Fenbendazole and Breast Cancer: Pyroptosis, Case Reports & What the Research Shows

Fenbendazole — a decades-old veterinary antiparasitic — has quietly accumulated a body of preclinical evidence suggesting it may interfere with cancer cell survival through several distinct mechanisms. In breast cancer specifically, a landmark 2025 paper published in Frontiers in Pharmacology revealed an entirely new dimension: fenbendazole can trigger pyroptosis, an inflammatory form of programmed cell death, by activating the caspase-3/GSDME signaling axis and simultaneously dismantling the glycolytic machinery that breast cancer cells depend on for energy. This is not the same mechanism described in earlier benzimidazole research — it is something more nuanced, and more targeted.

This article covers the full picture of what current research shows about fenbendazole and breast cancer: the 2025 pyroptosis study in detail, the in vivo mouse efficacy data, earlier mechanisms involving microtubule disruption and p53 stabilization, the documented case of an 83-year-old woman with Stage IV ER+ disease who achieved complete remission while taking 222 mg/day, practical considerations for triple-negative breast cancer, the American Cancer Society's perspective, and an honest assessment of liver safety. This is an educational deep-dive for researchers, patients, and caregivers — not a treatment recommendation.

🔬 What Is Pyroptosis — and Why Does It Matter in Breast Cancer?

Pyroptosis is a form of programmed cell death distinct from apoptosis. While apoptosis is typically a quiet, immunologically silent process, pyroptosis is characterized by cell swelling, plasma membrane pore formation, and the release of pro-inflammatory cytokines (particularly IL-1β and IL-18). In the context of cancer, this distinction matters considerably: pyroptotic death activates the immune system, potentially recruiting immune effector cells to the tumor site and reshaping the local tumor microenvironment.

The molecular switch governing pyroptosis is the gasdermin (GSDM) protein family. When cleaved by activated caspases, gasdermin proteins insert into the plasma membrane, creating pores that cause cell lysis and cytokine release. In cancer cells, GSDME (gasdermin E) is a particularly relevant target — and it sits downstream of caspase-3, the same executioner caspase involved in apoptosis. The caspase-3/GSDME axis therefore represents a bifurcation point: activation of caspase-3 can result in either apoptosis or pyroptosis, depending on GSDME expression levels in the target cell.

This is the pathway that fenbendazole appears to exploit in breast cancer cells, according to the 2025 Frontiers study — and it represents a mechanistic advance over what was previously understood about the drug's anticancer activity.

Cell Death Type	Key Features	Immune Activation	Key Mediators
Apoptosis	Membrane blebbing, cell shrinkage, silent	Minimal / immunosuppressive	Caspase-3, Bcl-2 family
Pyroptosis	Cell swelling, membrane pores, cytokine release	Strong pro-inflammatory	Caspase-1/3, GSDMD/GSDME

🔬 The 2025 Frontiers in Pharmacology Pyroptosis Study: What It Found

Published in July 2025, the study titled "Fenbendazole induces pyroptosis in breast cancer cells through HK2/caspase-3/GSDME signaling pathway" by Pan, Jin, Huang and colleagues represents the first direct demonstration that fenbendazole can activate the pyroptotic machinery in breast cancer (Frontiers in Pharmacology, 2025). The work used EMT6 mouse mammary carcinoma cells in vitro and a Balb/c xenograft model in vivo.

In Vitro Findings

Treating EMT6 cells with fenbendazole at increasing concentrations produced a dose-dependent reduction in cell viability, as measured by CCK-8 assay. Crucially, the researchers also observed characteristic pyroptotic morphology under microscopy: cells swelled, developed membrane bubbles, and lysed — patterns consistent with gasdermin-mediated membrane disruption, not typical apoptotic shrinkage. Importantly, the control cell line HC11 (normal mouse mammary epithelial cells) showed no significant toxicity at the same concentrations, suggesting a degree of selectivity for cancer cells.

Western blot and qPCR analysis confirmed upregulation of:

• Cleaved caspase-3 — the activated form of the executioner caspase
• GSDME-N terminal fragment (GSDME-NT) — the membrane-pore-forming product of GSDME cleavage
• IL-1β and IL-18 — canonical pyroptosis-associated pro-inflammatory cytokines
• LDH release — a marker of membrane rupture and cell lysis

When the researchers inhibited caspase-3 pharmacologically (using Z-DEVD-FMK) or knocked down GSDME using siRNA, pyroptosis was significantly attenuated — confirming that the caspase-3/GSDME axis is causally required for fenbendazole's pyroptotic effect, not merely correlative.

