Ivermectin in Cancer Research

Ivermectin is a worm and mite medicine whose discovery won a share of the 2015 Nobel Prize, and in the last fifteen years it has also been tested against cancer cells in the laboratory. This page sets one point from a 2026 integrative-oncology presentation — that ivermectin is one of the most useful antiparasitic drugs against cancer — beside the published research: what the cell and mouse studies found, how the doses used in those studies compare with what reaches human blood, what the first human trials have reported so far, and what is known about high-dose harm.

What the Presentation Said
From Worm Medicine to the Cancer Laboratory
What Cell-Culture Studies Report
What Mouse Studies Report
The Dose Question: Laboratory Dish Versus Human Blood
Registered Human Trials
What a Worm-in-a-Dish Demonstration Shows
High Doses, Interactions and Reported Harm
Where Ivermectin Already Has a Role in Cancer Care
How the Claim Compares With the Research
What Is Not Known
Connections
Key Research Papers
Featured Videos

What the Presentation Said

In a 2026 webinar on cancer and parasites, the medical director of an integrative cancer clinic turned from herbal parasite cleanses to antiparasitic medicines. The speaker named mebendazole and ivermectin as the clinic's preferred drugs, ahead of fenbendazole, and said that ivermectin "just has so many properties."

The speaker's reasoning, as presented:

Several antiparasitic drugs show anti-cancer activity through a number of independent mechanisms: changes to tumour signalling, disruption of microtubules (the internal scaffolding a cell needs to divide), and effects on the immune system and the tumour's surroundings. On this basis the speaker described them as candidates for "repurposing" in cancer care — using an existing approved drug for a new disease.
A short video was shown under the heading of ivermectin's possible anti-cancer mechanisms. In it, a narrator adds a de-wormer paste to worms in a dish; the worms at first seem unaffected, then spasm and stop moving, and the narrator explains that the medicine works by slowly paralysing the parasites.
The speaker then cited a six-month observational study of ivermectin combined with mebendazole in people with cancer, reading out percentages for tumour shrinkage, stable disease and "no evidence of disease". That study has its own page: The 2026 Ivermectin and Mebendazole Observational Study.
In the question period, answering a question about stomach cancer, the speaker said that ivermectin and mebendazole "can be useful."

The presentation did not name a laboratory study, an animal study or a clinical trial of ivermectin on its own. This page therefore looks at the general claim — that ivermectin acts against cancer — and at each mechanism named, against the published record.

From Worm Medicine to the Cancer Laboratory

Ivermectin is made from avermectins, compounds produced by a soil bacterium found in Japan. It has been used in people since the 1980s against river blindness (onchocerciasis), the threadworm Strongyloides, scabies and head lice. Its history, approved uses and the full COVID-19 record are on the site's main Ivermectin page.

In worms and insects, ivermectin opens a type of chloride channel — a gate in the cell membrane that lets chloride ions in — that is controlled by the messenger glutamate. These glutamate-gated channels exist only in invertebrates. Chloride flooding into the worm's nerve and muscle cells silences them, and the worm is paralysed. In mammals, a pump in the blood-brain barrier called P-glycoprotein pushes most of the drug back out of the brain, which is why approved doses are tolerated (Kaur and colleagues, 2024).

None of that explains an effect on cancer, because human tumour cells do not have the worm's glutamate-gated channel. The cancer interest began instead with drug-screening experiments. In 2010 a Toronto group screened a library of already-approved drugs against leukaemia cells and found that ivermectin killed them in the dish (Sharmeen and colleagues, 2010). Since then reviews have collected studies on breast, ovarian, colon, prostate, lung, liver, pancreatic, blood and brain cancers (Tang and colleagues, 2021; Robalino and colleagues, 2025).

What Cell-Culture Studies Report

Everything in this section was done in cell culture — cancer cells growing in plastic dishes or flasks — sometimes with a follow-up experiment in mice. Cell culture is the first screening step for a possible drug. Most compounds that kill cancer cells in a dish never become cancer treatments.

