Evidence map›Paper›PMID 36121385›Full record

ArticleMolecular cancer therapeutics2022

Anticancer Activity of ST101, A Novel Antagonist of CCAAT/Enhancer Binding Protein β.

Emad Darvishi, Lila Ghamsari, Siok F Leong, Ricardo Ramirez, Mark Koester, Erin Gallagher, Miao Yu, Jody M Mason, Gene Merutka, Barry J Kappel and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Next-generation therapeutics for glioblastoma: Challenges and future directions.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Emad DarvishiSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0003-4209-6162
Lila GhamsariSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0002-8914-2114
Siok F LeongSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0003-0011-3999
Ricardo RamirezSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0003-3453-6164
Mark KoesterSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0003-4559-6568
Erin GallagherSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0002-6020-9418
Miao YuDepartment of Biology & Biochemistry, University of Bath, Claverton Down, Bath, United Kingdom.ORCID 0000-0003-1743-4043
Jody M MasonDepartment of Biology & Biochemistry, University of Bath, Claverton Down, Bath, United Kingdom.ORCID 0000-0002-4118-1958
Gene MerutkaSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0001-5447-2554
Barry J KappelSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0002-0344-8826
Jim A RotoloSapience Therapeutics, Inc., Harrison, New York.ORCID 0000-0003-4195-6167
Io Therapeutics (United States) · USUniversity of Bath · GB

Funding

Efficacy and PK/PD of a C/EBP beta antagonist in orthotopic breast cancerR43CA250786 · NCI · SAPIENCE THERAPEUTICS, INC. · PI ROTOLO, JIM · 2020 to 2020
$255k
NCI NIH HHS R43 CA250786
6 · The paper itself

Abstract

CCAAT/enhancer binding protein β (C/EBPβ) is a basic leucine zipper (bZIP) family transcription factor, which is upregulated or overactivated in many cancers, resulting in a gene expression profile that drives oncogenesis. C/EBPβ dimerization regulates binding to DNA at the canonical TTGCGCAA motif and subsequent transcriptional activity, suggesting that disruption of dimerization represents a powerful approach to inhibit this previously "undruggable" oncogenic target. Here we describe the mechanism of action and antitumor activity of ST101, a novel and selective peptide antagonist of C/EBPβ that is currently in clinical evaluation in patients with advanced solid tumors. ST101 binds the leucine zipper domain of C/EBPβ, preventing its dimerization and enhancing ubiquitin-proteasome dependent C/EBPβ degradation. ST101 exposure attenuates transcription of C/EBPβ target genes, including a significant decrease in expression of survival, transcription factors, and cell-cycle-related proteins. The result of ST101 exposure is potent, tumor-specific in vitro cytotoxic activity in cancer cell lines including glioblastoma, breast, melanoma, prostate, and lung cancer, whereas normal human immune and epithelial cells are not impacted. Further, in mouse xenograft models ST101 exposure results in potent tumor growth inhibition or regression, both as a single agent and in combination studies. These data provide the First Disclosure of ST101, and support continued clinical development of ST101 as a novel strategy for targeting C/EBPβ-dependent cancers.

Indexed as

Antineoplastic AgentsCCAAT-Enhancer-Binding Protein-betaAnimalsCell Cycle ProteinsCell LineHumansMiceNeoplasms, ExperimentalProtein BindingAntineoplastic AgentsCCAAT-Enhancer-Binding Protein-betaCell Cycle Proteins

Identifiers

PMID36121385
PMCPMC9630826
OpenAlexW4296325200

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.