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Oxazole, 4-(chloromethyl)-2-[(1E)-2-[4-(trifluoromethyl)phenyl]ethenyl]- is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

366016-66-2

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366016-66-2 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 366016-66-2 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 3,6,6,0,1 and 6 respectively; the second part has 2 digits, 6 and 6 respectively.
Calculate Digit Verification of CAS Registry Number 366016-66:
(8*3)+(7*6)+(6*6)+(5*0)+(4*1)+(3*6)+(2*6)+(1*6)=142
142 % 10 = 2
So 366016-66-2 is a valid CAS Registry Number.

366016-66-2Relevant academic research and scientific papers

A Facile Total Synthesis of Mubritinib

Wang, Rong,Cui, Menghan,Yang, Qing,Kuang, Chunxiang

, p. 978 - 982 (2021/02/03)

A five-step, practical, and concise total synthesis of mubritinib is described. The synthesis utilized Friedel-Crafts acylation, click reaction, reduction, and demethylation for the construction of the triazole ring system as key steps. Another important feature of this synthesis is the Bredereck oxazole synthesis. The main advantages of this process are the improved yield and decreased number of reaction steps, which paves the way for the industrial-scale synthesis of mubritinib.

Identification of a novel toxicophore in anti-cancer chemotherapeutics that targets mitochondrial respiratory complex i

Allen, Timothy E. H.,Chung, Injae,Fischer, Peter,Hardy, Rachel,Harvey, Robert F.,Hirst, Judy,Kellam, Barrie,Macfarlane, Marion,Mistry, Sarah,Pryde, Kenneth R.,Serreli, Riccardo,Stephenson, Zo? A.,Stoneley, Mark,Willis, Anne E.

, (2020/06/10)

Disruption of mitochondrial function selectively targets tumour cells that are dependent on oxidative phosphorylation. However, due to their high energy demands, cardiac cells are disproportionately targeted by mitochondrial toxins resulting in a loss of cardiac function. An analysis of the effects of mubritinib on cardiac cells showed that this drug did not inhibit HER2 as reported, but directly inhibits mitochondrial respiratory complex I, reducing cardiac-cell beat rate, with prolonged exposure resulting in cell death. We used a library of chemical variants of mubritinib and showed that modifying the 1H-1,2,3-triazole altered complex I inhibition, identifying the heterocyclic 1,3-nitrogen motif as the toxicophore. The same toxicophore is present in a second anti-cancer therapeutic carboxyamidotriazole (CAI) and we demonstrate that CAI also functions through complex I inhibition, mediated by the toxicophore. Complex I inhibition is directly linked to anti-cancer cell activity, with toxicophore modification ablating the desired effects of these compounds on cancer cell proliferation and apoptosis.

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