Evidence map›Paper›PMID 42562963›Full record

ReviewProstate cancer and prostatic diseases2026

From fungus fighter to cancer slayer: itraconazole as a multifaceted candidate for drug-resistant prostate cancer.

Luciano O Souza, Despoina G Papoutsi, José M A Moreira

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In one paragraph

Review in Prostate cancer and prostatic diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

3 authors.

Luciano O SouzaDepartment of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Despoina G PapoutsiDepartment of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
José M A MoreiraDepartment of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. jomo@sund.ku.dk.ORCID http://orcid.org/0000-0002-9944-1214

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetastatic castration-resistant prostate cancer (mCRPC) remains a lethal disease state with limited durable responses to existing therapies, including taxane-based chemotherapy. Resistance mechanisms are multifactorial and incompletely addressed by current treatments. Drug repurposing offers an accelerated pathway for the development of novel therapeutic strategies in treatment-resistant disease.

methodsThis review synthesizes preclinical mechanistic data and clinical experience with itraconazole (ITZ), a clinically approved triazole antifungal, across prostate cancer and other malignancies. We evaluate the signaling pathways targeted by ITZ, barriers to its clinical translation, and opportunities for biomarker-driven combination therapy.

resultsITZ functions as a pleiotropic anticancer compound that modulates multiple pathways implicated in prostate cancer progression and therapeutic resistance, including Hedgehog/GLI, PI3K/AKT/mTOR, and Wnt/β-catenin signaling, as well as drug efflux transporters. Preclinical studies demonstrate that ITZ reverses ABCB1-mediated docetaxel resistance, suppresses Hedgehog/GLI1 signaling, and inhibits cancer cell proliferation and invasion. Despite compelling mechanistic rationale, clinical activity in mCRPC has been modest, with limited durable responses, underscoring a translational disconnect. Advancement of ITZ into clinical practice is constrained by pharmacokinetic challenges, dose-limiting toxicities, and the lack of validated predictive biomarkers to identify responsive patient subsets. Emerging evidence further suggests potential synergy with immune checkpoint inhibitors through tumor microenvironment modulation, though this remains unexplored in prostate cancer.

conclusionsITZ represents a potential adjunctive strategy to standard therapies within rationally designed, biomarker-stratified combination regimens for mCRPC. Target populations include patients with PTEN-null tumors (elevated Hh/GLI and PI3K/AKT signaling), ABCB1-overexpressing tumors (taxane resistance), or those progressing after AR pathway inhibitor therapy. Clinical advancement will require pharmacological optimization, development and validation of patient stratification biomarkers (GLI1/PTCH1, PTEN status, ABCB1 expression), and integration with therapies targeting complementary resistance pathways.

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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.