Leukaemia cells and chloride

In the 2010 screening study, ivermectin killed acute myeloid leukaemia cells at "low micromolar" concentrations, and killed them more readily than normal blood-forming cells. It raised the chloride level inside leukaemia cells, made the cells swell, and increased reactive oxygen species (chemically aggressive forms of oxygen that damage cells); blocking that oxygen stress reduced the cell death. Ivermectin also added to the effect of two standard leukaemia drugs, cytarabine and daunorubicin, and delayed tumour growth in three mouse models of leukaemia (Sharmeen and colleagues, 2010).

Breast cancer cells: growth signals and "self-eating"

A 2016 study reported that ivermectin lowered the amount of an enzyme called PAK1 in breast cancer cells. PAK1 passes on growth signals through a chain of proteins known as Akt and mechanistic target of rapamycin (mTOR). With that chain switched down, the cells entered autophagy — a process in which a cell breaks down its own contents — of a type that halted growth rather than killing the cells outright. The same effect slowed the growth of human breast tumours transplanted into mice (Dou and colleagues, 2016).

A Mexican group found that ivermectin preferentially reduced the survival of "cancer stem-like cells" in one breast cancer cell line — a small subset of cells thought to regrow tumours after treatment — and lowered the activity of genes that keep those cells in a stem-like state. The chemotherapy drug paclitaxel showed the opposite pattern. Growth was inhibited across a range of 0.2 to 8 micromolar (Dominguez-Gomez and colleagues, 2018).

In 2025 a Thai group tested ivermectin on breast cancer cells that had become resistant to the hormone treatments tamoxifen and fulvestrant. The concentration that halved growth in 24 hours was about 9 micromolar. At that level, cell movement fell by more than half and invasion through a barrier fell by 62% and 35% in the two cell lines, alongside lower levels of proteins in the Wnt signalling pathway, which helps cancer cells spread (Rujimongkon and colleagues, 2025).

A 28-cell-line test

To answer the question of whether earlier studies had used unrealistically high doses, the Mexican group treated 28 cancer cell lines with 5 micromolar ivermectin. Three breast cancer lines and one ovarian line were the most sensitive; a prostate cancer line was the most resistant. In sensitive cells ivermectin stopped the cell cycle at its first stage, and it worked together with the chemotherapy drugs docetaxel and cyclophosphamide and with tamoxifen. It also shrank tumours in mice. The authors described 5 micromolar as a clinically feasible concentration and concluded that their results support clinical testing (Juarez and colleagues, 2020). The next section but one looks at how that figure compares with measured human blood levels.

Brain tumours

A 2024 review of glioma (the commonest primary brain cancer) gathered laboratory work in which ivermectin suppressed glioma cells by several routes, including programmed cell death and changes to tumour signalling pathways (Hu and colleagues, 2024). The review is a summary of cell and animal work, not of patients.

What the mechanisms have in common

Across these studies, the effects reported are many and different: chloride and oxygen stress, PAK1–Akt–mechanistic target of rapamycin, Wnt, a signalling protein called STAT3, stem-cell genes, and the cell cycle (Tang and colleagues, 2021; Robalino and colleagues, 2025). One drug touching many pathways can be read two ways — as broad activity, or as a sign of a general stress effect at high concentration. The cell studies themselves cannot tell those apart.

One mechanism named in the presentation, microtubule disruption, belongs to a different drug family. Microtubule binding is how mebendazole, albendazole and fenbendazole act on worms and on cancer cells in the laboratory (Chai and colleagues, 2021); it is not one of the main mechanisms the ivermectin reviews describe. The benzimidazoles are covered on Mebendazole, Fenbendazole and Albendazole in Cancer Research.

What Mouse Studies Report

The animal evidence comes from mice carrying transplanted human or mouse tumours. Several of the cell studies above added a mouse experiment in which ivermectin slowed tumour growth or reduced tumour size and weight (Sharmeen and colleagues, 2010; Dou and colleagues, 2016; Juarez and colleagues, 2020).

