQ for 48 h resulted in increased levels of Mitotracker staining, mitochondrial DNA content, and mitochondrially encoded cytochrome c oxidase subunit 1 (MTCO1) protein. Moreover, we observed that PQQ treatment induces deacetylation of the peroxisome proliferator-activated receptor-γ-coactivator 1α (PGC-1α) and facilitates its nuclear translocation and target gene expression but does not affect its protein levels, implying increased activity of the NAD+-dependent protein deacetylase sirtuin 1 (SIRT1). Indeed, treatment with a SIRT1 selective inhibitor, EX-527, hampered the ability of PQQ to stimulate PGC-1α-mediated mitochondrial biogenesis. We also found that the PQQ treatment caused a concentration-dependent increase in the cellular NAD+ levels, but not the total NAD+ and NADH levels. Our results suggest that PQQ-inducible mitochondrial biogenesis can be attributed to activation of the SIRT1/PGC-1α signaling pathway by enhancing cellular NAD+ formation.

Title

Pyrroloquinoline Quinone, a Redox-Active o-Quinone, Stimulates Mitochondrial Biogenesis by Activating the SIRT1/PGC-1α Signaling Pathway.

Author

Saihara K1, Kamikubo R1,2, Ikemoto K3, Uchida K2, Akagawa M1.

Publish date

2017 Dec 19


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