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David W. Fry

Researcher at Pfizer

Publications -  31
Citations -  3258

David W. Fry is an academic researcher from Pfizer. The author has contributed to research in topics: Receptor tyrosine kinase & Tyrosine kinase. The author has an hindex of 18, co-authored 31 publications receiving 3001 citations. Previous affiliations of David W. Fry include Autonomous University of Barcelona.

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Journal Article

Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts

TL;DR: Results indicate that inhibition of Cdk4/6 alone is sufficient to cause tumor regression and a net reduction in tumor burden in some tumors.
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Discovery of a potent and selective inhibitor of cyclin-dependent kinase 4/6.

TL;DR: It is demonstrated that the modification of pyrido[2,3-d]pyrimidin-7-ones to include a 2-aminopyridine side chain at the C2-position provides inhibitors with exquisite selectivity for Cdk4/6 in vitro.
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Drug‐induced ubiquitylation and degradation of ErbB receptor tyrosine kinases: implications for cancer therapy

TL;DR: An unexpected activity of TKIs is reported: along with inhibition of tyrosine phosphorylation, they enhance ubiquitylation and accelerate endocytosis and subsequent intracellular destruction of ErbB‐2 molecules.
Journal Article

PD153035, a tyrosine kinase inhibitor, prevents epidermal growth factor receptor activation and inhibits growth of cancer cells in a receptor number-dependent manner.

TL;DR: C Cotreatment with C225, an anti-EGF receptor-blocking monoclonal antibody, further enhanced the antitumor activity of PD153035, suggesting mechanisms of action for C225 other than competition with ligand binding.
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CI-1033, a pan-erbB tyrosine kinase inhibitor.

TL;DR: In vitro studies of human cancer cell lines indicate that CI-1033 results in prompt, potent, and sustained inhibition of tyrosine kinase activity, which holds significant potential for use in a broad range of solid tumors.