The immune checkpoint study

The mouse study with the most influence on human trials came from a California group in 2021. Immune checkpoint inhibitors are antibody drugs that release a brake — a protein called PD-1 on immune T cells — so the immune system can attack cancer. They work poorly in "cold" tumours that few immune cells enter. In mice with breast tumours, ivermectin caused a form of cancer-cell death that alerts the immune system, drew T cells into the tumours, and reduced immune-suppressing cells (Draganov and colleagues, 2021).

Two findings from that paper are often left out when it is quoted:

Neither drug alone worked in the mice. The authors state that "neither agent alone showed efficacy in vivo." Only the combination of ivermectin with an anti-PD-1 antibody limited tumour growth and produced complete responses, and it reduced relapse after treatment around surgery and in metastatic disease.
The paper now carries an editorial expression of concern. In June 2026 the journal reported that several images in one figure (Figure 4d and 4f, pictures of individual treated mice) were highly similar to one another. The authors had issued a correction removing some duplicated data, further similarities were then found, and the authors stated that the original data are no longer available. The journal advises readers to interpret the data with caution (Editorial Expression of Concern, 2026).

Mouse tumours are a weak predictor of human results in general: the doses, the timing and the tumours themselves differ from cancer in people.

The Dose Question: Laboratory Dish Versus Human Blood

A drug can only act on a tumour at the concentration that reaches it. For ivermectin, the gap between dish and blood is the most discussed problem in the field.

What the label reports

The United States prescribing label reports that after a single 12-milligram dose (an average of 165 micrograms per kilogram) in fasting healthy volunteers, mean peak blood levels of the main component were 46.6 and 30.6 nanograms per millilitre in two studies, reached about four hours after the dose. The plasma half-life is about 18 hours (U.S. Food and Drug Administration (FDA) Stromectol label).

The label gives the molecular weight of that main component as 875.10. Converted, 46.6 nanograms per millilitre is about 0.05 micromolar. The cell studies above used 0.2 to about 9 micromolar, and the 28-cell-line test used 5 micromolar — roughly 100 times the average peak level after a standard dose.

Higher doses

A placebo-controlled dose-escalation study in 68 healthy adults tested 30 or 60 milligrams three times a week and single doses of 90 or 120 milligrams — up to about ten times the highest approved dose of 200 micrograms per kilogram. Drug exposure rose roughly in proportion to dose, taking the drug with food raised exposure 2.6-fold, and the researchers found no sign of brain or nerve toxicity, measured mainly by pupil size, with side effects similar to placebo (Guzzo and colleagues, 2002). Even at ten times the standard exposure, average blood levels would sit at the low end of the range used in the dish experiments.

The case for "achievable"

Researchers who support clinical testing argue the gap is smaller than it looks. The leukaemia study described its mouse doses as "pharmacologically achievable" (Sharmeen and colleagues, 2010), and the 28-cell-line study chose 5 micromolar as "clinically feasible" (Juarez and colleagues, 2020). Ivermectin is very fat-soluble, and how much gathers in tumour tissue compared with blood has not been measured in patients. A 2025 review points to its poor water solubility and low availability as reasons new formulations are being studied (Robalino and colleagues, 2025). The question is open; it is the main reason trials measure drug levels in patients.

Registered Human Trials

A search of ClinicalTrials.gov (the United States registry of clinical studies) for "ivermectin cancer", checked on 23 October 2026, returned two registered trials testing ivermectin as a cancer treatment. Neither has posted results to the registry.

Ivermectin with an immune checkpoint inhibitor in triple-negative breast cancer

The first, a phase I/II trial (NCT05318469) that grew out of the 2021 mouse study, enrols people with metastatic triple-negative breast cancer — a form that lacks the three receptors targeted by hormone and HER2 drugs. Participants receive the anti-PD-1 antibody balstilimab (or pembrolizumab, according to the current registry entry) intravenously every three weeks, plus oral ivermectin on the first three days of each week. A phase I trial looks mainly at safety and dose; phase II looks at whether tumours shrink. The registry lists it as recruiting, with a planned 34 participants, a start date of 13 October 2023 and estimated completion in October 2026.

