Mebendazole for Thyroid Cancer: Promising Research or Premature Hype?

Thyroid cancer represents the most common endocrine malignancy worldwide. Among its subtypes, papillary thyroid cancer (PTC) accounts for roughly 80% of diagnosed cases. Although most patients experience favorable outcomes, a subset develops persistent or progressive disease. In these cases, tumors may dedifferentiate into anaplastic thyroid cancer (ATC) — an aggressive form with a median survival of just 5 to 6 months and a 1-year survival rate of approximately 20%. Because standard therapies often fail in advanced disease, researchers continue to explore safer and more effective treatment strategies.

Why This Matters
Anaplastic thyroid cancer is one of the most lethal human malignancies. Patients with radioiodine-refractory disease face extremely limited options, making drug repurposing research a critical area of investigation.

This comprehensive analysis examines the preclinical evidence, pharmacological challenges, and clinical translation barriers facing mebendazole as a potential thyroid cancer therapy. We evaluate the biological mechanisms, compare it to related benzimidazoles like fenbendazole, and assess what would be required for rigorous clinical validation.

The Role of Mebendazole in Thyroid Cancer Research

Recent preclinical research has examined mebendazole, a benzimidazole compound traditionally used as an antiparasitic medication, for its potential activity against thyroid cancer. A study conducted at Johns Hopkins University by Williamson et al. (2020) evaluated whether this well-known drug could suppress tumor growth and prevent metastasis, particularly during early disease stages before widespread progression occurs. Mebendazole belongs to the same benzimidazole class as fenbendazole and shares key structural and biological properties.

Illustration: Thyroid cellular pathways targeted by benzimidazole compounds

Mebendazole for Thyroid Cancer: Promising Research or Premature Hype?

In Vitro Activity Against Thyroid Cancer Cells

Laboratory experiments demonstrated that mebendazole inhibited growth across several human thyroid cancer cell lines. The compound reduced viability in both papillary (B-CPAP) and anaplastic (8505c) thyroid cancer cells. Researchers observed strong cytotoxic effects at low micromolar concentrations, causing:

• G2/M cell cycle arrest — blocking cancer cells from dividing
• Late-stage apoptosis — programmed cell death via activation of the caspase-3 pathway
• Inhibition of phosphorylated Akt and Stat3 — key survival signaling pathways in cancer
• Reduction of Gli1 — a transcription factor linked to tumor invasion

Illustration: Stages of apoptosis in cancer cells induced by benzimidazole treatment

In aggressive anaplastic thyroid cancer cells, mebendazole also significantly reduced migratory and invasive behavior in wound healing and transwell invasion assays. Because these traits drive rapid disease spread, limiting them represents an important therapeutic goal.

Key In Vitro Findings — Mebendazole vs Thyroid Cancer Cells

• Growth inhibition in both PTC (B-CPAP) and ATC (8505c) cell lines
• G2/M arrest and caspase-3-mediated apoptosis confirmed
• Reduced migration and invasion in aggressive ATC cells
• Inhibition of Akt, Stat3 and Gli1 signaling pathways

In Vivo Findings in Thyroid Cancer Models

To further evaluate therapeutic potential, researchers tested mebendazole in orthotopic thyroid cancer models — meaning tumor cells were implanted directly in the thyroid region to mimic natural disease. Results were striking:

Endpoint	PTC Model (B-CPAP)	ATC Model (8505c)
Tumor response	Significant regression	Growth arrest
Ki-67 (proliferation)	Reduced	Reduced
VEGF / vascularity	Decreased (CD31+)	Decreased (CD31+)
Lung metastasis	Prevented	Significantly reduced

Most notably, daily oral administration prevented established thyroid tumors from spreading to the lungs. Lung metastasis commonly occurs in anaplastic thyroid cancer and is a leading cause of death. In contrast, untreated control animals developed extensive pulmonary metastases. Reduced VEGF expression also suggests the drug impairs blood vessel formation needed for tumor growth.

Clinical Relevance and At-Risk Patient Groups

These findings hold particular relevance for the estimated 20–30% of papillary thyroid cancer patients who experience persistent or progressive disease. This group faces a higher risk of dedifferentiation into ATC — a transformation that dramatically worsens prognosis.

