Fenbendazole is widely known as a broad-spectrum antiparasitic drug used to treat internal parasites. It belongs to the benzimidazole family, a class of compounds that work by binding to β-tubulin, a structural protein essential for forming microtubules in parasitic worms. Microtubules act like the internal scaffolding of a cell; when they are disrupted, parasites cannot absorb nutrients and eventually die (Prichard, 1979). Beyond its approved use, fenbendazole has become a major subject of interest in off-label oncology due to multiple scientific studies showing strong anticancer effects in laboratory research.

This article provides a clear and comprehensive explanation of fenbendazole’s anticancer mechanisms, including treatment and prevention relevance. 

1. Why Fenbendazole Entered Cancer Research
 

Interest in fenbendazole as an anticancer compound intensified after research revealed that many benzimidazoles interfere with microtubules—the same cellular structures targeted by major chemotherapy drugs. Fenbendazole targets multiple cancer-related pathways simultaneously, including microtubules, glucose metabolism, p53 signalling, mitochondrial function, and programmed cell-death pathways. Multi-target drugs are of great interest in oncology because tumours often adapt quickly to single-target therapies. It is important to note that fenbendazole has a long track record of low toxicity in animals, which makes it a particularly attractive candidate for drug repurposing. 
                                                                               
 

2. Microtubule Disruption – How Fenbendazole Interferes With Cancer Cell Division
 

Microtubules are tiny hollow tubes that form part of the cell’s internal skeleton (the cytoskeleton). They are essential for maintaining cell shape, transporting molecules, and, most importantly, separating chromosomes during cell division. When microtubules are destabilised, cells cannot divide properly.

Fenbendazole binds to β-tubulin and prevents microtubules from forming correctly. Dogra et al. (2018) demonstrated that fenbendazole disorganises the microtubule network, blocks mitosis (cell division), activates stress-response pathways, and suppresses tumour growth in mice.

An analogy helps: microtubules are like the “rails” a cell uses to divide. Fenbendazole removes sections of these rails, making division impossible.

This microtubule-based anticancer mechanism has been confirmed in colorectal cancer (Park et al., 2022), ovarian cancer (Wang et al., 2024), lung cancer (Dogra et al., 2018), and cervical cancer (Lei et al., 2025).
 

3. Metabolic Inhibition – Fenbendazole Starves Cancer Cells
 

Cancer cells rely heavily on altered metabolism, especially high glucose uptake and glycolysis, known as the Warburg effect. This metabolic strategy allows them to produce energy quickly, even if inefficiently, to support rapid division.             

Nguyen et al. (2024) showed that fenbendazole significantly disrupts tumour metabolism by reducing glucose uptake, inhibiting GLUT1 (glucose transporter 1), reducing activity of glycolytic enzymes, and lowering ATP production.



Analogy: if cancer cells are engines constantly revving at maximum speed, fenbendazole partially closes the fuel valve.

Because metabolic rewiring occurs early in cancer formation, this mechanism is frequently cited by people using fenbendazole off-label for preventive purposes.

4. Triggering Cancer Cell Death – Apoptosis, Mitotic Catastrophe, Pyroptosis
 

Fenbendazole can induce multiple forms of programmed cell death, each with distinct mechanisms. Below are clear definitions and explanations of how fenbendazole triggers each.

Apoptosis
 

Definition: apoptosis is a clean, controlled form of programmed cell death in which the cell dismantles itself without causing inflammation. It is the body’s natural method for removing damaged or dangerous cells.

Dogra et al. (2018) demonstrated that fenbendazole activates the tumour-suppressor protein p53. When p53 is triggered, the cell checks its DNA; if damage is too severe, p53 instructs the cell to undergo apoptosis.

Thus, fenbendazole helps encourage the elimination of mutated or unstable cells.

Mitotic Catastrophe
 

Definition: mitotic catastrophe is a form of cell death resulting from failed or abnormal cell division. It occurs when chromosomes are not separated properly or when the spindle apparatus is defective.

Wang et al. (2024) showed that fenbendazole causes chromosome missegregation and mitotic failure in ovarian cancer cells, ultimately leading to cell death. This pathway is especially effective against fast-dividing tumours.

Pyroptosis
 

Definition: pyroptosis is a highly inflammatory form of programmed cell death characterised by cell swelling, membrane rupture, and release of immune-stimulating molecules. It is mediated by a protein family called gasdermins.

Pan et al. (2025) discovered that fenbendazole induces pyroptosis in breast cancer cells by triggering metabolic stress and activating gasdermin proteins. This type of cell death not only kills tumour cells but may also recruit immune cells to target the tumour environment.

Fenbendazole’s ability to activate multiple death pathways simultaneously is unusual and makes it stand out among repurposing candidates.