The only results so far are conference abstracts, not a peer-reviewed paper. A 2025 abstract reported:

Nine patients enrolled, median age 52, heavily pretreated (a median of five earlier lines of treatment for metastatic disease); six had already received a checkpoint inhibitor.
Ivermectin doses tested: 30, 45 and 60 milligrams a day on those three days a week. The first two dose levels were completed; the 60-milligram level was still to come.
Side effects judged treatment-related: rash in two patients (grade 1, mild), and one patient each with anaemia (grade 3), diarrhoea, taste change, muscle weakness, vomiting (all grade 1) and an underactive thyroid (grade 2). The one serious adverse event was attributed to the disease.
Of eight patients who could be assessed, one had a partial response (tumour shrinkage of at least 30%), one had stable disease and six had progressive disease. Median time without progression was 2.5 months. The four-month clinical benefit rate was 37.5% (95% confidence interval 15.3% to 91.7%).
The authors concluded that the combination was safe and well tolerated and that the clinical benefit rate was encouraging enough to continue (Yuan and colleagues, 2025).

This is an uncontrolled study of eight evaluable people, without a comparison group receiving the antibody alone. It cannot show whether ivermectin added anything to the checkpoint inhibitor. The trial design states that the phase II part will judge the combination promising only if at least 3 of 25 patients respond (Yuan and colleagues, 2024).

A second trial not yet open

The second (NCT07487805), registered in March 2026 at a Florida university, is a randomised phase II trial planned for 80 adults with solid tumours who are already receiving a checkpoint inhibitor. It compares two ivermectin doses — 200 and 400 micrograms per kilogram, taken on three days a week for four weeks — and its main measure is a change in activated immune T cells in the blood after two weeks, not tumour response. It is listed as not yet recruiting, with an estimated start in December 2026. Its registry entry states that clinical data "remain virtually absent," and gives as one reason for the trial that it is unknown whether ivermectin enhances or "potentially compromises" anti-cancer immunity.

Other registry entries

The same search also returned a trial of ivermectin and losartan for COVID-19 in people who had cancer (NCT04447235), terminated after a futility analysis showed no difference between arms; it tested COVID-19 treatment, not cancer treatment. A privately sponsored 2011 study of a mix of anti-infective drugs for cancer is listed with status unknown and no results.

The observational study the presentation cited

The 2025 study of ivermectin with mebendazole that the speaker described is covered in full on its own page, The 2026 Ivermectin and Mebendazole Observational Study. Its outcomes were reported by the patients themselves through online surveys, without a comparison group. PubMed now lists the published paper as retracted by the journal's editor in October 2026.

No randomised controlled trial of ivermectin for any cancer has been published. A 2025 review for oncologists states that evidence in humans is limited, "with no large-scale randomized controlled trials" (Patel and colleagues, 2025).

What a Worm-in-a-Dish Demonstration Shows

The video shown in the presentation followed a familiar format: a veterinary de-wormer paste is added to live worms in a dish, and over time they spasm and stop moving. Exactly which product, how much of it, and which worm species were used are not stated in the transcript.

What a demonstration like this does show:

That a de-wormer, put directly onto worms at the concentration of a paste made for large animals, paralyses and kills them. For ivermectin this is the expected result: the drug opens the glutamate-gated chloride channels in worm nerve and muscle cells, which paralyses them (Kaur and colleagues, 2024). The slow onset followed by spasm and stillness the narrator described fits that paralysing action.

What it does not show:

Anything about cancer. Human cancer cells do not have the worm's glutamate-gated chloride channel, so the way ivermectin kills a worm is not the way it acts on tumour cells in the laboratory studies above.
Anything about the human body. A paste poured onto a worm is not a dose swallowed by a person; after a standard dose, blood levels are measured in nanograms per millilitre (U.S. Food and Drug Administration Stromectol label).
That the person treated has parasites. The video shows that the paste kills worms in a dish; it does not show that a patient's tumour, or the patient, contains worms.
That a veterinary product is safe for people. In poison-centre data and case reports, people who took veterinary ivermectin took higher doses and more often had confusion and other brain effects (see the next section).