Mebendazole’s long-standing safety record strengthens its appeal for further investigation. The drug has been widely used in pediatric and adult populations for decades with minimal toxicity. This profile suggests potential use as an adjunct therapy alongside surgery, radiotherapy, or targeted treatments, pending clinical validation. Patients with radioiodine-refractory disease, who often have very limited options, represent a particularly compelling target population.

Furthermore, patients with poorly differentiated thyroid carcinoma (PDTC)—an intermediate-grade malignancy between well-differentiated PTC and undifferentiated ATC—may represent an ideal population for early clinical investigation. PDTC exhibits moderate proliferation rates and variable radioiodine avidity, creating a therapeutic window where mebendazole's multi-targeted mechanism could provide clinical benefit without the dose-limiting challenges posed by fully dedifferentiated disease.

Mechanisms of Action: Why Mebendazole May Work

Beyond its direct cytotoxic effects, mebendazole acts through multiple complementary pathways:

• Tubulin disruption — interferes with microtubule polymerization, blocking cell division
• Anti-angiogenic activity — inhibits VEGF expression and reduces tumor blood supply
• Kinase inhibition — blocks BCR-ABL and BRAF kinases at nanomolar concentrations
• Immune modulation — may stimulate anti-tumor immune responses
• Pro-apoptotic signaling — activates caspase pathways in cancer cells while sparing healthy cells

Additionally, recent research suggests mebendazole may exhibit immunomodulatory effects in the tumor microenvironment. Studies in other cancer types have shown that the drug can polarize tumor-associated macrophages from an immunosuppressive M2 phenotype to a pro-inflammatory M1 state, potentially enhancing immune recognition of cancer cells. Whether this mechanism operates in thyroid cancer specifically awaits investigation, but it represents another pathway through which benzimidazoles might complement conventional immunotherapy approaches currently being explored for aggressive thyroid malignancies.

Related Compounds: Fenbendazole

Within the same benzimidazole family, fenbendazole has attracted attention for its possible anticancer activity in preclinical settings. Reports describe activity in several cancer models, although controlled clinical data remain limited. As a result, fenbendazole research continues largely outside formal oncology frameworks.

By comparison, mebendazole benefits from extensive clinical use and regulatory familiarity. This background supports its further evaluation in oncology-focused research, particularly for aggressive thyroid cancers.

The Benzimidazole Class: Not All Dewormers Are Equal

Mebendazole belongs to the benzimidazole family of antiparasitic drugs, which includes fenbendazole and albendazole. While all three share a core mechanism—disrupting microtubule assembly in both parasitic and mammalian cells—they differ significantly in regulatory status, human pharmacokinetic data, and clinical evidence base.

Feature	Mebendazole	Fenbendazole	Albendazole
Regulatory status	FDA-approved (human)	Veterinary only	FDA-approved (human)
Bioavailability	5–20% (polymorph-dependent)	<20–25% (animal data)	~30% (metabolized to active form)
Half-life (human)	2–6 hours	Unknown (10–15h in animals)	8–12 hours
BBB penetration	Documented	Not established	Limited
Cancer trials (any type)	Phase I/II (glioma, other)	None	Limited
Quality control	Pharmaceutical-grade	Veterinary standards	Pharmaceutical-grade

Why This Matters for Thyroid Cancer Research: Mebendazole's human-approved status and documented blood-brain barrier penetration make it a more attractive candidate for clinical investigation than fenbendazole. The Johns Hopkins research cited earlier specifically chose mebendazole over other benzimidazoles for these reasons.

The Bioavailability Problem: Polymorph C and Dose Escalation

One of the most critical—yet often overlooked—challenges in repurposing mebendazole for cancer is its extremely poor oral bioavailability. Standard formulations achieve only 5–20% systemic absorption, with most of the drug never entering the bloodstream.

The Polymorph Factor

Mebendazole exists in three crystalline forms (polymorphs A, B, and C), which differ dramatically in dissolution rate and bioavailability:

• Polymorph A — Most stable, but poorest solubility (reaches only 19% of the plasma AUC achieved by Polymorph C in mouse models)
• Polymorph B — Highest solubility, but associated with greater toxicity
• Polymorph C — Optimal balance of bioavailability and safety; preferred for oncology research

In a pivotal study, researchers at Johns Hopkins patented an enhanced Polymorph C formulation containing at least 90% pure Polymorph C. This formulation achieved superior plasma concentrations and tumor penetration compared to standard preparations. The difference is not trivial: using the wrong polymorph can result in subtherapeutic tissue concentrations even at high oral doses.

