Structural Basis of p97 Inhibition by the Site-Selective Anticancer Compound CB-5083.


Journal

Molecular pharmacology
ISSN: 1521-0111
Titre abrégé: Mol Pharmacol
Pays: United States
ID NLM: 0035623

Informations de publication

Date de publication:
03 2019
Historique:
received: 10 09 2018
accepted: 20 12 2018
pubmed: 29 12 2018
medline: 18 6 2019
entrez: 29 12 2018
Statut: ppublish

Résumé

Inhibition of p97, a key player in the ubiquitin-proteasome degradation pathway, has been proposed as a treatment of cancer. This concept was nearly realized recently when a potent p97 inhibitor, 1-[4-(benzylamino)-5H,7H,8H-pyrano[4,3-d]pyrimidin-2-yl]-2-methyl-1H-indole-4-carboxamide (CB-5083), was developed and demonstrated broad antitumor activity in various tumor models. CB-5083 functions as a competitive inhibitor that binds selectively to the ATP-binding site of the D2 domain, although both the D1 and D2 ATPase sites of p97 are highly similar. Despite its promising anticancer activity, CB-5083 failed its phase I clinical trials due to an unexpected off-target effect, which necessitates further improvement of the inhibitor. In this study, we determined the crystal structure of N-terminal domain-truncated p97 in complex with CB-5083. It provides a structural basis for the specificity of CB-5083 toward the D2 domain, offers an explanation in atomic detail for the mutations that confer resistance to CB-5083, and establishes a foundation for future structure-guided efforts to develop the next generation of p97 inhibitors.

Identifiants

pubmed: 30591537
pii: mol.118.114256
doi: 10.1124/mol.118.114256
pmc: PMC6355941
doi:

Substances chimiques

Antineoplastic Agents 0
CB-5083 0
Indoles 0
Nuclear Proteins 0
Pyrimidines 0
Adenosine Triphosphate 8L70Q75FXE
Adenosine Triphosphatases EC 3.6.1.-
p97 ATPase EC 3.6.1.-

Types de publication

Journal Article Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

286-293

Informations de copyright

U.S. Government work not protected by U.S. copyright.

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Auteurs

Wai Kwan Tang (WK)

Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Taivan Odzorig (T)

Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Whitney Jin (W)

Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Di Xia (D)

Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland xiad@mail.nih.gov.

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Classifications MeSH