High Doses, Interactions and Reported Harm

At approved doses for parasitic infections, ivermectin has a long safety record; the side effects and the main hazards, including the Loa loa reaction, are set out on the Ivermectin page. Cancer use raises different questions, because it involves higher doses, repeated doses for weeks or months, and people who are often taking several other drugs.

What a 2026 toxicology review reports

A 2026 review of human and animal toxicity reports that controlled trials in healthy volunteers found ivermectin generally well tolerated even well above approved doses. Real-world reports, in contrast, describe rare but severe brain toxicity — encephalopathy, seizures, coma and death — after overdoses and, in susceptible people, at standard doses. The common thread is the blood-brain barrier pump P-glycoprotein: when it is impaired or saturated, more drug enters the brain. In animals, repeated high doses can cause structural brain damage and injury to other organs. The review notes a large rise in toxic exposures during the COVID-19 pandemic, many from veterinary products (Yilmaz and colleagues, 2026).

Why this matters for people with cancer

Drug interactions. Drugs that block the P-glycoprotein pump may raise the amount of ivermectin reaching the brain (Yilmaz and colleagues, 2026), and people with cancer often take several medicines at once. Reactions reported after marketing and listed on the U.S. Food and Drug Administration label include seizures, hepatitis and raised liver enzymes (U.S. Food and Drug Administration Stromectol label).
A published case. A 73-year-old woman with metastatic breast cancer took high doses of ivermectin on her own, based on information found online. She developed confusion, generalised seizures and respiratory failure and needed a breathing machine; she recovered fully within 48 hours (Saperstein and colleagues, 2026).
Self-medication. A 2025 review for oncologists describes observational studies and case reports of self-medication driven by social media, with toxicity in some cancer patients, and the ethical problem that patients may set aside proven treatments (Patel and colleagues, 2025).
A specialty review's statement. A 2025 review of ivermectin in gynaecological cancers found that the data on human cancers are lacking and limited to cell lines; its authors state that they "do not recommend and strongly caution" its use to treat those cancers (Mujumdar and colleagues, 2025).

In the triple-negative breast cancer trial, doses of 30 to 45 milligrams a day on three days a week, given with a checkpoint inhibitor under trial monitoring, produced mostly mild side effects in nine patients (Yuan and colleagues, 2025). That is a small, closely watched group and does not describe the safety of unsupervised use.

Decisions about cancer treatment and antiparasitic medicines belong with a clinician.

Where Ivermectin Already Has a Role in Cancer Care

Ivermectin does have an established role for some people with cancer — not against the tumour, but against a parasite that cancer treatment can make deadly.

The threadworm Strongyloides stercoralis can live quietly in the gut for decades. When the immune system is suppressed, it can multiply out of control (hyperinfection) and spread through the body (disseminated disease). A systematic review of 244 published cases of severe strongyloidiasis found that steroids were the main trigger in 67% — often given for underlying conditions such as lymphomas — and that the fatality rate was 60% for hyperinfection and 68.5% for disseminated disease. The authors call screening, including a blood antibody test, mandatory for high-risk people about to receive immune-suppressing drugs who live or have lived where the worm is common, and name ivermectin the gold-standard treatment (Buonfrate and colleagues, 2013).

A 2025 case report describes a patient receiving immunotherapy for metastatic kidney cancer who developed a rash first taken for an immunotherapy side effect. It did not respond to steroids; the patient's travel history and a laboratory test showed Strongyloides infection of the skin. Ivermectin cleared it, and immunotherapy was restarted without further skin problems (Cornillon and colleagues, 2025). More on the worm is on the Strongyloides page.

This is a real and documented point where parasites, cancer and ivermectin meet, though it is a different point from the one the presentation made.

How the Claim Compares With the Research

What the research supports

Ivermectin slows or kills many kinds of cancer cells in cell culture and slows transplanted tumours in mice, through several different signalling pathways (Tang and colleagues, 2021; Juarez and colleagues, 2020).
It is being studied as a "repurposed" drug, and registered human trials exist (ClinicalTrials.gov, NCT05318469 and NCT07487805).
Effects on the immune system and the tumour's surroundings were reported in mice (Draganov and colleagues, 2021).
A de-wormer paralyses and kills worms on direct contact.

