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3,4-Dimethoxycinnamic acid

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-D3003

  • Specification : 98%

  • CAS number : 2316-26-9

  • Formula : C11H12O4

  • Molecular Weight : 208.21

  • Volume : 100mg

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Catalogue Number

BF-D3003

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

208.21

Appearance

powder

Botanical Source

leaves of Phyllostachys heterocycla

Structure Type

Phenylpropanoids

Category

SMILES

COC1=C(C=C(C=C1)C=CC(=O)O)OC

Synonyms

IUPAC Name

Density

1.2±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

144.0±17.2 °C

Boiling Point

367.4±27.0 °C at 760 mmHg

Melting Point

181-183 °C(lit.)

InChl

InChI=1S/C11H12O4/c1-14-9-5-3-8(4-6-11(12)13)7-10(9)15-2/h3-7H,1-2H3,(H,12,13)/b6-4+

InChl Key

HJBWJAPEBGSQPR-GQCTYLIASA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:2316-26-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31764941

Abstract

Conclusion

KEYWORDS

piper nigrum; 4-Coumarate:CoA ligase; Coumarate:CoA ligase-like; methylenedioxyphenyl moiety; piperine.

Title

4-Coumarate:coenzyme A ligase isoform 3 from Piper nigrum (Pn4CL3) catalyzes the CoA thioester formation of 3,4-methylenedioxycinnamic and piperic acids

Author

Zhehao Jin 1 2, Juraithip Wungsintaweekul 3, Sang-Hoon Kim 1, Jeong-Han Kim 1, Yongho Shin 1, Dae-Kyun Ro 4, Soo-Un Kim 1 2

Publish date

2020 Jan 17

PMID

28509424

Abstract

Neurodegenerative diseases are associated with accumulation of amyloid-type protein misfolding products. Prion protein (PrP) is known for its ability to aggregate into soluble oligomers that in turn associate into amyloid fibrils. Preventing the formation of these infective and neurotoxic entities represents a viable strategy to control prion diseases. Numerous attempts to find dietary compounds with anti-prion properties have been made; however, the most promising agent found so far was curcumin, which is poorly soluble and merely bioavailable. In the present work, we identify 3,4-dimethoxycinnamic acid (DMCA) which is a bioavailable coffee component as a perspective anti-prion compound. 3,4-Dimethoxycinnamic acid was found to bind potently to prion protein with a Kd of 405 nM. An in vitro study of DMCA effect on PrP oligomerization and fibrillization was undertaken using isothermal titration calorimetry (ITC), dynamic light scattering (DLS) and circular dichroism (CD) methodologies. We demonstrated that DMCA affects PrP oligomer formation reducing the oligomer content by 30-40%, and enhancing SH-SY5Y cell viability treated with prion oligomers. Molecular docking studies allowed to suggest a site where DMCA is able to bind stabilizing PrP tertiary structure. We suggest that DMCA is a perspective dietary compound for prophylaxis of neurodegenerative diseases that needs further research. Copyright © 2017 John Wiley & Sons, Ltd.

KEYWORDS

3,4-dimethoxycinnamic acid; amyloid aggregation; coffee metabolites; prion protein.

Title

Inhibition of Prion Propagation by 3,4-Dimethoxycinnamic Acid

Author

Ivan Zanyatkin 1, Yulia Stroylova 1 2, Sofia Tishina 1, Victor Stroylov 3, Aleksandra Melnikova 1, Thomas Haertle 4, Vladimir Muronetz 1

Publish date

2017 Jul;

PMID

26438837

Abstract

Atherosclerosis is the major cause of cardiovascular disease (CVD), the leading cause of death worldwide. Despite much focus on lipid abnormalities in atherosclerosis, it is clear that the immune system also has important pro- and antiatherogenic functions. The enzyme indoleamine-2,3-dioxygenase (IDO) catalyses degradation of the essential amino acid tryptophan into immunomodulatory metabolites. How IDO deficiency affects immune responses during atherogenesis is unknown and we explored potential mechanisms in models of murine and human atherosclerosis. IDO deficiency in hypercholesterolemic ApoE(-/-) mice caused a significant increase in lesion size and surrogate markers of plaque vulnerability. No significant changes in cholesterol levels were observed but decreases in IL-10 production were found in the peripheral blood, spleen and lymph node B cells of IDO-deficient compared with IDO-competent ApoE(-/-) mice. 3,4,-Dimethoxycinnamoyl anthranilic acid (3,4-DAA), an orally active synthetic derivative of the tryptophan metabolite anthranilic acid, but not l-kynurenine, enhanced production of IL-10 in cultured splenic B cells. Finally, 3,4-DAA treatment reduced lesion formation and inflammation after collar-induced arterial injury in ApoE(-/-) mice, and reduced cytokine and chemokine production in ex vivo human atheroma cell cultures. Our data demonstrate that endogenous production of tryptophan metabolites via IDO is an essential feedback loop that controls atherogenesis and athero-inflammation. We show that the IDO pathway induces production of IL-10 in B cells in vivo and in vitro, suggesting that IDO may induce immunoregulatory functions of B cells in atherosclerosis. The favorable effects of anthranilic acid derivatives in atherosclerosis indicate a novel approach toward therapy of CVD.

KEYWORDS

B cell; atherosclerosis; cardiovascular disease; indoleamine 2,3-dioxygenase; inflammation.

Title

Indoleamine 2,3-dioxygenase-1 is protective in atherosclerosis and its metabolites provide new opportunities for drug development

Author

Jennifer E Cole 1, Nagore Astola 1, Adam P Cribbs 1, Michael E Goddard 1, Inhye Park 1, Patricia Green 1, Alun H Davies 2, Richard O Williams 1, Marc Feldmann 3, Claudia Monaco 3

Publish date

2015 Oct 20;


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