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Catalogue Number : BN-O2104
Specification : 95%(HPLC)
CAS number : 87441-73-4
Formula : C15H20O4
Molecular Weight : 264.321
PUBCHEM ID : 435723
Volume : 10mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

This product is isolated and purified from the herbs of Carpesium abrotanoides L.

Structure Type



Standards;Natural Pytochemical;API




(1aR,2aS,5aR,6aR,7aR,9aR)-1a,7a-Dimethyl-5-methylenedecahydrobisoxireno[4,5:8,9]cyclodeca[1,2-b]furan-4(1aH)-one/1a,7a-Dimethyl-5-methylenedecahydrobisoxireno[4,5:8,9]cyclodeca[1,2-b]furan-4(1aH)-one/ERIOLIN,13/11,13-Dehydroeriolin/Bisoxireno[4,5:8,9]cyclodeca[1,2-b]furan-4(1aH)-one, decahydro-1a,7a-dimethyl-5-methylene-, (1aR,2aS,5aR,6aR,7aR,9aR)-/Bisoxireno[4,5:8,9]cyclodeca[1,2-b]furan-4(1aH)-one, decahydro-1a,7a-dimethyl-5-methylene-




1.2±0.1 g/cm3


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

Flash Point

185.2±28.8 °C

Boiling Point

415.0±45.0 °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#:87441-73-4) 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.




The crystal structures of four (E)-meth­oxy­benzaldehyde oxime derivatives, namely (2-meth­oxy­benzaldehyde oxime, 1, 2,3-di­meth­oxy­benzaldehyde oxime, 2, 4-di­meth­oxy­benzaldehyde oxime, 3, and 2,5-di­meth­oxy­benzaldehyde oxime, 4, are discussed. The arrangements of the 2-meth­oxy group and the H atom of the oxime unit are s-cis in compounds 1-3, but in both independent mol­ecules of compound 4, the arrangements are s-trans. There is also a difference in the conformation of the two mol­ecules in 4, involving the orientations of the 2- and 5-meth­oxy groups. The primary inter­molecular O—H(oxime)⋯O(hy­droxy) hydrogen bonds generate C(3) chains in 1 and 2. In contrast, in compound 3, the O—H(oxime)⋯O(hy­droxy) hydrogen bonds generate symmetric R 2 2(6) dimers. A more complex dimer is generated in 4 from the O—H(oxime)⋯O(hy­droxy) and C—H(2-meth­oxy)⋯O(hy­droxy) hydrogen bonds. In all cases, further inter­actions, C—H⋯O and C—H⋯π or π-π, generate three-dimensional arrays. Hirshfeld surface and fingerprint analyses are discussed.


crystal structure, oxime derivative, hydrogen bonding


Crystal structures and Hirshfeld surfaces of four meth­oxy­benzaldehyde oxime derivatives, 2-MeO-XC6H3C=NOH (X = H and 2-, 3- and 4-MeO): different conformations and hydrogen-bonding patterns


Ligia R. Gomes,a,b Marcus V. N. de Souza,c Cristiane F. Da Costa,c James L. Wardell,c,d and John Nicolson Lowd,*

Publish date

2018 Nov 1;




Reversine is a potent antitumor 2,6-diamino-substituted purine acting as an Aurora kinases inhibitor and interfering with cancer cell cycle progression. In this study we describe three reversine-related molecules, designed by docking calculation, that present structural modifications in the diamino units at positions 2 and 6. We investigated the conformations of the most stable prototropic tautomers of one of these molecules, the N6-cyclohexyl-N6-methyl-N2-phenyl-7H-purine-2,6-diamine (3), by Density Functional Theory (DFT) calculation in the gas phase, water and chloroform, the last solvent considered to give insights into the detection of broad signals in NMR analysis. In all cases the HN(9) tautomer resulted more stable than the HN(7) form, but the most stable conformations changed in different solvents. Molecules 1-3 were evaluated on MCF-7 breast and HCT116 colorectal cancer cell lines showing that, while being less cytotoxic than reversine, they still caused cell cycle arrest in G2/M phase and polyploidy. Unlike reversine, which produced a pronounced cell cycle arrest in G2/M phase in all the cell lines used, similar concentrations of 1-3 were effective only in cells where p53 was deleted or down-regulated. Therefore, our findings support a potential selective role of these structurally simplified, reversine-related molecules in p53-defective cancer cells.


reversine, microwave-assisted synthesis, molecular docking, cell cycle arrest, endoreduplication, p53


Synthesis of 2,6-Diamino-Substituted Purine Derivatives and Evaluation of Cell Cycle Arrest in Breast and Colorectal Cancer Cells


Bartolomeo Bosco,1 Andrea Defant,2 Andrea Messina,1 Tania Incitti,1 Denise Sighel,1,2 Angela Bozza,1 Yari Ciribilli,1 Alberto Inga,1 Simona Casarosa,1,* and Ines Mancini2,*

Publish date

2018 Aug;




Inflammation of the middle ear cavity (otitis media) and the abnormal deposition of bone at the otic capsule are common causes of conductive hearing impairment in children and adults. Although a host of environmental factors can contribute to these conditions, a genetic predisposition has an important role as well. Here, we analyze the Tail-short (Ts) mouse, which harbors a spontaneous semi-dominant mutation that causes skeletal defects and hearing loss. By genetic means, we show that the Ts phenotypes arise from an 18-kb deletion/insertion of the Rpl38 gene, encoding a ribosomal protein of the large subunit. We show that Ts mutants exhibit significantly elevated auditory-brain stem response thresholds and reduced distortion-product otoacoustic emissions, in the presence of normal endocochlear potentials and typical inner ear histology suggestive of a conductive hearing impairment. We locate the cause of the hearing impairment to the middle ear, demonstrating over-ossification at the round window ridge, ectopic deposition of cholesterol crystals in the middle ear cavity, enlarged Eustachian tube, and chronic otitis media with effusion all beginning at around 3 weeks after birth. Using specific antisera, we demonstrate that Rpl38 is an ∼8-kDa protein that is predominantly expressed in mature erythrocytes. Finally, using an Rpl38 cDNA transgene, we rescue the Ts phenotypes. Together, these data present a previously uncharacterized combination of interrelated middle ear pathologies and suggest Rpl38 deficiency as a model to dissect the causative relationships between neo-ossification, cholesterol crystal deposition, and Eustachian tubes in the etiology of otitis media.


Erythropoiesis, Genetic Diseases, Inflammation, Mouse Genetics, Ribosome Function, Otitis Media, Ribosomal Protein L38, Tail-short, Cholesterol Crystals, Conductive Hearing Loss


Ectopic Mineralization in the Middle Ear and Chronic Otitis Media with Effusion Caused by RPL38 Deficiency in the Tail-short (Ts) Mouse*An external file that holds a picture, illustration, etc. Object name is sbox.jpg


Konrad Noben-Trauth1 and Joseph R. Latoche

Publish date

2011 Jan 28;