5. Gene Expression Changes – A Broad, Multilevel Disruption
 

Gene expression refers to how cells interpret their DNA and produce proteins. Cancer cells must modify the expression of hundreds or thousands of genes to maintain their abnormal growth.

Wang et al. (2024) performed a transcriptomic analysis and found that fenbendazole alters over 1,700 genes, including many involved in mitosis, metabolism, DNA repair, apoptosis, and chromosome segregation.

This broad genetic disruption makes it far harder for cancer cells to adapt or become resistant.

6. Fenbendazole in Drug-Resistant Cancers
 

Drug resistance is one of the most serious challenges in oncology. Park et al. (2022) studied colorectal cancer cells resistant to the common chemotherapy drug 5-fluorouracil (5-FU). They found that fenbendazole induces apoptosis, triggers cell-cycle arrest, and kills resistant clones even when the p53 pathway is defective.

This suggests fenbendazole may attack fundamental cellular weaknesses that remain even when tumours become resistant to standard treatments.

7. Fenbendazole in Cancer Prevention – Scientific Rationale
 

Although officially unproven in humans, the rationale behind using fenbendazole off-label for cancer prevention involves four key mechanistic ideas.

• First, microtubule disruption may help remove early abnormal cells before they form tumours.

• Second, metabolic suppression prevents precancerous cells from acquiring the metabolic flexibility needed for tumour development.

• Third, activation of apoptosis and mitotic catastrophe may eliminate mutated cells that would otherwise survive.

• Fourth, fenbendazole’s broad gene-expression disruption may interfere with early tumour-initiating programs.
   

8. What the Scientific Community Currently Agrees On
 

Fenbendazole is promising due to strong preclinical data, multi-pathway action, and low animal toxicity. It may synergise with other drugs and appears effective in numerous drug-resistant cancer models. Its ability to target microtubules, disrupt glucose metabolism, impair mitochondrial function, and trigger several programmed cell-death pathways simultaneously — including p53-dependent apoptosis, mitotic catastrophe, and gasdermin-mediated pyroptosis — makes it mechanistically compelling. The compound also modulates stress-response networks such as HIF-1α and NF-κB, reduces antioxidant capacity in certain tumour types, and enhances the vulnerability of malignant cells to metabolic and chemotherapeutic pressure. This convergence of antimitotic, metabolic, and immunogenic mechanisms, together with favourable tolerability in animal studies, positions fenbendazole as a notable candidate for further scientific investigation and combination-strategy research.


 

References
 

Dogra, N., Kumar, A. and Mukhopadhyay, T. (2018) ‘Fenbendazole acts as a moderate microtubule destabilising agent and causes cancer cell death by modulating multiple cellular pathways’, Scientific Reports, 8, 11926.

Golla, U., Pan, Y. and Yang, H. (2024) ‘From Deworming to Oncology: Benzimidazoles as Emerging Anticancer Agents’, Cancers, 16(20), 3454.

Lei, X., Zhang, Y. and Huang, W. (2025) ‘Fenbendazole Exhibits Antitumor Activity Against Cervical Cancer Cells and Cancer-Associated Fibroblasts’, Molecules, 30(11), 2377.

Makis, W. (2025) ‘Fenbendazole as an Anticancer Agent? A Case Series of Self-Administration in Advanced Cancer’, Case Reports in Oncology, 18(1), 856–866.

Nguyen, J., Hassan, A. and Lee, D. (2024) ‘Fenbendazole Inhibits Glycolysis and Glucose Uptake in Human Cancer Cells’, Anticancer Research, 44(9), 3725–3734.

Pan, T., Li, R. and Zhong, W. (2025) ‘Fenbendazole Induces Pyroptosis in Breast Cancer Cells Through Metabolic Reprogramming’, Frontiers in Pharmacology, 16, 1596694.

Park, D., Kim, S. and Yoo, J. (2022) ‘Anti-Cancer Effects of Fenbendazole on 5-Fluorouracil-Resistant Colorectal Cancer Cells’, Oncology Letters, 24(1), 43.

Prichard, R. (1979) ‘Mode of Action of Benzimidazoles’, Parasitology, 79(2), 249–262.

Rahman, M., Singh, A. and Gupta, R. (2023) ‘Fenbendazole-Loaded Nanoparticles Enhance Anticancer Activity in Solid Tumours’, International Journal of Nanomedicine, 18, 6023–6041.

Wang, X., Zhao, Y. and Li, H. (2024) ‘Transcriptome Analysis Reveals the Anticancer Effects of Fenbendazole in Ovarian Cancer Cells and Xenograft Models’, BMC Cancer, 24, 13361.