Improved Binding Affinity and Pharmacokinetics Enable Sustained Degradation of BCL6 In Vivo.

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Authors

Huckvale, R
Harnden, AC
Cheung, K-MJ
Pierrat, OA
Talbot, R
Box, GM
Henley, AT
de Haven Brandon, AK
Hallsworth, AE
Bright, MD
Akpinar, HA
Miller, DSJ
Tarantino, D
Gowan, S
Hayes, A
Gunnell, EA
Brennan, A
Davis, OA
Johnson, LD
de Klerk, S
McAndrew, C
Le Bihan, Y-V
Meniconi, M
Burke, R
Kirkin, V
van Montfort, RLM
Raynaud, FI
Rossanese, OW
Bellenie, BR
Hoelder, S

Document Type

Journal Article

Date

2022-06-23

Date Accepted

2022-06-03

Abstract

The transcriptional repressor BCL6 is an oncogenic driver found to be deregulated in lymphoid malignancies. Herein, we report the optimization of our previously reported benzimidazolone molecular glue-type degrader CCT369260 to CCT373566, a highly potent probe suitable for sustained depletion of BCL6 in vivo. We observed a sharp degradation SAR, where subtle structural changes conveyed the ability to induce degradation of BCL6. CCT373566 showed modest in vivo efficacy in a lymphoma xenograft mouse model following oral dosing.

Citation

Journal of Medicinal Chemistry, 2022, 65 (12), pp. 8191 - 8207

Source Title

Journal of Medicinal Chemistry

Publisher

AMER CHEMICAL SOC

ISSN

0022-2623

eISSN

1520-4804
1520-4804

Research Team

Hit Discov Struct Design
Clinical Pharma & Trials
Directorate Canc Ther
Medicinal Chemistry 4

Notes