Clinical Reality Check: Most over-the-counter mebendazole products do not specify polymorph composition. Patients attempting self-treatment may unknowingly use formulations with minimal systemic absorption.

Dose Escalation in Cancer Trials

Because of the bioavailability barrier, cancer-focused trials have tested doses far exceeding standard antiparasitic regimens:

• Standard antiparasitic dose: 100 mg twice daily for 3 days
• Experimental cancer doses: 25–200 mg/kg/day (equivalent to 1,750–14,000 mg/day for a 70 kg adult)
• Target serum concentration: ~1 µM (~300 ng/mL), based on in vitro IC₅₀ data

Some trials have implemented therapeutic drug monitoring (TDM) to individually adjust doses based on measured plasma levels, given the high inter-patient variability in absorption.

From Mice to Humans: The Concentration Gap

While the Johns Hopkins orthotopic thyroid cancer models showed "stunning" efficacy, translating these results to human patients faces a critical pharmacokinetic challenge.

The Mouse vs Human Plasma Level Problem

In the thyroid cancer study, mice received daily oral mebendazole at doses that achieved effective tissue concentrations. However, the therapeutic window in rodents does not directly translate to humans:

• IC₅₀ in thyroid cancer cells (in vitro): Low micromolar range (~2–5 µM = 560–1,400 ng/mL)
• Achievable human plasma (standard dose): Often <100 ng/mL
• Achievable human plasma (high-dose protocols): 300–800 ng/mL (with TDM and Polymorph C)

This creates a 2- to 5-fold concentration gap even with dose escalation. While it's possible that:

1. Tissue concentrations exceed plasma levels in some organs
2. Chronic exposure produces cumulative effects not captured in in vitro IC₅₀ measurements
3. Combination with other agents reduces the required mebendazole threshold

...these remain unproven hypotheses in the context of human thyroid cancer.

Thyroid-Specific Mechanisms: Why This Organ May Respond

Despite the pharmacokinetic challenges, there are biological reasons to believe thyroid tissue might be particularly vulnerable to benzimidazole activity:

High Proliferative Index in Aggressive Subtypes

Anaplastic thyroid cancer (ATC) exhibits one of the highest proliferation rates among solid tumors, with Ki-67 indices often exceeding 50–80%. Because mebendazole arrests cells in the G2/M phase of mitosis, rapidly dividing ATC cells may be disproportionately sensitive compared to slower-growing cancers.

BRAF and RAS-Driven Signaling

The majority of papillary thyroid cancers harbor BRAF V600E mutations (40–45%) or RAS mutations (10–20%). The Johns Hopkins data showed that mebendazole inhibits phosphorylated Akt and Stat3—downstream effectors of these oncogenic drivers. This suggests potential synergy with BRAF inhibitors (e.g., vemurafenib, dabrafenib) in BRAF-mutant disease.

Vascular Dependence

Thyroid tumors are highly vascular, relying on robust angiogenesis for growth and metastatic spread. The observed reduction in VEGF expression and CD31+ vascularity in the mouse models indicates that mebendazole's anti-angiogenic properties may be particularly effective in this cancer type.

The Lung Metastasis Prevention Finding: A Breakthrough or Statistical Artifact?

Perhaps the most striking result from the Johns Hopkins orthotopic thyroid cancer study was the near-complete prevention of pulmonary metastasis in mebendazole-treated animals. This finding warrants deeper examination because lung metastases represent the primary cause of death in advanced thyroid cancer.

What the Data Showed

In the B-CPAP (papillary) and 8505c (anaplastic) thyroid cancer models, untreated control mice developed extensive lung metastases by the study endpoint. In contrast, mice receiving daily oral mebendazole showed:

• Complete absence of lung metastases in most treated animals
• Significantly reduced metastatic burden in the few cases where lung lesions did appear
• Reduced expression of invasion markers (Gli1, matrix metalloproteinases)
• Decreased tumor cell migration and invasion in transwell assays (in vitro correlate)

Proposed Anti-Metastatic Mechanisms

Several biological mechanisms may explain this anti-metastatic activity:

1. Inhibition of Epithelial-Mesenchymal Transition (EMT)
Cancer cells must undergo EMT to detach from the primary tumor, invade surrounding tissue, and enter the bloodstream. Mebendazole's suppression of Gli1—a key transcription factor in the Hedgehog signaling pathway—may block this transition. Gli1 is known to promote EMT and stemness in multiple cancer types.

