Achieving In Vivo Target Depletion through the Discovery and Optimization of Benzimidazolone BCL6 Degraders.

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Authors

Bellenie, BR
Cheung, K-MJ
Varela, A
Pierrat, OA
Collie, GW
Box, GM
Bright, MD
Gowan, S
Hayes, A
Rodrigues, MJ
Shetty, KN
Carter, M
Davis, OA
Henley, AT
Innocenti, P
Johnson, LD
Liu, M
de Klerk, S
Le Bihan, Y-V
Lloyd, MG
McAndrew, PC
Shehu, E
Talbot, R
Woodward, HL
Burke, R
Kirkin, V
van Montfort, RLM
Raynaud, FI
Rossanese, OW
Hoelder, S

Document Type

Journal Article

Date

2020-04-23

Date Accepted

Date Available

Abstract

Deregulation of the transcriptional repressor BCL6 enables tumorigenesis of germinal center B-cells, and hence BCL6 has been proposed as a therapeutic target for the treatment of diffuse large B-cell lymphoma (DLBCL). Herein we report the discovery of a series of benzimidazolone inhibitors of the protein-protein interaction between BCL6 and its co-repressors. A subset of these inhibitors were found to cause rapid degradation of BCL6, and optimization of pharmacokinetic properties led to the discovery of 5-((5-chloro-2-((3R,5S)-4,4-difluoro-3,5-dimethylpiperidin-1-yl)pyrimidin-4-yl)amino)-3-(3-hydroxy-3-methylbutyl)-1-methyl-1,3-dihydro-2H-benzo[d]imidazol-2-one (CCT369260), which reduces BCL6 levels in a lymphoma xenograft mouse model following oral dosing.

Citation

Journal of medicinal chemistry, 2020, 63 (8), pp. 4047 - 4068

Source Title

Publisher

AMER CHEMICAL SOC

ISSN

0022-2623

eISSN

1520-4804

Research Team

Cancer Pharmacology & Stress Response (CPSR)
Clinical Pharmacology & Trials (including Drug Metabolism & Pharmacokinetics Group)
Medicinal Chemistry 4 (including Analytical Chemistry)
Hit Discovery & Structural Design

Notes