128039-27-0

Upstream product

• 104-92-7 1-bromo-4-methoxy-benzene 
• 5024-70-4 11H-dibenzo[b,f]oxepin-10-one 
• 25563-02-4 2-(2-phenoxyphenyl)acetic acid 
• 25562-98-5 2-phenoxybenzyl cyanide 
• 5888-53-9 2-phenoxybenzyl chloride 
• 13807-84-6 (2-phenoxyphenyl)methanol 
• 19434-34-5 2-(phenoxy)benzaldehyde 
• 108-95-2 phenol 
• 446-52-6 2-Fluorobenzaldehyde 
• 128039-26-9 1-(p-methoxyphenyl)-2-(o-(phenyloxy)phenyl)ethyne 

Downstream Products

• 144836-66-8 5-bromo-6-(p-methoxyphenyl)dibenzoxepine 

Relevant academic research and scientific papers

Electrophilic addition to o-ArY-substituted phenylalkynes. A highly selective cyclization controlled by heteroatoms

Treatment of o-(phenyloxy)phenylalkyne 1 with HC104 or HBF4 gave dibenz [b, f]oxepin 2, whereas the sulfur analogue, o-(phenylthio)phenyl-alkyne 3, provided 1-phenyl 1-1-benzothiophenium salts 4.

Synthesis of targeted dibenzo[b,f]thiepines and dibenzo[b,f]oxepines as potential lead molecules with promising anti-breast cancer activity

A targeted library of substituted dibenzo[b,f]thiepines and dibenzo[b,f]oxepines (prototypes I, II and III), and structurally analogous to tamoxifen have been synthesized as a new class of anti-breast cancer agents. All the prototype molecules exhibited potential antiproliferative activity against ER + ve and ER-ve breast cancer cell lines. Dibenzo[b,f]thiepine prototypes were found to be more active. Of all the compound tested, 14b exhibited potent in-vitro antiproliferative activity at 1.33 μM and 5 μM concentration in MCF-7 and MDA-MB-231 cell lines and was devoid of any cytotoxicity in normal HEK cells even at 50 μM. Cell cycle analysis showed that the compound 14b inhibited cell proliferation due to G0/G1 arrest in MCF-7 cells. Annexin-V FITC and PI staining experiments confirmed that the cell inhibition was primarily due to apoptosis and not by necrosis, which was also supported by LDH release assay experiment. Molecular docking studies showed better binding interaction of the new dibenzo[b,f]thiepine analogue 14b with the estrogen receptor (ER) as compared to 4-hydroxy-tamoxifen and this enhanced binding might be responsible for its estrogen antagonistic activity that induces cell cycle arrest, apoptosis and inhibition of breast cancer cells.

Electrophile-induced Intramolecular Cyclization of ortho-(Aryloxy)phenylalkynes to Dibenzoxepines

Reaction of o-(aryloxy)phenylalkynes with electrophiles such as perchloric acid, tetrafluoroboric acid, benzenesulfenyl chloride, and iodine monochloride yielded dibenzoxepine derivatives.Cyclization to the dibenzoxepines competed with 1,2-addit