M
Matthew J. Fuchter
Researcher at Imperial College London
Publications - 159
Citations - 6834
Matthew J. Fuchter is an academic researcher from Imperial College London. The author has contributed to research in topics: Chemistry & Medicine. The author has an hindex of 36, co-authored 134 publications receiving 4871 citations. Previous affiliations of Matthew J. Fuchter include Emory University & University of London.
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Journal ArticleDOI
Development of a Photo-Cross-Linkable Diaminoquinazoline Inhibitor for Target Identification in Plasmodium falciparum.
Alexandra S. Lubin,Ainoa Rueda-Zubiaurre,Holly Matthews,Hella Baumann,Fabio R. Fisher,Julia Morales-Sanfrutos,Kate Hadavizadeh,Flore Nardella,Edward W. Tate,Jake Baum,Artur Scherf,Artur Scherf,Artur Scherf,Matthew J. Fuchter +13 more
TL;DR: Initial pull-down proteomics experiments identified 104 proteins from different classes, many of which are essential, highlighting the suitability of the developed probe as a valuable tool for target identification in Plasmodium falciparum.
Journal ArticleDOI
Highly Selective High-Speed Circularly Polarized Photodiodes Based on π-Conjugated Polymers
Matthew D. Ward,Jessica Wade,Xingyuan Shi,Jenny Nelson,Alasdair J. Campbell,Matthew J. Fuchter +5 more
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Development of a cyclin-dependent kinase inhibitor devoid of ABC transporter-dependent drug resistance.
Maciej Kaliszczak,Hetal Patel,Sebastian H. B. Kroll,Laurence Carroll,Graham Smith,Sean Delaney,Dean A. Heathcote,Alexander Bondke,Matthew J. Fuchter,R. C. Coombes,Anthony G. M. Barrett,Simak Ali,Eric O. Aboagye +12 more
TL;DR: A promising pyrazolo[1,5-a]pyrimidine compound devoid of ABC transporter interaction is identified, highly suitable for further preclinical and clinical evaluation for the treatment of cancer.
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Highly ligand efficient and selective N-2-(Thioethyl)picolinamide histone deacetylase inhibitors inspired by the natural product psammaplin A.
TL;DR: It is found that the HDAC potency and isoform selectivity provided by the oxime unit of psammaplin A could be reproduced by using carefully chosen heterocyclic frameworks.
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The transcriptional repressor REV-ERB as a novel target for disease
TL;DR: Current understanding of the function of REV-ERB, modulation by endogenous factors and synthetic ligands, and the involvement of REB in select human diseases are reviewed and the need for higher quality ligands to aid in robust validation of this exciting target is demonstrated.