59455-11-7

Upstream product

• 352-13-6 4-flourophenylmagnesium bromide 
• 460-00-4 1-Bromo-4-fluorobenzene 
• 337506-83-9 1,1-bis(4-fluorophenyl)butane-1,4-diol 

Downstream Products

• 57668-61-8 4,4'-(4-bromobutane-1,1-diyl)bis(fluorobenzene) 
• 64630-52-0 4,4-bis-(4-fluoro-phenyl)-butylamine 
• 1841-17-4 8-[4,4-bis(4-fluorophenyl)-but-3-enyl]-1-phenyl-1,3,8-triazaspiro[4.5]decan-4-one 
• 97182-50-8 methyl 1-[4,4-bis-(4'-fluorophenyl)-3-butenyl]-3-pyrrolidineacetate 
• 97182-51-9 1-[4,4-bis-(4'-fluorophenyl)-3-butenyl]-3-pyrrolidineacetic acid hydrochloride 

Relevant academic research and scientific papers

Ring-opening reaction of methylenecyclopropanes with LiCl, LiBr or NaI in acetic acid

The methylenecyclopropanes 1 react with LiCl, LiBr or NaI at 80°C to give the corresponding gem-disubstituted homoallylic halides 2 in good to excellent yields in acetic acid. In some cases, the ring-opening reaction can be completed within 5 min to give

Design, synthesis and structure-activity relationship study of novel urea compounds as FGFR1 inhibitors to treat metastatic triple-negative breast cancer

Triple-negative breast cancer (TNBC) is an aggressive type of cancer characterized by higher metastatic and reoccurrence rates, where approximately one-third of TNBC patients suffer from the metastasis in the brain. At the same time, TNBC shows good responses to chemotherapy, a feature that fuels the search for novel compounds with therapeutic potential in this area. Recently, we have identified novel urea-based compounds with cytotoxicity against selected cell lines and with the ability to cross the blood-brain barrier in vivo. We have synthesized and analyzed a library of more than 40 compounds to elucidate the key features responsible for the observed activity. We have also identified FGFR1 as a molecular target that is affected by the presence of these compounds, confirming our data using in silico model. Overall, we envision that these compounds can be further developed for the potential treatment of metastatic breast cancer.

Fluspirilene Analogs Activate the 20S Proteasome and Overcome Proteasome Impairment by Intrinsically Disordered Protein Oligomers

Oligomerization of aggregation-prone intrinsically disordered proteins (IDPs), such as α-synuclein, amyloid β, and tau, has been shown to be associated with the pathogenesis of several neurodegenerative diseases, including Parkinson's and Alzheimer's disease. The proteasome is charged with regulating cellular levels of IDPs, but this degradation pathway can become dysregulated leading to their accumulation and subsequent aggregation. Although the pathogenesis of these neurodegenerative diseases is still under intense investigation, it has been shown that the oligomeric forms of IDPs, including α-synuclein and amyloid β, can impair proteasome function. This leads to additional accumulation of the IDPs, further promoting disease progression. Herein, we report the use of small molecule activators of the 20S subcomplex of the proteasome to restore impaired 20S proteasome activity and prevent IDP accumulation and oligomerization. We found that fluspirilene and its new synthetic analog (16) show strong 20S proteasome enhancement (doubling 20S proteolytic activity at μ2 μM, with maximum fold enhancement of μ1000%), overcome impaired proteasome function, and prevent the accumulation of pathogenic IDPs. These findings provide support for the use of 20S enhancers as a possible therapeutic strategy to combat neurodegenerative diseases.

Synthesis and SAR study of diphenylbutylpiperidines as cell autophagy inducers

A novel series of diphenylbutylpiperidines as autophagy inducers was described and extensive SAR studies resulted in derivatives (15d-e, 15i-j) with 10-fold greater activity than the lead compounds 1 and 2. Meanwhile, a new synthetic route to diphenylbutyl bromide (6) from bromobenzene and γ-butyrolactone was also reported here.

DIPHENYLBUTYPIPERIDINE AUTOPHAGY INDUCERS

Autophagy inducing compounds, methods of their preparation and use, and kits containg said compounds are disclosed herein.