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Menadione

$64

  • Brand : BIOFRON

  • Catalogue Number : BD-D1363

  • Specification : 98%(HPLC)

  • CAS number : 58-27-5

  • Formula : C11H8O2

  • Molecular Weight : 172.18

  • PUBCHEM ID : 4055

  • Volume : 20MG

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Catalogue Number

BD-D1363

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

2-8℃

Molecular Weight

172.18

Appearance

White crystalline powder

Botanical Source

Structure Type

Quinones

Category

Standards;Natural Pytochemical;API

SMILES

CC1=CC(=O)C2=CC=CC=C2C1=O

Synonyms

Aquakay/Karcon/Kipca/Menadione/Synkay/Koaxin/Kaykot/Kanone/2-methyl-1,4-naphthalenedione/Kareon/2-methyl-naphthoquinone/Juva-K/2-methyl-1,4-naphthodione/VK3

IUPAC Name

2-methylnaphthalene-1,4-dione

Applications

Menadione, a synthetic naphthoquinone, can be converted to active vitamin K2 in vivo.Target: OthersMenadione (Vitamin K3) is a synthetic analogue of of 1,4-naphthoquinone with a methyl group in the 2-position. Menadione is used as a phosphatase inhibitor and an inhibitor of mitochondrial DNA polymerase γ (pol γ). Menadione can be used as an oxidative injury (free radical generator) inducing agent [1].

Density

1.225 g/cm3

Solubility

Methanol; Chloroform; Ethyl Acetate

Flash Point

113.8ºC

Boiling Point

304.5ºC at 760 mmHg

Melting Point

105-107 °C(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2914690000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:58-27-5) 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

27237971

Abstract

Previous studies have demonstrated vitamin K3 had a great relief to smooth muscle spastic disorders, but no researches have yet pinpointed its possible anti-contractile activity in the uterus. Here, we evaluated the effect of vitamin K3 on myometrial contractility and explored the possible mechanisms of vitamin K3 action. Myograph apparatus were used to record the changes in contractility of isolated mouse uterine strips in a tissue bath. Uterine strips were exposed to vitamin K3 or vehicle. Vitamin K3 suppressed spontaneous contractions in a concentration dependent manner. It significantly decreased the contractile frequency induced by PGF2ɑ but not their amplitude (expect 58.0 μM). Prior incubation with vitamin K3 reduced the effectiveness of PGF2ɑ-induced contraction. The antispasmodic effect of vitamin K3 was also sensitive to potassium channel blockers, such as tetraethylammonium, 4-aminopyridine, iberiotoxin) but not to the nitric oxide related pathway blockers. High concentrations (29.0, 58.0 μM) of vitamin K3 weakened the Ca(2+) dose response and inhibited phase 1 contraction (intracellular stored calcium release). These dates suggest that vitamin K3 specifically suppresses myometrial contractility by affecting calcium and potassium channels; thus, this approach has potential therapy for uterine contractile activity related disorders.

Copyright © 2016 Elsevier Inc. All rights reserved.

KEYWORDS

Calcium; In vitro; Potassium channel; Uterine contraction; Vitamin K3

Title

Vitamin K3 inhibits mouse uterine contraction in vitro via interference with the calcium transfer and the potassium channels.

Author

Zhang XX1, Lu LM2, Wang L3.

Publish date

2016 Aug 5

PMID

27230476

Abstract

Protein misfolding and aggregation have been associated with several human diseases such as Alzheimer’s, Parkinson’s and familial amyloid polyneuropathy etc. In this study, anti-fibrillation activity of vitamin k3 and its effect on the kinetics of amyloid formation of hen egg white lysozyme (HEWL) and Aβ-42 peptide were investigated. Here, in combination with Thioflavin T (ThT) fluorescence assay, circular dichroism (CD), transmission electron microscopy and cell cytotoxicity assay, we demonstrated that vitamin k3 significantly inhibits fibril formation as well as the inhibitory effect is dose dependent manner. Our experimental studies inferred that vitamin k3 exert its neuro protective effect against amyloid induced cytotoxicity through concerted pathway, modifying the aggregation formation towards formation of nontoxic aggregates. Molecular docking demonstrated that vitamin k3 mediated inhibition of HEWL and Aβ-42 fibrillogenesis may be initiated by interacting with proteolytic resistant and aggregation prone regions respectively. This work would provide an insight into the mechanism of protein aggregation inhibition by vitamin k3; pave the way for discovery of other small molecules that may exert similar effect against amyloid formation and its associated neurodegenerative diseases.

Title

Vitamin k3 inhibits protein aggregation: Implication in the treatment of amyloid diseases.

Author

Alam P1, Chaturvedi SK1, Siddiqi MK1, Rajpoot RK2, Ajmal MR1, Zaman M1, Khan RH1.

Publish date

2016 May 27

PMID

32099380

Abstract

PURPOSE:
Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer and its incidence continues to rise yearly. Photodynamic therapy (PDT) is a non-invasive form of cancer therapy, which utilizes the combined action of a photosensitizer, light, and oxygen molecules to selectively cause cellular damage to tumor cells. Vitamin K3 (VitK3) has been shown to induce apoptosis and inhibit the growth of tumor cells in humans. The purpose of this study was to determine the effect of VitK3 and ultraviolet radiation B (UVB) on oxidative damage, proliferation and apoptosis of A431 cells.

METHODS:
CCK-8 assay was used to detect cell proliferation; Hoechst staining, TUNEL assay and flow cytometry analysis were used to detect apoptosis. Western Blot was perfomed to measure the expression of apoptosis-related proteins. Flow cytometry analysis was employed to detect the reactive oxygen species (ROS) levels and mitochondrial membrane potential. Finally, the role of VitK3 in combination with UVB on the proliferation and apoptosis of A431 cells was investigated using mice xenograft models.

RESULTS:
We found that the co-treatment of VitK3 combined with UVB more significantly inhibited the growth and proliferation of A431 cells than either VitK3 or UVB alone. Hoechst 33258 staining and flow cytometry analysis revealed that apoptosis was more pronounced in the VitK3-UVB group compared to the VitK3 and UVB groups. Moreover, flow cytometry analysis showed that ROS and the depolarization of the mitochondrial membrane potential were higher in all the co-treatment groups compared to the control, VitK3, and UVB groups. The VitK3-UVB group exhibited a significantly lower tumor growth rate in mouse xenograft models.

CONCLUSION:
This study reveals that VitK3 combined with UVB inhibits the growth and induces apoptosis of A431 cells in vitro and suppresses tumor growth and promotes apoptosis of cSCC in vivo.

© 2019 Shi et al.

KEYWORDS

depolarization; oxidative; photodynamic; photosensitizer

Title

Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells.

Author

Shi S#1, Zheng G#2,3, Yang C#4, Chen X2, Yan Q1, Jiang F1, Jiang X1, Xin Y1, Jiang G2.

Publish date

2019 Dec 31