HK2 and the Glycolysis Connection

Perhaps the most novel finding of the 2025 study is the link between fenbendazole, hexokinase 2 (HK2), and the pyroptotic pathway. HK2 is the rate-limiting enzyme of glycolysis — it phosphorylates glucose to glucose-6-phosphate, committing it to the glycolytic pathway. Cancer cells typically overexpress HK2 as part of the Warburg effect, their pathological reliance on aerobic glycolysis for energy and biosynthetic precursors.

The study found that fenbendazole significantly downregulates HK2 expression, leading to:

• Reduced glucose consumption in EMT6 cells
• Decreased lactate production (a glycolysis byproduct)
• Lower intracellular ATP levels

Mechanistically, this appears to occur through p53 upregulation: fenbendazole stabilizes p53, which transcriptionally suppresses HK2 expression. The downstream metabolic disruption then feeds into the caspase-3/GSDME axis, amplifying pyroptosis. When the researchers used 2-DG (an HK2 inhibitor) alongside fenbendazole, pyroptosis was enhanced; when they added ATP (activating HK2), the pyroptotic effect was reversed — directly demonstrating that HK2 modulation is mechanistically upstream of the pyroptotic outcome.

Mechanism	Molecular Target	Functional Outcome	Evidence Type
Pyroptosis induction	Caspase-3 → GSDME-NT	Inflammatory cancer cell death, membrane pore formation	In vitro, in vivo (2025)
Glycolysis suppression	HK2 downregulation	Reduced glucose uptake, lactate, ATP	In vitro (2025)
p53 stabilization	Tumor suppressor p53	Transcriptional suppression of HK2; apoptosis facilitation	In vitro, NSCLC model (2018)
Microtubule disruption	β-tubulin polymerization	Mitotic arrest, cell cycle block	In vitro multiple cell lines (2018)
GLUT transporter downregulation	GLUT1/GLUT4	Reduced glucose entry into cancer cells	In vitro (2018)
BAX/caspase-3 cascade	Mitochondrial apoptosis pathway	Apoptosis upstream of GSDME cleavage	In vitro (2025)

In Vivo Mouse Results: Medium-Dose FBZ vs. Cisplatin

The in vivo component of the study used Balb/c mice implanted with EMT6 mammary carcinoma xenografts. Animals were treated with three doses of fenbendazole (low: 12.5 mg/kg, medium: 25 mg/kg, high: 50 mg/kg, administered intraperitoneally every 3 days for 21 days) and compared to a cisplatin-treated group (DDP, clinical equivalent dose) and untreated controls.

Key in vivo results:

• Medium-dose FBZ (25 mg/kg) produced tumor volume and weight reduction statistically comparable to cisplatin — a standard cytotoxic chemotherapy agent
• All three FBZ doses produced dose-dependent tumor growth inhibition
• Histopathology of excised tumors showed pyroptotic-like cell morphology and disrupted tumor architecture in FBZ-treated animals
• Consistent with in vitro findings, FBZ-treated xenografts showed elevated LDH, IL-18, and IL-1β in tumor tissue — confirming active pyroptosis in vivo

Safety Comparison: FBZ vs. Cisplatin In Vivo

The toxicity profile comparison in this study is clinically striking. While medium-dose FBZ achieved efficacy comparable to cisplatin, the systemic toxicity profiles were markedly different:

Parameter	Medium-Dose FBZ (25 mg/kg)	Cisplatin (DDP)
Body weight change	No significant loss	Significant weight loss (P < 0.01)
Liver/kidney weights	Unchanged	Significantly increased (P < 0.01)
ALT (liver enzyme)	Lower than control	Significantly elevated (P < 0.01)
AST	Unchanged	Significantly elevated (P < 0.01)
BUN (kidney marker)	Unchanged	Significantly elevated (P < 0.01)
Histopathology	Normal liver/kidney tissue	Hepatocyte condensation/fragmentation, glomerular enlargement

📌 Important context: These results are in mouse models using intraperitoneal injection, not oral human dosing. The extrapolation to human use requires significant caution. Nonetheless, the safety differential between FBZ and cisplatin in this preclinical model is notable, and it aligns with the broader benzimidazole safety data from veterinary use.

