Evidence map›Paper›PMID 36988504›Full record

ArticleAging2023

Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolytic.

Fares Al-Mansour, Abdullah Alraddadi, Buwei He, Anes Saleh, Marta Poblocka, Wael Alzahrani, Shaun Cowley, Salvador Macip

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
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  16. Article
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

8 authors at 1 institution in 3 countries.

Fares Al-MansourMechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom.
Abdullah AlraddadiMechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom.
Buwei HeMechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom.
Anes SalehMechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom.
Marta PoblockaMechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom.
Wael AlzahraniMechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom.
Shaun CowleyDepartment of Molecular and Cell Biology, University of Leicester, Leicester LE1 7RH, United Kingdom.
Salvador MacipMechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom.
University of Leicester · GB

Funding

Medical Research Council MR/W00190X/1
6 · The paper itself

Abstract

The accumulation of senescent cells has an important role in the phenotypical changes observed in ageing and in many age-related pathologies. Thus, the strategies designed to prevent these effects, collectively known as senotherapies, have a strong clinical potential. Senolytics are a type of senotherapy aimed at specifically eliminating senescent cells from tissues. Several small molecule compounds with senolytic properties have already been identified, but their specificity and range of action are variable. Because of this, potential novel senolytics are being actively investigated. Given the involvement of HDACs and the PI3K pathway in senescence, we hypothesized that the dual inhibitor CUDC-907, a drug already in clinical trials for its antineoplastic effects, could have senolytic effects. Here, we show that CUDC-907 was indeed able to selectively induce apoptosis in cells driven to senesce by p53 expression, but not when senescence happened in the absence of p53. Consistent with this, CUDC-907 showed senolytic properties in different models of stress-induced senescence. Our results also indicate that the senolytic functions of CUDC-907 depend on the inhibitory effects of both HDACs and PI3K, which leads to an increase in p53 and a reduction in BH3 pro-survival proteins. Taken together, our results show that CUDC-907 has the potential to be a clinically relevant senolytic in pathological conditions in which stress-induced senescence is involved.

Indexed as

Histone Deacetylase InhibitorsPhosphatidylinositol 3-KinasesCellular SenescenceMorpholinesPhosphoinositide-3 Kinase InhibitorsPyrimidinesSenotherapeuticsTumor Suppressor Protein p53CUDC-907Histone Deacetylase InhibitorsMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPyrimidinesSenotherapeuticsTumor Suppressor Protein p53CUDC-907HDACPI3Ksenescencesenolytics

Identifiers

PMID36988504
PMCPMC10120895
OpenAlexW4361301939

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.