What it supports only in part

The immune effect in mice appeared only when ivermectin was combined with a checkpoint inhibitor, not with ivermectin alone, and the key paper now carries an expression of concern over duplicated images (Draganov and colleagues, 2021; Editorial Expression of Concern, 2026).
The only human tumour-response data from a registered trial are a conference abstract on eight evaluable patients: one partial response, one stable disease, six progressions, with no comparison group (Yuan and colleagues, 2025).
Most cell studies used concentrations around 100 times the average peak blood level after a standard dose (U.S. Food and Drug Administration Stromectol label). Whether higher doses or tumour tissue close that gap has not been shown in patients.

What the research does not match

Microtubule disruption, named in the presentation among antiparasitic anti-cancer mechanisms, is the mechanism of mebendazole and related benzimidazoles (Chai and colleagues, 2021), not a main mechanism reported for ivermectin.
How a worm dies from ivermectin — through a chloride channel found only in invertebrates — is not how it acts on human cancer cells.

What has no research at all

No randomised controlled trial of ivermectin for any cancer has been published (Patel and colleagues, 2025).
No study was found of ivermectin in stomach cancer patients, the cancer the speaker was asked about.
No study was found showing that ivermectin works against cancer by killing parasites inside tumours.

What Is Not Known

Whether ivermectin, alone or with other treatment, changes survival or tumour growth in any human cancer. No controlled trial has answered this.
Whether the drug reaches tumour tissue at the concentrations that work in the dish, at doses people tolerate over weeks or months.
Whether ivermectin helps or harms immunotherapy in people. The new Florida trial was designed partly because this is unknown (ClinicalTrials.gov, NCT07487805).
What happens with long-term repeated dosing alongside chemotherapy, hormone therapy or targeted drugs.
How many people with cancer take ivermectin on their own, and how often harm results; case reports describe cases but do not measure how often they occur (Saperstein and colleagues, 2026).
Whether the mouse findings of the 2021 checkpoint study stand, given the journal's expression of concern and the unavailability of the original data.

