Optimization of an Imidazo[1,2

Authors :: William, McCoull
Scott, Boyd
Martin R, Brown
Muireann, Coen
Olga, Collingwood
Nichola L, Davies
Ann, Doherty
Gary, Fairley
Kristin, Goldberg
Elizabeth, Hardaker
Guang, He
Edward J, Hennessy
Philip, Hopcroft
George, Hodgson
Anne, Jackson
Xiefeng, Jiang
Ankur, Karmokar
Anne-Laure, Lainé
Nicola, Lindsay
Yumeng, Mao
Roshini, Markandu
Lindsay, McMurray
Neville, McLean
Lorraine, Mooney
Helen, Musgrove
J Willem M, Nissink
Alexander, Pflug
Venkatesh Pilla, Reddy
Philip B, Rawlins
Emma, Rivers
Marianne, Schimpl
Graham F, Smith
Sharon, Tentarelli
Jon, Travers
Robert I, Troup
Josephine, Walton
Cheng, Wang
Stephen, Wilkinson
Beth, Williamson
Jon, Winter-Holt
Dejian, Yang
Yuting, Zheng
Qianxiu, Zhu
Paul D, Smith
Source :: Journal of medicinal chemistry. 64(18)
Publication Year :: 2021
Abstract: Inhibition of Mer and Axl kinases has been implicated as a potential way to improve the efficacy of current immuno-oncology therapeutics by restoring the innate immune response in the tumor microenvironment. Highly selective dual Mer/Axl kinase inhibitors are required to validate this hypothesis. Starting from hits from a DNA-encoded library screen, we optimized an imidazo[1,2

Subjects :: Male
Molecular Structure
c-Mer Tyrosine Kinase
Pyridines
Imidazoles
Mice, Nude
Receptor Protein-Tyrosine Kinases
Antineoplastic Agents
Axl Receptor Tyrosine Kinase
Mice, Inbred C57BL
Structure-Activity Relationship
Cell Line, Tumor
Neoplasms
Proto-Oncogene Proteins
Animals
Female
Drug Screening Assays, Antitumor
Protein Kinase Inhibitors
Cell Proliferation

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