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  • Brand : BIOFRON

  • Catalogue Number : AV-C10183

  • Specification : 98%

  • CAS number : 55486-06-1

  • Formula : C17H14O6

  • Molecular Weight : 314.29

  • PUBCHEM ID : 5316819

  • Volume : 5mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Structure Type



Standards;Natural Pytochemical;API




(Z)-2-(3,4-Dihydroxyphenyl)vinyl (2E)-3-(3,4-dihydroxyphenyl)acrylate/2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-, (Z)-2-(3,4-dihydroxyphenyl)ethenyl ester, (2E)-


[(Z)-2-(3,4-dihydroxyphenyl)ethenyl] (E)-3-(3,4-dihydroxyphenyl)prop-2-enoate


1.5±0.1 g/cm3


neurodegeneration, Parkinson’s disease, vasoactive intestinal peptide, agonist, microglia, regulatory T cells, alpha-synuclein, 6-hydroxydopamine

Flash Point

219.4±23.6 °C

Boiling Point

587.4±50.0 °C at 760 mmHg

Melting Point



InChl Key


WGK Germany


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#:55486-06-1) 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.




A paradigm shift has emerged in Parkinson’s disease (PD) highlighting the prominent role of CD4+ Tregs in pathogenesis and treatment. Bench to bedside research, conducted by others and our own laboratories, advanced a neuroprotective role for Tregs making pharmacologic transformation of immediate need. Herein, a vasoactive intestinal peptide receptor-2 (VIPR2) peptide agonist, LBT-3627, was developed as a neuroprotectant for PD-associated dopaminergic neurodegeneration. Employing both 6-hydroxydopamine (6-OHDA) and α-synuclein (α-Syn) overexpression models in rats, the sequential administration of LBT-3627 increased Treg activity without altering cell numbers both in na?ve animals and during progressive nigrostriatal degeneration. LBT-3627 administration was linked to reductions of inflammatory microglia, increased survival of dopaminergic neurons, and improved striatal densities. While α-Syn overexpression resulted in reduced Treg activity, LBT-3627 rescued these functional deficits. This occurred in a dose-dependent manner closely mimicking neuroprotection. Taken together, these data provide the basis for the use of VIPR2 agonists as potent therapeutic immune modulating agents to restore Treg activity, attenuate neuroinflammation, and interdict dopaminergic neurodegeneration in PD. The data underscore an important role of immunity in PD pathogenesis.


neurodegeneration, Parkinson’s disease, vasoactive intestinal peptide, agonist, microglia, regulatory T cells, alpha-synuclein, 6-hydroxydopamine


A Synthetic Agonist to Vasoactive Intestinal Peptide Receptor-2 Induces Regulatory T Cell Neuroprotective Activities in Models of Parkinson’s Disease


R. Lee Mosley, Yaman Lu, Katherine E. Olson, Jatin Machhi, Wenhui Yan, Krista L. Namminga, Jenell R. Smith, Scott J. Shandler, Howard E. Gendelman