2. Vascular Normalization
The reduction in tumor vascularity (CD31+ staining) suggests mebendazole limits the formation of new blood vessels. Paradoxically, this "vascular normalization" may also reduce the shedding of circulating tumor cells (CTCs) into the bloodstream by decreasing leaky, aberrant tumor vessels.

3. Microenvironment Modulation
Emerging evidence suggests benzimidazoles may alter the tumor microenvironment by:

• Reducing stromal cell activation
• Inhibiting cancer-associated fibroblasts (CAFs)
• Polarizing tumor-associated macrophages toward an anti-tumor M1 phenotype

These changes could create a microenvironment less permissive to metastatic seeding.

The Translation Question

While prevention of lung metastases in mice is scientifically compelling, translating this to human patients faces major obstacles:

• Treatment timing: The mice received mebendazole starting at or shortly after tumor implantation—analogous to treating micrometastatic disease in humans, not established macro-metastases
• Dose-response relationship: The effective dose in mice may not be safely achievable in humans given bioavailability constraints
• Species differences: Mouse models of metastasis often overestimate human responses due to differences in immune surveillance and vascular biology

Comparative Analysis: Mebendazole vs Other Repurposed Drugs in Thyroid Cancer

Mebendazole is not the only repurposed drug being explored for thyroid cancer. How does its preclinical evidence compare to other candidates?

Drug	Original Use	Thyroid Cancer Evidence	Clinical Trials
Mebendazole	Anthelmintic	Strong preclinical (JHU 2020): tumor regression, metastasis prevention	None
Metformin	Diabetes	Observational: reduced recurrence in diabetic PTC patients	Retrospective only
Atorvastatin	Cholesterol	Preclinical: inhibits mevalonate pathway, reduces cell viability	Part of COC Protocol
Ivermectin	Antiparasitic	Weak preclinical; anecdotal case series (2026)	None
Sorafenib	Kidney/liver cancer	Strong clinical evidence in radioiodine-refractory DTC	FDA-approved

Key Insight: Mebendazole has stronger preclinical thyroid cancer data than many other repurposed agents, yet remains further from clinical validation than drugs with weaker biological evidence but better funding or commercial interest.

Future Research Directions and Unanswered Questions

For mebendazole to transition from "interesting preclinical finding" to "viable clinical option," several critical questions must be addressed:

1. Optimized Formulation Development

The biggest barrier is bioavailability. Future research should focus on:

• Nano-formulations: Lipid nanoparticles, SMEDDS (self-microemulsifying drug delivery systems), or mesoporous silica carriers
• Polymorph C standardization: Ensuring ≥90% pure Polymorph C in pharmaceutical-grade products
• Cyclodextrin complexation: Improving aqueous solubility without altering the active molecule

2. Biomarker-Driven Patient Selection

Not all thyroid cancers are biologically identical. Research should identify which patient subgroups are most likely to respond:

• High Ki-67 proliferation index (>50%)
• BRAF V600E-mutant disease (for combination with BRAF inhibitors)
• Tumors with high Gli1 or Hedgehog pathway activation
• Radioiodine-refractory disease with measurable lung metastases

3. Pharmacokinetic/Pharmacodynamic Modeling in Humans

Before launching efficacy trials, dose-finding studies should establish:

• The minimum plasma concentration required for biological activity (target ≥300 ng/mL based on in vitro IC₅₀)
• Inter-patient variability and factors influencing absorption (genetics, gut microbiome, food intake)
• Safe maximum tolerated dose with enhanced formulations

4. Combination Regimen Optimization

Given the complexity of cancer biology, mebendazole is unlikely to succeed as monotherapy in advanced disease. Rational combinations to test include:

• Mebendazole + dabrafenib/trametinib (for BRAF-mutant ATC)
• Mebendazole + lenvatinib (dual anti-angiogenic + anti-proliferative)
• Mebendazole + radiation (for unresectable local disease)
• Mebendazole + immunotherapy (PD-1 inhibitors for microsatellite-instable thyroid cancers)