📌 Established Mechanisms: Microtubules, p53, and GLUT Transporters

The pyroptosis discovery builds on a foundation of earlier mechanistic work. The most-cited study establishing fenbendazole's anticancer credentials is a 2018 paper by Dogra, Kumar, and Mukhopadhyay in Scientific Reports (Nature), which demonstrated three interconnected mechanisms in human non-small cell lung cancer (NSCLC) cells (PMC6103891):

1. Microtubule Disruption

Fenbendazole, like all benzimidazoles, binds to β-tubulin and interferes with microtubule polymerization. Cancer cells undergoing mitosis depend on intact spindle formation; disrupting microtubule dynamics causes mitotic arrest and cell death. This mechanism is shared with well-established cancer drugs such as paclitaxel and vincristine, though fenbendazole is described as a "moderate" destabilizer rather than a potent one. The 2018 paper demonstrated this in A549 NSCLC cells using tubulin polymerization assays and immunofluorescence microscopy.

2. p53 Stabilization

The 2018 study also showed that fenbendazole significantly upregulates and stabilizes p53, the master tumor suppressor protein often called the "guardian of the genome." In the majority of cancer cells that retain functional p53 (approximately 50% of all cancers), p53 stabilization activates transcriptional programs leading to cell cycle arrest, DNA repair engagement, or apoptosis. The 2025 pyroptosis study extends this observation: p53 upregulation by fenbendazole appears to transcriptionally suppress HK2, creating the metabolic vulnerability that feeds into the pyroptotic cascade.

3. GLUT Transporter Downregulation

Fenbendazole was shown in the 2018 study to reduce expression of GLUT transporters (primarily GLUT1 and GLUT4) on the cancer cell surface. GLUT transporters are responsible for importing glucose into cells; cancer cells overexpress them to fuel their voracious glycolytic demands. Reducing GLUT expression limits glucose entry, complementing the HK2 suppression documented in the 2025 pyroptosis study. Together, these two mechanisms — less glucose entering the cell, and reduced capacity to phosphorylate and metabolize what does enter — create compounding metabolic stress in cancer cells.

💡 Synergy insight: The metabolic mechanisms (GLUT downregulation + HK2 suppression) and the cell death mechanisms (microtubule disruption + p53 stabilization + caspase-3/GSDME pyroptosis) may act in concert. Metabolic stress can sensitize cancer cells to pyroptotic death, while pyroptotic signaling further disrupts metabolism — creating a potentially self-reinforcing cycle.

For readers interested in how fenbendazole compares mechanistically with other benzimidazoles, see our article on Fenbendazole vs. Mebendazole.

🩺 Stage IV Breast Cancer Case Report: From Hospice to Complete Remission

Published in May 2025 in a peer-reviewed case series by Makis, Baghli, and Martinez (PMC12215191), Case 1 of the series describes one of the most clinically compelling fenbendazole reports in the breast cancer literature to date.

Patient Profile and Diagnosis

An 83-year-old woman with a history of ER+ breast cancer originally diagnosed in 2009 (treated with bilateral mastectomy, reconstruction, and aromatase inhibitors) presented in October 2021 with recurrence as fully metastatic Stage IV ER+/PR+, HER2-negative breast cancer. The disease burden was extensive:

• Liver metastases confirmed by fine needle aspiration (including a left lobe lesion measuring 2.9×1.7 cm, SUV max 5.6 on PET/CT)
• Ascites requiring biliary stent placement for obstruction
• Extensive bone metastases: T10, T12, L1-L5, S1-S2, iliac bones (L4 lesion: 5.0×2.9 cm lytic, SUV max 6.8)
• Multiple lung lesions: 6 hypermetabolic nodules, largest 2.8×1.5 cm in the right upper lobe (SUV max 8.4)

She declined chemotherapy and radiation (with the exception noted below) and was placed on hospice care. This baseline context is important for interpreting the subsequent clinical course.