Publish date





Structures are reported for six closely related salts of tris­(bipyrid­yl)iron(II) cations, namely tris­(2,2′-bi­pyridine)­iron(II) bis­(1,1,3,3-tetra­cyano-2-meth­oxy­propenide) 0.776-hydrate, [Fe(C10H8N2)3](C8H3N4O)2.0.776H2O, (I), tris­(2,2′-bi­pyridine)­iron(II) 1,1,3,3-tetra­cyano-2-(propyl­sulfan­yl)propenide perchlor­ate, [Fe(C10H8N2)3](C10H7N4S)(ClO4), (II), tris­(5,5′-dimethyl-2,2′-bi­pyridine)­iron(II) 1,1,3,3-tetra­cyano-2-meth­oxy­propenide tetra­fluorido­borate ethanol 0.926-solvate, [Fe(C12H12N2)3](C8H3N4O)(BF4).0.926C2H2O, (III), tris­(5,5′-dimethyl-2,2′-bi­pyridine)­iron(II) 1,1,3,3-tetra­cyano-2-eth­oxy­propenide tetra­fluorido­borate, [Fe(C12H12N2)3](C9H5N4O)(BF4), (IV), tris­(5,5′-dimethyl-2,2′-bi­pyridine)­iron(II) 1,1,3,3-tetra­cyano-2-(ethyl­sufanyl)propenide tetra­fluorido­borate, [Fe(C12H12N2)3](C9H5N4S)(BF4), (V), and tris­(5,5′-dimethyl-2,2′-bi­pyri­dine)­iron(II) 1,1,3,3-tetra­cyano-2-prop­oxypropenide tetra­fluorido­borate, [Fe(C12H12N2)3](C10H7N4O)(BF4), (VI). In compound (I), one of the anions is disordered over two sets of atomic sites with equal occupancies while, in the second anion, just one of the C(CN)2 units is disordered, again over two sets of atomic sites with equal occupancies: the anionic components are linked by multiple C?H?N hydrogen bonds to form a three-dimensional framework. In compound (II), the polynitrile anion is disordered over two sets of atomic sites with occupancies in the approximate ratio 3:1, while the perchlorate anion is disordered over three sets of atomic sites: there are C?N?π inter­actions between the cations and the polynitrile anion. The polynitrile anion in compound (III) is fully ordered, but the tetra­fluorido­borate anion is disordered over two sets of atomic sites with occupancies 0.671?(4) and 0.329?(4): the cations and the tetra­fluorido­borate anions are linked by C?H?F inter­actions to form an inter­rupted chain. Compounds (IV) and (V) are isostructural and all of the ionic components are fully ordered in both of them: the cations and tetra­fluorido­borate anions are linked into C 2 2(12) chains. The polynitrile anion in compound (VI) is disordered over two sets of atomic sites with approximately equal occupancies, and here the chains formed by the cations and the tetra­fluorido­borate anions are of the C 2 2(13) type.


synthesis, tris­(bipyrid­yl)iron(II) complexes, polynitrile anions, crystal structure, disorder, hydrogen bonding, C?N?π inter­actions, supra­molecular assembly


Six tris­(bipyrid­yl)iron(II) complexes with 2-substituted 1,1,3,3-tetra­cyano­propenide, perchlorate and tetra­fluorido­borate anions; order versus disorder, hydrogen bonding and C?N?π inter­actions


Abderezak Addala,a Zouaoui Setifi,b,a,* Yukio Morimoto,c BeNat Artetxe,d Takashi Matsumoto,e Juan M. Gutierrez-Zorrilla,d and Christopher Glidewellf

Publish date

2018 Dec 1




The mitochondrial electron transport chain complexes are organized into supercomplexes (SCs) of defined stoichiometry, which have been proposed to regulate electron flux via substrate channeling. We demonstrate that CoQ trapping in the isolated SC I+III2 limits complex (C)I turnover, arguing against channeling. The SC structure, resolved at up to 3.8 a in four distinct states, suggests that CoQ oxidation may be rate limiting because of unequal access of CoQ to the active sites of CIII2. CI shows a transition between “closed” and “open” conformations, accompanied by the striking rotation of a key transmembrane helix. Furthermore, the state of CI affects the conformational flexibility within CIII2, demonstrating crosstalk between the enzymes. CoQ was identified at only three of the four binding sites in CIII2, suggesting that interaction with CI disrupts CIII2 symmetry in a functionally relevant manner. Together, these observations indicate a more nuanced functional role for the SCs.


bioenergetics, supercomplex, respiration, oxidative phosphorylation, mitochondria, complex i, cytochrome bc1 complex, protein structure, oxidoreductas, cryoEM


Structures of Respiratory Supercomplex I+III2 Reveal Functional and Conformational Crosstalk


James A. Letts, Karol Fiedorczuk, Gianluca Degliesposti, Mark Skehel, Leonid A. Sazanov

Publish date

2019 Sep 19;

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