Evidence map›Paper›PMID 42847058›Full record

ArticleJournal of clinical haematology2025

Repurposing Nilotinib as a Selective P38β Inhibitor in Hematopoietic Malignancies: Clinical Evidence and Mechanistic Insights.

Xu Hannah Zhang, Jack Hsiang, Sangkil Nam, Hongzhi Li, Yate-Ching Yuan, Xiwei Wu, Susan Hmwe, Roger Moore, Steven T Rosen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical haematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Xu Hannah ZhangDepartment of Hematology & Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Jack HsiangDepartment of Hematology & Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Sangkil NamHigh Throughput Screening Core Shared research facility, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Hongzhi LiBioinformatics Core Shared Research Facilities, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Yate-Ching YuanBioinformatics Core Shared Research Facilities, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Xiwei WuIntegrative Genomics Core Shared Research Facilities, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Susan HmweDepartment of System Clinical Trial Technology & Data Solutions Department, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Roger MooreIntegrated Mass Spectrometry Core Facility, Beckman Research Institute, City of Hope, Duarte, CA, USA.
Steven T RosenDepartment of Hematology & Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA, USA.

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI STANLEY R. HAMILTON · 1985 to 2026
$86.3M
Targeting p38 gamma signaling to advance Cutaneous T Cell Lymphoma TherapyR01CA233922 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI ROSEN, STEVEN TERRY · 2019 to 2023
$3.4M
NCI NIH HHS P30 CA033572NCI NIH HHS R01 CA233922
6 · The paper itself

Abstract

Background: Cutaneous T cell lymphoma (CTCL) is an incurable cancer characterized by elevated p38β and p38γ and downregulated tumor-suppressive p38α. Objectives: We aimed to identify selective p38β inhibitors and investigate their mechanisms and therapeutic implications in hematologic malignancies. Methods: A high-throughput screen of Food and Drug Administration (FDA)-approved compounds was conducted to identify p38β inhibitors. Results: Nilotinib was identified as a selective p38β inhibitor (~25-fold over p38α). Its inhibition of p38β led to compensatory activation of p38γ, driving Epithelial-to-Mesenchymal Transition (EMT) and potential toxicities. Combining Nilotinib with p38γ inhibitors (e.g., CSH71 or Paclitaxel) produced synergistic anti-tumor effects in CTCL and leukemia cells. Clinical and FDA Adverse Event Reporting System (FAERS) data revealed higher toxicity rates for Nilotinib in Ph Conclusion: Nilotinib selectively inhibits p38β but activates p38γ, potentially reducing therapeutic selectivity. Combining it with p38γ inhibitors may enhance efficacy and reduce toxicity across hematologic malignancies.

Indexed as

Chronic myeloid leukemiaClinical trialsCutaneous T cell lymphomaNilotinibPaclitaxel

Identifiers

PMID42847058
PMCPMC13645396

What OpenQuestion holds

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Registered trials

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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.