Published July 24, 2025 | Version Supplemental material
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Antitumor Efficacy of 1,2,4-Triazole-Based VCP/p97 Allosteric Inhibitors

  • 1. ROR icon Frederick National Laboratory for Cancer Research
  • 2. ROR icon University of Pittsburgh
  • 3. Department of Medicinal Chemistry, Curia Global Inc, 33 Riverside Ave, Rensselaer, New York 12144, United States.
  • 4. ROR icon California Institute of Technology
  • 5. Department of Medicinal Chemistry, The Conventus, Curia Global Inc, 1001 Main St, Buffalo, New York 14203, United States.

Abstract

The AAA ATPase p97 (VCP) plays a crucial role in maintaining protein homeostasis through the ubiquitin-proteosome pathway, as well as other mechanisms. Due to the increased mutational load and protein quality control failures in cancer cells, p97 is a potential target for cancer therapy. Here, we highlight the optimization of the previously reported 3-thioalkyl-1,2,4-triazol-pyridyl allosteric inhibitor scaffold and identify two compounds (25 and 38) with low-nanomolar biochemical potency, submicromolar cellular inhibition, in vivo effects on biomarkers of VCP inhibition, and antitumor efficacy in mouse xenograft tumor models. Furthermore, compound 38 demonstrated robust inhibition of VCP ATP-site mutant proteins and growth of cells resistant to the known ATP-competitive inhibitor CB-5083.

Copyright and License

© 2025 American Chemical Society.

Acknowledgement

The authors acknowledge Barbara Mroczkowski (NCI), James Doroshow (NCI), and John Giraldes (NCI), contributing members of the Division of Cancer Treatment and Diagnosis (DCTD) at the National Cancer Institute (NCI), the Chemical Biology Consortium for project support, Michelle Arkin (UCSF) Han-Jie Zhou and Ronan Le Moigne (Cleave Biosciences–currently at ESSA Pharma) James Burnett (UPitt) and Po-Lin Chou (ASU) Stephan Stern, Krishna Kattel and Ruvanthi Kularatne (NCL) and Ray Deshaies (Caltech, Amgen) for helpful discussions; and Desirae Crocker (UPitt), Taber Maskrey (UPitt), and Zhizhou Yue (UPitt) for experimental contributions.

Funding

The project was funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under Chemical Biology Consortium Contract No. HHSN261200800001E.

Contributions

All authors have given approval to the final version of the manuscript. N.G., D.M.H., and P.W. wrote the manuscript. D.M.H., P.W., M.G.L., E.J.C., M.L., S.J., Z.V., P.M., and W.D.P. designed and/or synthesized compounds. F.W. and S.L. obtained biochemical and cell-based data in Tables 12, and 5. F.T. performed biomarker analysis. G.M.S., A.F., W.J.M., and N.G. helped with design of in vivo experiments. A.S., M.W., T.F.C., P.W., and D.M.H. supervised and directed experiments. D.M.H., P.W., and M.W. acquired funding.

Conflict of Interest

The authors declare no competing financial interest.

Supplemental Material

Plasmids for protein purification, antibodies for Western blots, methods for measuring MDCK cell permeability, additional xenograft studies, resistance mutants of VCP, NCI-60 cell line data, and spectral data for final compounds (PDF)

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Additional details

Identifiers

Related works

Describes
Journal Article: 40605370 (PMID)

Funding

National Cancer Institute
HHSN261200800001E

Dates

Submitted
2025-02-25
Updated
2025-06-13
Accepted
2025-06-23
Available
2025-07-03
Published online

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