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Multiparameter Lead Optimization to Give an Oral Checkpoint Kinase 1 (CHK1) Inhibitor Clinical Candidate: (R)-5-((4-((Morpholin-2-ylmethyl)amino)-5-(trifluoromethyl)pyridin-2-yl)amino)pyrazine-2-carbonitrile (CCT245737).

Title: Multiparameter Lead Optimization to Give an Oral Checkpoint Kinase 1 (CHK1) Inhibitor Clinical Candidate: (R)-5-((4-((Morpholin-2-ylmethyl)amino)-5-(trifluoromethyl)pyridin-2-yl)amino)pyrazine-2-carbonitrile (CCT245737).
Authors: Osborne, JD; Matthews, TP; McHardy, T; Proisy, N; Cheung, K-MJ; Lainchbury, M; Brown, N; Walton, MI; Eve, PD; Boxall, KJ; Hayes, A; Henley, AT; Valenti, MR; De Haven Brandon, AK; Box, G; Jamin, Y; Robinson, SP; Westwood, IM; van Montfort, RLM; Leonard, PM; Lamers, MBAC; Reader, JC; Aherne, GW; Raynaud, FI; Eccles, SA; Garrett, MD; Collins, I
Contributors: Matthews, Thomas; McHardy, Tatiana; Jamin, Yann; Robinson, Simon; Van Montfort, Robert; Raynaud, Florence; Collins, Ian
Publisher Information: AMER CHEMICAL SOC
Publication Year: 2016
Collection: The Institute of Cancer Research (ICR): Publications Repository
Subject Terms: Humans; 4-Aminopyridine; Pyrazines; Protein Kinase Inhibitors; Molecular Structure; Structure-Activity Relationship; Dose-Response Relationship; Drug; Models; Molecular; Checkpoint Kinase 1
Description: Multiparameter optimization of a series of 5-((4-aminopyridin-2-yl)amino)pyrazine-2-carbonitriles resulted in the identification of a potent and selective oral CHK1 preclinical development candidate with in vivo efficacy as a potentiator of deoxyribonucleic acid (DNA) damaging chemotherapy and as a single agent. Cellular mechanism of action assays were used to give an integrated assessment of compound selectivity during optimization resulting in a highly CHK1 selective adenosine triphosphate (ATP) competitive inhibitor. A single substituent vector directed away from the CHK1 kinase active site was unexpectedly found to drive the selective cellular efficacy of the compounds. Both CHK1 potency and off-target human ether-a-go-go-related gene (hERG) ion channel inhibition were dependent on lipophilicity and basicity in this series. Optimization of CHK1 cellular potency and in vivo pharmacokinetic-pharmacodynamic (PK-PD) properties gave a compound with low predicted doses and exposures in humans which mitigated the residual weak in vitro hERG inhibition.
Document Type: article in journal/newspaper
File Description: Print-Electronic; 5237; application/pdf
Language: English
ISSN: 1520-4804; 0022-2623
Relation: Journal of medicinal chemistry, 2016, 59 (11), pp. 5221 - 5237; https://repository.icr.ac.uk/handle/internal/46
DOI: 10.1021/acs.jmedchem.5b01938
Availability: https://doi.org/10.1021/acs.jmedchem.5b01938; https://repository.icr.ac.uk/handle/internal/46
Rights: https://creativecommons.org/licenses/by/4.0
Accession Number: edsbas.F369CA00
Database: BASE