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Poster Display session

155P - Targeting colorectal cancer by sequestration of beta-catenin in nuclear condensates

Date

27 Jun 2024

Session

Poster Display session

Presenters

Kip West

Citation

Annals of Oncology (2024) 35 (suppl_1): S1-S74. 10.1016/annonc/annonc1477

Authors

K.A. West1, C. Salojin1, D. Baumann1, A. Talbot1, T. Durand-Reville1, S. Sirdeshmukh1, U. Zanelli2, I. Klein1, A. Boija1

Author affiliations

  • 1 Dewpoint Therapeutics, Inc., Boston/US
  • 2 Dewpoint Therapeutics GmbH, Frankfurt am Main/DE

Resources

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Abstract 155P

Background

Many malignancies are driven by aberrant activation of the beta catenin signaling pathway, notably colorectal cancer (CRC). Despite extensive biological insights into the underlying mechanism, targeted therapeutic approaches have largely been unsuccessful, deeming beta catenin ‘undruggable’. Recent research has shed light on the essential role of biomolecular condensates in orchestrating numerous cellular processes and biological pathways through membraneless compartmentalization of biomolecules. In this study, we apply emerging insights gleaned from condensate biology to discover small molecules, condensate-modifying compounds (c-mods), that inhibit the transcriptionally hyperactive beta-catenin found in CRC via sequestration within nuclear depot condensates.

Methods

We employed high content, high throughput phenotypic screening to identify and optimize small molecules that drive beta catenin into nuclear puncta. Cancer cell proliferation was quantified using CTG assays and gene expression profiles obtained using qPCR assays. Visualization of phospho-beta-catenin in nuclear depot condensates was accomplished by employing immunofluorescent IHC analysis. C-mods were profiled in xenograft and PDX models of CRC.

Results

We have identified c-mods that induce beta catenin depot condensates. We demonstrate that c-mods act on-pathway and selectively kill cancer cells both in vitro and ex vivo. Oral dosing of c-mods, as single agents, in xenograft and PDX CRC mouse models exhibits competitive tumor growth inhibition. In PK/PD studies in CRC xenografts, c-mod tumor exposure correlates with dose-dependent modulation of beta catenin-driven gene transcription; IHC of tumors from these studies demonstrates robust beta catenin depot formation. Finally, combination treatment of c-mods with the standard of care in CRC enhanced its anti-tumor activity in a CRC xenograft model, highlighting the potential for first-line therapeutic intervention in CRC.

Conclusions

These findings underscore the potential of condensate biology in targeting challenging, high-value oncology targets, historically deemed ‘undruggable’, and pioneering novel medicines for cancer patients with critical unmet medical needs.

Legal entity responsible for the study

Dewpoint Therapeutics, Inc.

Funding

Dewpoint Therapeutics, Inc.

Disclosure

K.A. West, C. Salojin, D. Baumann, A. Talbot, T. Durand-Reville, S. Sirdeshmukh, U. Zanelli, I. Klein, A. Boija: Financial Interests, Personal, Full or part-time Employment: Dewpoint Therapeutics.

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