Itraconazole Reverts ABCB1-Mediated Docetaxel Resistance in Prostate Cancer
Open accessAbstract
Docetaxel (DTX) was the first chemotherapeutic agent to demonstrate significant efficacy in the treatment of men with metastatic castration-resistant prostate cancer. However, response to DTX is generally short-lived, and relapse eventually occurs due to emergence of drug-resistance. We previously established two DTX-resistant prostate cancer cell lines, LNCaP R and C4-2B R , derived from the androgen‐dependent LNCaP cell line, and from the LNCaP lineage-derived androgen-independent C4-2B sub-line, respectively. Using an unbiased drug screen, we identify itraconazole (ITZ), an oral antifungal drug, as a compound that can efficiently re-sensitize drug-resistant LNCaP R and C4-2B R prostate cancer cells to DTX treatment. ITZ can re-sensitize multiple DTX-resistant cell models, not only in prostate cancer derived cells, such as PC-3 and DU145, but also in docetaxel-resistant breast cancer cells. This effect is dependent on expression of ATP-binding cassette (ABC) transporter protein ABCB1, also known as P-glycoprotein (P-gp). Molecular modeling of ITZ bound to ABCB1, indicates that ITZ binds tightly to the inward-facing form of ABCB1 thereby inhibiting the transport of DTX. Our results suggest that ITZ may provide a feasible approach to re-sensitization of DTX resistant cells, which would add to the life-prolonging effects of DTX in men with metastatic castration-resistant prostate cancer.
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ITZ synergy with docetaxel has been inferred against prostate and MCF-7 drug-resistant breast cancer cells.
“Regarding hedgehog signaling pathway, its synergy with docetaxel has been inferred against prostate and MCF-7 drug-resistant-breast cancer cells, though prior mechanisms has been also stated.85,94,95”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [85]
The Results report that itraconazole reversed docetaxel resistance in prostate cancer cell lines, but explicitly say it failed to reverse resistance in MCF-7R breast cancer cells. The Discussion attributes the observed prostate-cell effect to ABCB1 inhibition, not an established hedgehog-signaling mechanism. Page numbers are not available in the supplied copy. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredITZ synergy with docetaxel has been inferred against prostate and MCF-7 drug-resistant breast cancer cells.
“Regarding hedgehog signaling pathway, its synergy with docetaxel has been inferred against prostate and MCF-7 drug-resistant-breast cancer cells, though prior mechanisms has been also stated.85,94,95”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [94]
The Results report that itraconazole combined with docetaxel reversed resistance in prostate cancer cell lines (Figure 2). But the breast cancer Results state that itraconazole failed to reverse docetaxel resistance in MCF-7R cells (Figure 3A), contrary to that part of the claim. The Discussion attributes the observed effect to ABCB1 inhibition, not to hedgehog-pathway inhibition. (LLM, conf=0.89)
Experimental — accuracy not yet measuredITZ has acceptable synergistic effects with various anticancer agents, including paclitaxel, cisplatin, and docetaxel, mainly through antiangiogenic pathways, hedgehog signaling inhibition, and effects on drug efflux pumps.
“Accordingly, ITZ has deciphered acceptable synergistic effects with various anticancer agents, including paclitaxel, cisplatin, and docetaxel, mainly through mechanisms such as antiangiogenic pathways, hedgehog signaling inhibition, and effects on drug efflux pumps.”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [85]
The Results and Discussion (pages unavailable) report that itraconazole reverses docetaxel resistance in cancer cell lines by inhibiting ABCB1-mediated drug efflux. The Introduction mentions paclitaxel as an ABCB1 substrate, but the paper does not report an itraconazole combination effect with paclitaxel or cisplatin. It describes hedgehog inhibition as a possible mechanism in another cell line, not the established mechanism for its docetaxel result, and does not establish an antiangiogenic mechanism for the claimed combinations. (LLM, conf=0.88)
Experimental — accuracy not yet measuredITZ can re-sensitize a variety of docetaxel-resistant cell types, including docetaxel-resistant breast cancer cells and prostate cancer PC-3 and DU145 cells.
“ITZ can re-sensitize a variety of DTX-resistant cell types, including docetaxel-resistant breast cancer cells as well as cells derived from prostate cancer, including PC-3 and DU145.”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [85]
ITZ might offer a workable method for re-sensitizing docetaxel-resistant cells, enhancing the treatment's ability to prolong life in men with metastatic castration-resistant prostate cancer.
“These findings implied that ITZ might offer a workable method for re-sensitizing DTX-resistant cells, enhancing the treatment's ability to prolong life in men with metastatic castration-resistant prostate cancer.”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [85]
ITZ effectively re-sensitizes drug-resistant LNCaPR and C4-2BR prostate cancer cells to docetaxel treatment.
“An objective drug screen was used in this study to determine that the oral antifungal medication ITZ effectively re-sensitizes drug-resistant LNCaPR and C4-2BR prostate cancer cells to DTX treatment.”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [85]
Expression of the ATP-binding cassette transporter protein ABCB1 (P-glycoprotein) is necessary for ITZ re-sensitization of docetaxel-resistant cells.
“The expression of the ATP-binding cassette (ABC) transporter protein ABCB1, often referred to as P-glycoprotein (P-gp), is necessary for this action.”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [85]
ITZ binds firmly to the inward-facing form of ABCB1, blocking the transport of docetaxel.
“ITZ binds firmly to the inward-facing form of ABCB1, blocking the transport of DTX, according to molecular modeling of ITZ bound to ABCB1.”
From Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights (2026) · cites this paper as [85]
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Self-citationPreclinical evaluation of itraconazole in docetaxel-resistant prostate cancer xenograft models
Souza, L. O., Bartels, A., & Moreira, J. M. A. (2026) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2026.179218
Self-citationItraconazole induced ferroptosis in acute myeloid leukemia cells through TP53INP1
Qi, Y., Han, C., Lin, Y., Cheng, S., She, Y., Zhang, M., Xie, H., Guangming, Y., & Zeng, D. (2026) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2026.1890539
Sun, Y. (2026) · Pakistan Journal of Pharmaceutical Sciences · doi:10.36721/pjps/2026.40.15730.1
- Authors
- Lima, T. S., Souza, L. O., Iglesias-Gato, D., Elversang, J., Jørgensen, F. S., Kallunki, T., Røder, M. A., Brasso, K., & Moreira, J. M. A.
- Affiliations
- University of Copenhagen (DK)
- Copenhagen University Hospital (DK)
- Corresponding author
- Moreira, José M.A.
- ORCID
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2022-06-03
- Volume
- 13
- Pages
- 869461-869461
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC9203833
- OpenAlex
- W4281623335
- Cited by
- 26
- References
- 50
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 3 · 2023: 6 · 2022: 2
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (BEX 13421/13-1)
- Kræftens Bekæmpelse (R90-A6109)
- Danmarks Grundforskningsfond (DNRF125)
- Topics
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
- Keywords
- itraconazole, docetaxel resistance, P-glycoprotein, ABC transporters, castration-resistant prostate cancer, drug re-sensitization, LNCaP cells, breast cancer, molecular modeling, antifungal drug repurposing
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