Clinical Dosing Strategies and Safety Monitoring

For patients and clinicians considering mebendazole as part of an investigational or adjunctive protocol, the following evidence-based considerations apply:

Recommended Monitoring

• Liver function tests (LFTs): Baseline, then every 2–4 weeks during high-dose therapy (monitor ALT, AST, GGT)
• Complete blood count (CBC): Monitor for neutropenia, particularly at doses >500 mg/day
• Therapeutic drug monitoring: Plasma mebendazole levels if available (target ~300–800 ng/mL)
• Avoid in Gilbert's syndrome: Case reports document severe hepatotoxicity due to impaired glucuronidation

Drug Interactions

Mebendazole is metabolized via hepatic glucuronidation. Co-administration with cimetidine (a CYP inhibitor) has been shown to increase plasma levels—potentially useful for enhancing bioavailability, but also increasing toxicity risk. Conversely, strong CYP inducers (rifampin, phenytoin) may reduce efficacy.

Fat Co-Administration

Taking mebendazole with a high-fat meal modestly improves bioavailability (typically 1.5- to 2-fold increase). This simple intervention is often recommended in investigational protocols.

Documented Cases and Anecdotal Reports

While controlled clinical trials are absent, isolated case reports and anecdotal accounts have emerged describing mebendazole use in advanced thyroid cancer patients. These reports must be interpreted with extreme caution, as they lack the rigor of peer-reviewed trials.

The 2026 OneDayMD Case Series

In January 2026, a controversial case series described eight patients with metastatic thyroid cancer treated with high-dose mebendazole (200 mg twice daily) plus ivermectin. According to the report:

• 2 of 8 patients experienced partial tumor regression or symptom improvement
• 6 of 8 patients showed disease progression despite treatment
• All patients were also receiving concurrent treatments, making attribution impossible

This 25% "response rate" is not evidence of efficacy — it represents uncontrolled observations in a tiny, heterogeneous cohort. The authors themselves acknowledged that "resolution of metastatic lesions" could not be definitively attributed to the benzimidazole regimen versus other interventions.

Integration into Multi-Drug Protocols

Mebendazole appears as a component in several investigational multi-drug protocols promoted by alternative oncology practitioners:

• Care Oncology Protocol (COC): Combines mebendazole with metformin, doxycycline, and atorvastatin
• Dr. William Makis Protocol: Includes mebendazole alongside ivermectin, fenbendazole, and vitamin C
• Jane McLelland Metabolic Approach: Uses mebendazole as part of a "metabolic blockade" strategy

Importantly, none of these protocols have published survival data in peer-reviewed journals. Their inclusion of mebendazole is based on preclinical rationale rather than clinical proof.

Critical Distinction: "Included in a protocol" ≠ "proven effective." Many investigational protocols incorporate promising preclinical agents without validation, creating a gap between biological plausibility and patient outcomes.

Combination Strategies: Synergy Potential with Standard Therapy

One of the more scientifically interesting aspects of mebendazole research involves its potential to enhance conventional cancer therapies rather than replace them.

Synergy with BRAF Inhibitors

Approximately 40–45% of papillary thyroid cancers harbor the BRAF V600E mutation. While BRAF inhibitors (vemurafenib, dabrafenib) have shown activity, resistance commonly develops. Preclinical data suggest mebendazole may:

• Inhibit phosphorylated Akt and Stat3 — downstream escape pathways that mediate BRAF inhibitor resistance
• Suppress Gli1 transcription factor — implicated in tumor invasion and stemness
• Provide dual microtubule + kinase inhibition, attacking cancer cells through complementary mechanisms

A theoretical combination regimen might pair dabrafenib + trametinib (FDA-approved for BRAF-mutant ATC) with mebendazole to delay or prevent resistance. However, this remains entirely hypothetical without clinical validation.

Chemosensitization in Aggressive ATC

Anaplastic thyroid cancer is often treated with palliative chemotherapy (doxorubicin, cisplatin, paclitaxel). Because mebendazole:

1. Disrupts microtubules (similar to paclitaxel)
2. Reduces tumor vascularity (potentially improving drug delivery)
3. Inhibits survival signaling pathways

...it could theoretically act as a chemosensitizer, making resistant tumors more vulnerable to cytotoxic agents. A 2016 study by Williamson et al. demonstrated this concept in colon cancer models, where mebendazole combined with a non-steroidal anti-inflammatory (NSAID) reduced tumor initiation more effectively than either agent alone.