Treatment Timeline and Protocol

Date	Event / Intervention
October 2021	Stage IV diagnosis; EGD/ERCP with biliary stent; FNA liver mets confirmed; placed on hospice
November 22, 2021	Started fenbendazole 222 mg/day (continuous)
December 2021	Fulvestrant injections initiated; PET/CT confirms extensive metastatic disease (CA 27.29 = 316)
January 2022	Targeted radiation to 2 painful spinal metastases (T10/L4) — rapid pain relief achieved
April 20, 2022	Follow-up PET scan: no abnormal metabolic activity detected
June 2022	No evidence of active disease (NED); all treatments discontinued except FBZ, vitamin D (5,000 IU), multivitamin
July 2022	CA 27.29: 36.6 (from 316); transient elevated ALT/AST, normalized weeks later
February 2023	CA 27.29: 26.5 (within normal range)
Ongoing (~3 years)	Recurrence-free; follow-up every 3–6 months; no adverse effects from FBZ

CA 27.29 Tumor Marker Trajectory

CA 27.29 is the primary serum tumor marker used to monitor breast cancer disease burden. A value above 38 U/mL is generally considered elevated. The trajectory in this case is remarkable:

• November 2021 (baseline): CA 27.29 = 316 U/mL — far above normal, consistent with extensive metastatic disease
• July 2022 (7 months after starting FBZ): CA 27.29 = 36.6 U/mL — an ~88% reduction, now within normal range
• February 2023: CA 27.29 = 26.5 U/mL — remained normal
• Subsequent follow-up: All values remained normal through approximately 3 years of follow-up

⭐ Clinical note: The case authors (Makis et al.) are careful to note that the patient received three concurrent interventions — fenbendazole, fulvestrant (an estrogen receptor degrader/blocker), and targeted radiation to two spinal lesions. Attributing the complete response to any single agent is not scientifically defensible from a case report. However, the authors point out that fulvestrant monotherapy in heavily pre-treated ER+ metastatic breast cancer typically yields an objective response rate of approximately 15–20%, and complete remission of this magnitude and duration in a patient with liver, lung, and extensive bone metastases who had declined chemotherapy would be extraordinary for fulvestrant alone.

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Products Referenced in This Article

Pharmaceutical-grade fenbendazole discussed in the research above — lab-tested at 99% purity with certificates of analysis.

Disclaimer: For convenience only. Consult a licensed professional.

⚠️ Safety Considerations: Liver Monitoring and DILI Risk

Any honest discussion of fenbendazole must include a clear-eyed look at its hepatotoxicity potential. While the drug has a long veterinary safety record and the 2025 in vivo study showed FBZ did not elevate liver enzymes in mice (unlike cisplatin), published human case reports document real cases of drug-induced liver injury (DILI) — some severe — associated with fenbendazole self-administration.

Documented DILI Cases

ACG Case Reports Journal (2024) — Histologically Confirmed Severe DILI: A 67-year-old woman self-administering fenbendazole for premalignant skin lesions developed jaundice and marked liver enzyme elevation (PMC11068125). RUCAM score: 9 (highly probable). Pattern: severe hepatocellular DILI. Resolution occurred approximately 3 months after stopping fenbendazole. This is notable as the first histologically confirmed case of fenbendazole-induced DILI in humans.

World Journal of Clinical Cases (2026) — DILI vs. Immunotherapy Hepatitis: A 47-year-old woman with metastatic colon cancer on nivolumab/relatlimab developed severe hepatocellular injury (ALT 2407 U/L, AST 2435 U/L, bilirubin 3.1 mg/dL) within 7 days of escalating her fenbendazole dose from 222 mg three times weekly to 222 mg daily — a 2.3-fold weekly exposure increase (PMC12836008). RUCAM score: 8 (probable). This case is clinically important for two reasons: it illustrates dose-dependent toxicity, and it highlights the diagnostic complexity when patients on immunotherapy self-administer fenbendazole (DILI can mimic immune-related hepatitis).

The 2026 case also notes a mechanistic explanation: fenbendazole activates CYP1A1 and CYP1A2 enzymes, which can generate reactive metabolites or interfere with the metabolism of co-administered drugs. It also appears to deplete hepatic glutathione — an essential antioxidant — increasing hepatocyte vulnerability to oxidative stress from other medications or metabolic challenges.

Liver Monitoring Recommendations

Based on published DILI cases and expert commentary, practitioners who supervise patients using fenbendazole generally recommend the following monitoring framework:

Timepoint	Tests	Action Threshold
Baseline (before starting)	ALT, AST, ALP, total bilirubin, GGT	Caution if baseline elevations present; consult physician
Week 2–4	ALT, AST, bilirubin	Discontinue if ALT/AST >3× upper limit of normal (ULN)
Month 2–3	Full hepatic panel	Discontinue if ALT/AST >3× ULN or bilirubin rising
Ongoing (every 2–3 months)	ALT, AST	Immediate cessation + medical evaluation if jaundice, dark urine, or right upper quadrant pain

⚠️ Interaction risk: The 2026 case strongly suggests that dose escalation dramatically increases DILI risk. Patients on immunotherapy (checkpoint inhibitors such as nivolumab, pembrolizumab) face an additional diagnostic complication, as fenbendazole DILI can closely mimic immune-related hepatitis — potentially resulting in unnecessary corticosteroid use or premature discontinuation of life-prolonging immunotherapy. Anyone on immunotherapy should disclose fenbendazole use to their oncologist.