Connections

Key Research Papers

Sharmeen S, Skrtic M, Sukhai MA, et al. The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells. Blood. 2010;116(18):3593-603. PubMed PMID: 20644115
Dou Q, Chen HN, Wang K, et al. Ivermectin Induces Cytostatic Autophagy by Blocking the PAK1/Akt Axis in Breast Cancer. Cancer Research. 2016;76(15):4457-69. PubMed PMID: 27302166
Dominguez-Gomez G, Chavez-Blanco A, Medina-Franco JL, et al. Ivermectin as an inhibitor of cancer stem-like cells. Molecular Medicine Reports. 2018;17(2):3397-3403. PubMed PMID: 29257278
Juarez M, Schcolnik-Cabrera A, Dominguez-Gomez G, et al. Antitumor effects of ivermectin at clinically feasible concentrations support its clinical development as a repositioned cancer drug. Cancer Chemotherapy and Pharmacology. 2020;85(6):1153-1163. PubMed PMID: 32474842
Draganov D, Han Z, Rana A, et al. Ivermectin converts cold tumors hot and synergizes with immune checkpoint blockade for treatment of breast cancer. NPJ Breast Cancer. 2021;7(1):22. PubMed PMID: 33654071 (Editorial note: this paper has an author correction, 2026, and an editorial expression of concern, listed next.)
Editorial Expression of Concern: Ivermectin converts cold tumors hot and synergizes with immune checkpoint blockade for treatment of breast cancer. NPJ Breast Cancer. 2026;12(1):78. PubMed PMID: 42248882
Rujimongkon K, Adchariyasakulchai P, Meeprasertskul P, et al. Ivermectin inhibits epithelial-to-mesenchymal transition via Wnt signaling in endocrine-resistant breast cancer cells. PLoS One. 2025;20(6):e0326742. PubMed PMID: 40569965
Tang M, Hu X, Wang Y, et al. Ivermectin, a potential anticancer drug derived from an antiparasitic drug. Pharmacological Research. 2021;163:105207. PubMed PMID: 32971268
Hu X, Ju Y, Zhang YK. Ivermectin as a potential therapeutic strategy for glioma. Journal of Neuroscience Research. 2024;102(1):e25254. PubMed PMID: 37814994
Robalino KN, Vivanco-Galván O, Romero-Benavides JC, et al. Ivermectin as an Alternative Anticancer Agent: A Review of Its Chemical Properties and Therapeutic Potential. Pharmaceuticals (Basel). 2025;18(10):1459. PubMed PMID: 41155573
Kaur B, Blavo C, Parmar MS. Ivermectin: A Multifaceted Drug With a Potential Beyond Anti-parasitic Therapy. Cureus. 2024;16(3):e56025. PubMed PMID: 38606261
Chai JY, Jung BK, Hong SJ. Albendazole and Mebendazole as Anti-Parasitic and Anti-Cancer Agents: an Update. The Korean Journal of Parasitology. 2021;59(3):189-225. PubMed PMID: 34218593
Patel Y, Chawla J, Parmar MS. Ivermectin in Cancer Treatment: Should Healthcare Providers Caution or Explore Its Therapeutic Potential? Current Oncology Reports. 2025;27(9):1070-1079. PubMed PMID: 40715995
Mujumdar V, Huang M, Smith LC, et al. Ivermectin and gynecologic cancer: What's the data? Gynecologic Oncology Reports. 2025;60:101803. PubMed PMID: 40851910
Yuan Y, Shiao S, Tighiouart M, et al. Abstract PO1-19-07: A Phase I Study Accessing Immunotherapy Combination of Balstilimab and Ivermectin in Patients with Metastatic Triple Negative Breast Cancer. Cancer Research. 2024;84(9_Supplement):PO1-19-07. doi:10.1158/1538-7445.SABCS23-PO1-19-07
Yuan Y, Bitar JS, Walker M, et al. A phase I/II study evaluating the safety and efficacy of ivermectin in combination with balstilimab in patients with metastatic triple negative breast cancer. Journal of Clinical Oncology. 2025;43(16_suppl):e13146. doi:10.1200/JCO.2025.43.16_suppl.e13146
Guzzo CA, Furtek CI, Porras AG, et al. Safety, tolerability, and pharmacokinetics of escalating high doses of ivermectin in healthy adult subjects. Journal of Clinical Pharmacology. 2002;42(10):1122-33. PubMed PMID: 12362927
Yilmaz S, Göktaş B, Ateş İ, et al. Ivermectin Toxicity in Humans and Animals: Clinical Spectrum, Mechanisms, and Management. Journal of Applied Toxicology. 2026;46(6):1856-1870. PubMed PMID: 41837342
Saperstein Y, Bou Sanayeh E, Boazak P, et al. Life-threatening neurotoxicity following off-label ivermectin use in metastatic breast cancer: a case report. Postgraduate Medicine. 2026;138(4):391-395. PubMed PMID: 42170801
Buonfrate D, Requena-Mendez A, Angheben A, et al. Severe strongyloidiasis: a systematic review of case reports. BMC Infectious Diseases. 2013;13:78. PubMed PMID: 23394259
Cornillon P, Beguinot M, Maillet D, et al. Cutaneous Anguillulosis During Immunotherapy for Metastatic Renal Cell Carcinoma. Medicina (Kaunas). 2025;61(2):339. PubMed PMID: 40005455

PubMed Topic Searches

Other Sources

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ClinicalTrials.gov. Ivermectin Combined With Immune Checkpoint Inhibition in Cancer (NCT07487805). clinicaltrials.gov
ClinicalTrials.gov. Early Treatment With Ivermectin and Losartan for Cancer Patients With COVID-19 Infection (NCT04447235). clinicaltrials.gov
U.S. Food and Drug Administration. Stromectol (ivermectin) tablets, prescribing information, 2009. accessdata.fda.gov