Radiation Sensitization

External beam radiation therapy (EBRT) is a cornerstone of ATC management. Mebendazole's anti-angiogenic properties—particularly its inhibition of VEGF expression—may enhance radiation efficacy by:

• Normalizing aberrant tumor vasculature, improving oxygenation (hypoxic tumors are radiation-resistant)
• Preventing radiation-induced angiogenic rebound
• Inducing cell cycle arrest in G2/M phase, the most radiosensitive cell cycle stage

These mechanisms have been explored in glioma models but remain untested in thyroid cancer.

What Would a Definitive Clinical Trial Look Like?

If funding and regulatory hurdles were overcome, a well-designed Phase II trial for mebendazole in thyroid cancer might include:

Trial Design Elements

• Population: Radioiodine-refractory papillary thyroid cancer with measurable disease, or unresectable anaplastic thyroid cancer
• Intervention: Enhanced Polymorph C formulation at escalating doses (50–200 mg/kg/day), taken with high-fat meals
• Control arm: Best supportive care or FDA-approved targeted therapy (lenvatinib, sorafenib)
• Primary endpoint: Objective response rate (ORR) per RECIST 1.1 criteria at 6 months
• Secondary endpoints: Progression-free survival, overall survival, toxicity (CTCAE grading), quality of life
• Correlative studies: Plasma drug levels (TDM), tumor biopsy for pharmacodynamic markers (Ki-67, p-Akt, VEGF)

Biomarker Stratification

An ideal trial would stratify patients by:

• BRAF mutation status (V600E vs wild-type)
• Tumor proliferation index (Ki-67 >50% vs <50%)
• Prior tyrosine kinase inhibitor exposure (naive vs refractory)

This stratification could identify subgroups most likely to benefit from benzimidazole therapy.

The Missing Clinical Evidence: Why No Thyroid Cancer Trials Exist

Despite the compelling preclinical data published in 2020, no registered clinical trials have evaluated mebendazole specifically for thyroid cancer as of early 2026. Several factors explain this gap:

1. Regulatory and Funding Barriers

Mebendazole is off-patent and inexpensive (<$1 per dose). Pharmaceutical companies lack financial incentive to sponsor trials for a generic drug with no exclusivity potential. Academic-led trials require independent funding, which is difficult to secure for repurposing studies.

2. Bioavailability Uncertainty

The poor and variable oral absorption creates uncertainty about whether effective human doses can be achieved safely. Until a validated, enhanced-bioavailability formulation (such as the Johns Hopkins Polymorph C patent) becomes commercially available, designing a definitive trial remains challenging.

3. Competing Targeted Therapies

For radioiodine-refractory thyroid cancer, FDA-approved targeted agents now exist:

• Lenvatinib (VEGFR/FGFR inhibitor)
• Sorafenib (multi-kinase inhibitor)
• Dabrafenib + trametinib (for BRAF V600E-mutant ATC)

Clinical trial sponsors prioritize novel agents over repurposed generics, even when preclinical data are strong.

4. Anecdotal Use Without Systematic Reporting

Mebendazole is sometimes used "off-label" in integrative oncology clinics as part of multi-drug protocols. However, these cases are rarely documented in peer-reviewed literature, making it impossible to assess real-world efficacy or safety signals.

The Evidence Gap: Preclinical promise without clinical validation creates a frustrating scenario for patients with limited options. The drug remains investigational in the oncology context, regardless of its antiparasitic approval.

Conclusion

Preclinical evidence suggests that mebendazole may suppress tumor growth and reduce metastasis in thyroid cancer models, including highly aggressive anaplastic disease. Its favorable safety profile and demonstrated biological activity make it a strong candidate for further investigation.

Summary — What the Research Demonstrates

• Mebendazole inhibits PTC and ATC cell growth in vitro at low concentrations
• Tumor regression and growth arrest confirmed in orthotopic animal models
• Daily oral administration prevented lung metastasis in thyroid cancer models
• Anti-angiogenic and multi-kinase inhibitory effects observed
• Favorable safety profile supports further clinical investigation

Although additional studies and clinical trials are necessary, this research highlights the broader potential of drug repurposing in oncology. As scientists seek more effective strategies for advanced thyroid cancer, mebendazole may represent a promising avenue for future therapeutic development.

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