📌 The breast cancer case note: The 83-year-old patient in the PMC12215191 case series did experience transient ALT/AST elevation in July 2022 (approximately 7 months after starting FBZ). The authors noted the elevation was mild and normalized within weeks without discontinuing FBZ, and the cause was unclear (possibly fulvestrant, FBZ, or their interaction). This did not preclude sustained complete remission but underscores the importance of hepatic monitoring.

💡 Triple-Negative Breast Cancer: A Special Consideration

Triple-negative breast cancer (TNBC) — characterized by absence of estrogen receptor, progesterone receptor, and HER2 amplification — is the most challenging breast cancer subtype. It lacks the druggable targets (ER, PR, HER2) that define the treatment landscape for other subtypes, making it more dependent on cytotoxic chemotherapy and, more recently, immunotherapy (checkpoint inhibitors). TNBC is associated with higher rates of early recurrence and reduced survival compared to hormone receptor-positive subtypes.

Several lines of evidence suggest fenbendazole may have particular relevance in TNBC:

• The 2025 Frontiers study used EMT6 cells — a model of highly aggressive murine mammary carcinoma that shares characteristics with human TNBC, including rapid growth kinetics and resistance to hormonal therapies. The pyroptosis and HK2-suppression mechanisms demonstrated in this model are not estrogen receptor-dependent.
• Cisplatin — the comparator drug in the 2025 in vivo study — is itself a standard-of-care option in TNBC, which gives the FBZ-vs-cisplatin comparison added clinical relevance for this subtype specifically.
• TNBC cells are known to highly overexpress GLUT1 and rely heavily on aerobic glycolysis for energy — precisely the metabolic vulnerability that FBZ's GLUT downregulation and HK2 suppression mechanisms target.
• The pyroptosis pathway activated by FBZ releases pro-inflammatory cytokines (IL-1β, IL-18) that could theoretically enhance immune recognition of tumor cells — potentially complementing checkpoint inhibitor immunotherapy, which is now part of the TNBC standard of care (pembrolizumab + chemotherapy in early and metastatic TNBC).

A Phase I/II clinical trial (NCT05318469) at Cedars-Sinai Medical Center is currently evaluating ivermectin combined with immune checkpoint inhibitors specifically in metastatic triple-negative breast cancer — a related antiparasitic approach that reflects growing institutional interest in repurposed antiparasitic drugs in this subtype.

📌 Research gap: No published preclinical study has directly compared fenbendazole efficacy across ER+, HER2+, and TNBC cell lines in a head-to-head format. The claim of particular TNBC activity is biologically plausible but not yet rigorously established. Human clinical data specific to FBZ in TNBC does not exist.

⭐ How This Fits the Joe Tippens Protocol Framework

The widespread interest in fenbendazole as an anticancer agent traces in large part to the story of Joe Tippens, a small-cell lung cancer patient who reportedly achieved complete remission after adding fenbendazole (among other supplements) to his prescribed pembrolizumab immunotherapy. The Joe Tippens Protocol typically combines fenbendazole 222 mg/day (or 444 mg/day) with vitamin E succinate, curcumin, and CBD oil — taken on a cycling schedule of 3 days on, 4 days off, though continuous dosing is also used.

The dose used in the PMC12215191 breast cancer case (222 mg/day, continuous) aligns with the lower end of the Tippens Protocol dosing range. For comprehensive dosing context and cycle schedules, see our Fenbendazole Dosage Guide. For comparisons with related antiparasitic approaches, see Ivermectin in Cancer Protocols and our comparison of Fenbendazole vs. Ivermectin.

Within the broader ISOM metabolic oncology framework, fenbendazole is used as part of a multi-target strategy alongside ivermectin, vitamin C, vitamin D3, curcumin, and metabolic interventions such as ketogenic diet and intermittent fasting. The compounding mechanisms — microtubule disruption, metabolic suppression, p53 activation, and now pyroptosis — make fenbendazole one of the more mechanistically interesting candidates in this space.

