T
Teresa Klinowska
Researcher at AstraZeneca
Publications - 69
Citations - 4616
Teresa Klinowska is an academic researcher from AstraZeneca. The author has contributed to research in topics: Cancer & Breast cancer. The author has an hindex of 23, co-authored 61 publications receiving 3733 citations. Previous affiliations of Teresa Klinowska include University of Manchester.
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Journal ArticleDOI
AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer
Darren Cross,Susan Ashton,Serban Ghiorghiu,Cath Eberlein,Caroline A. Nebhan,Paula J. Spitzler,Jonathon P. Orme,M. Raymond V. Finlay,Richard A. Ward,Martine J. Mellor,Gareth D Hughes,Amar Rahi,Vivien Jacobs,Monica Red Brewer,Eiki Ichihara,Jing Sun,Hailing Jin,Peter Ballard,Katherine Al-Kadhimi,Rachel Rowlinson,Teresa Klinowska,Graham Richmond,Mireille Cantarini,Dong Wan Kim,Malcolm R Ranson,William Pao +25 more
TL;DR: A novel structurally distinct third-generation EGFR TKI that irreversibly and selectively targets both sensitizing and resistant T790M(+) mutant EGFR while harboring less activity toward wild-type EGFR is reported.
Journal ArticleDOI
AZD4547: An Orally Bioavailable, Potent, and Selective Inhibitor of the Fibroblast Growth Factor Receptor Tyrosine Kinase Family
Paul R. Gavine,Lorraine Mooney,Elaine Kilgour,Andrew Peter Thomas,Katherine Al-Kadhimi,Sarah Beck,Claire Rooney,Tanya Coleman,Dawn Baker,Martine J. Mellor,A. Nigel Brooks,Teresa Klinowska +11 more
TL;DR: The findings show that AZD4547 is a novel selective small-molecule inhibitor of FGFR with potent antitumor activity against FGFR-deregulated tumors in preclinical models and is under clinical investigation for the treatment ofFGFR-dependent tumors.
Journal ArticleDOI
Discovery of a potent and selective EGFR inhibitor (AZD9291) of both sensitizing and T790M resistance mutations that spares the wild type form of the receptor
M. Raymond V. Finlay,Mark J. Anderton,Susan Ashton,Peter Ballard,Paul A. Bethel,Matthew R. Box,Robert Hugh Bradbury,Simon J. Brown,Sam Butterworth,Andrew D. Campbell,Christopher G. Chorley,Nicola Colclough,Darren Cross,Gordon S. Currie,Matthew Grist,Lorraine A. Hassall,George B. Hill,Daniel S. James,Michael James,Paul D. Kemmitt,Teresa Klinowska,Gillian M. Lamont,Scott G. Lamont,Nathaniel G. Martin,Heather L. McFarland,Martine J. Mellor,Jonathon P. Orme,David Perkins,Paula Perkins,Graham Richmond,Peter D. Smith,Richard A. Ward,Michael J. Waring,David Whittaker,Stuart L. Wells,Gail L. Wrigley +35 more
TL;DR: Following observations of significant tumor inhibition in preclinical models, the clinical candidate AZD9291 was administered clinically to patients with T790M positive EGFR-TKI resistant NSCLC and early efficacy has been observed, accompanied by an encouraging safety profile.
Journal ArticleDOI
Overcoming mTOR resistance mutations with a new-generation mTOR inhibitor
Vanessa Rodrik-Outmezguine,Masanori Okaniwa,Zhan Yao,Chris J. Novotny,Claire McWhirter,Arpitha Banaji,Helen Won,Wai Wong,M.F. Berger,Elisa de Stanchina,Derek Barratt,Sabina Cosulich,Teresa Klinowska,Neal Rosen,Kevan M. Shokat,Kevan M. Shokat +15 more
TL;DR: A new class of mTOR inhibitors is reported which overcomes resistance to existing first and second generation inhibitors and exploits the unique juxtaposition of two drug binding pockets to create a bivalent interaction that allows inhibition of these resistant mutants.
Journal ArticleDOI
Structure- and Reactivity-Based Development of Covalent Inhibitors of the Activating and Gatekeeper Mutant Forms of the Epidermal Growth Factor Receptor (EGFR)
Richard A. Ward,Mark J. Anderton,Susan Ashton,Paul A. Bethel,Matthew R. Box,Sam Butterworth,Nicola Colclough,Christopher G. Chorley,Claudio Chuaqui,Darren Cross,Les A. Dakin,Judit E. Debreczeni,Cath Eberlein,M. Raymond V. Finlay,George B. Hill,Matthew Grist,Teresa Klinowska,Clare Lane,Scott W. Martin,Jonathon P. Orme,Peter D. Smith,Fengjiang Wang,Michael J. Waring +22 more
TL;DR: A novel series of small-molecule inhibitors developed to target the double mutant form of the epidermal growth factor receptor (EGFR) tyrosine kinase, which is resistant to treatment with gefitinib and erlotinib, demonstrates high levels of activity and shows selectivity over wild-type EGFR.