🩺 The American Cancer Society's Position

The American Cancer Society maintains a clear and cautionary stance on fenbendazole for cancer treatment, summarized on their website (cancer.org). Their position, as of their October 2025 update, includes several key points worth acknowledging directly:

• Not FDA approved for human use: Fenbendazole is approved for veterinary use only. There are no approved human dosing guidelines, no pharmacokinetic data in cancer patients, and no safety monitoring protocols established through clinical trials.
• No completed human clinical trials: While preclinical (laboratory and animal) data exists, no randomized controlled trial has evaluated fenbendazole in human cancer patients. Anecdotal case reports, however compelling, cannot establish efficacy or safety.
• Potential risks acknowledged: The ACS specifically calls out liver damage risk, potential interactions with standard cancer treatments, and the possibility of reducing efficacy of proven therapies if patients substitute FBZ for conventional treatment.
• Acknowledged early-stage science: The ACS does acknowledge "some early promise against cancer cells in laboratory and animal studies" — a meaningful concession from a conservative mainstream oncology body.
• Recommendation: Patients interested in fenbendazole should discuss it openly with their oncologist, and the ACS encourages exploring clinical trial eligibility rather than unmonitored self-administration.

Dr. Petros Grivas, quoted in the ACS article: "No proven benefit but several potential risks — I do not prescribe it."

This is a reasonable institutional position given the current evidence base. The absence of proof is not proof of absence — and the 2025 pyroptosis study, along with the growing case series literature, provides grounds for optimism about future clinical investigation. But the ACS position is not wrong to demand rigorous human trial data before endorsing clinical use.

✅ Fenbendazole and Breast Cancer: Putting It All Together

The research landscape on fenbendazole and breast cancer in 2025–2026 can be summarized across three tiers of evidence:

Tier 1 — Preclinical (laboratory and animal): Robust and growing. The 2025 Frontiers pyroptosis study adds a novel, well-characterized mechanism to an already substantial preclinical profile. Multiple independent laboratories have now confirmed FBZ's anticancer activity across various cell lines and animal models. The mechanisms — pyroptosis induction, glycolysis suppression, microtubule disruption, p53 stabilization, GLUT downregulation — are biologically plausible and pharmacologically coherent.

Tier 2 — Case reports and series: Suggestive but not definitive. The PMC12215191 case series (Makis et al., 2025) provides physician-documented, biomarker-tracked accounts of apparent complete or near-complete remission in Stage IV cancer patients using fenbendazole within multimodal regimens. The breast cancer case is particularly striking given the disease burden at baseline and the 3-year sustained NED status. However, as with all case reports, confounding by concurrent treatments, spontaneous remission (rare but documented in breast cancer), and selection bias limits causal attribution.

Tier 3 — Controlled human trials: Absent. This is the critical gap. Without randomized controlled trials, questions about optimal dosing, patient selection, combination strategies, and comparative efficacy remain unanswered. The ACS position is grounded in this reality.

For patients navigating these questions, transparency with the oncology team is paramount. Sharing relevant literature (including this post's references), disclosing all supplements and off-label medications, and undergoing regular hepatic monitoring are the practical essentials for anyone considering fenbendazole as part of a comprehensive cancer protocol.

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Scientific References

1. Pan T, Jin S, Huang X, Xin Q, Yang W, Dong L, Li L. (2025). Fenbendazole induces pyroptosis in breast cancer cells through HK2/caspase-3/GSDME signaling pathway. Frontiers in Pharmacology. doi:10.3389/fphar.2025.1596694
2. Makis W, Baghli I, Martinez P. (2025). Fenbendazole as an Anticancer Agent? A Case Series of Self-Administration in Three Stage IV Cancers. PMC. PMC12215191
3. Dogra N, Kumar A, Mukhopadhyay T. (2018). Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways. Scientific Reports (Nature), 8, 11926. PMC6103891
4. Hsieh YC, et al. (2024). Severe Drug-Induced Liver Injury Due to Self-administration of the Veterinary Anthelmintic Fenbendazole. ACG Case Reports Journal. PMC11068125
5. Chibber P, et al. (2026). Differentiating fenbendazole-induced liver injury from immunotherapy hepatitis — the importance of structured causality assessment: A case report. World Journal of Clinical Cases. PMC12836008
6. American Cancer Society. (2025). What to Know About Fenbendazole. cancer.org. cancer.org
7. ClinicalTrials.gov. NCT05318469: Ivermectin + Immunotherapy in Metastatic Triple-Negative Breast Cancer. NCT05318469