Treatments
Complementary and Alternative Treatments
- Physical treatments
- Repurposed Drugs – General
- No medication – Plan B
- Repurposed drugs and chemotherapy
- Repurposed drugs and radiation therapy
- FLCCC’s ranking of repurposed drugs
- Brain metastases and the blood-brain barrier
- Bombs, fire extinguishers, and timing
Fenbendazole and cancer
Content:
- Fenbendazole (scroll down)
- Parasitaere compariso (scroll to)
What is Fenbendazole
Fenbendazole is a drug primarily used to fight parasites in animals. In recent years, however, there has been an increasing interest in its potential use in cancer treatment, particularly following reports of successful treatment of certain types of cancer.
Fenbendazole against cancer
Although the precise mechanism behind fenbendazole’s potential cancer-fighting effect is not yet fully understood, researchers have identified several possible ways in which it may affect cancer cells:
- Inhibition of cell division Fenbendazole can interfere with the processes that govern how cancer cells divide and grow. This can lead to the cancer cells dying or stopping their reproduction.
- Starving cancer cells Some studies suggest that fenbendazole can limit cancer cells’ access to nutrients, which can lead to cell death.
- Modulating the immune system There are some theories that fenbendazole can affect the immune system in a way that makes it more effective at fighting cancer cells.
- Degradation of microtubules Microtubules are important structures in the cell that help maintain the cell’s shape and movement. Fenbendazole can affect these structures and thereby disrupt the function of the cancer cells. See below.
Fenbendazole’s impact on microtubules in cancer cells
One of the mechanisms through which fenbendazole is believed to affect cancer cells is, as mentioned above, by interacting with the cell’s microtubules.
What are microtubules
Microtubules are long, hollow protein filaments that function as the cell’s “skeleton.” They play a crucial role in a number of cellular processes, including:
Cell shape
- They help maintain the cell’s shape and structure.
Cell division
- Microtubules form mitotic spindles, which are necessary to separate the chromosomes during cell division.
Cell movement
- They are involved in the movement of cells and organelles within the cell.
How does fenbendazole affect microtubules
Fenbendazole functions as a so-called microtubule-destabilizing agent. This means it can disrupt the assembly and disassembly of microtubules. When the microtubule structure is disrupted, it can have several consequences for the cancer cell:
Inhibited cell division
- Cancer cells often divide faster than normal cells. By disrupting the formation of mitotic spindles, fenbendazole can prevent cancer cells from dividing normally. (Mitotic spindles are like the small, invisible “arms” inside a cell that pull the chromosomes (our genetic material) to each side when the cell divides. Imagine the chromosomes are beads on a string, and the spindle is the force pulling the string in two.)
Entrapment in mitosis
- Cancer cells can become trapped in mitosis (the cell division phase), leading to cell death.
Inhibited cell movement
- Disruption of microtubules can reduce cancer cells’ ability to move and spread to other parts of the body (metastasize).
Summary
By interacting with microtubules, fenbendazole can disrupt several crucial cellular processes in cancer cells, which can lead to inhibited growth, cell death, and decreased spread. It is this mechanism that makes fenbendazole a potentially interesting agent in cancer research—and as an adjuvant cancer treatment—until research perhaps one day picks up speed.
Important about absorption
Like Mebendazole (Vermox), this substance is fat-soluble. To ensure the substance is absorbed into the blood, where it must fight cancer cells, it must be taken with a high-fat meal (at least 40g of fat is optimal, but less can suffice).
Research status and limitations
Limited clinical research has been conducted on the use of fenbendazole for treating cancer. The available studies are small and have been retrospective or observational. As a result, there is not enough evidence to establish whether fenbendazole is effective or safe for treating cancer in humans. However, many testimonies of extensive and convincing effects exist here. As well as in this group on Facebook.
Varying results
- The results of studies with fenbendazole have been very varied, and there is no guarantee that it will work for all types of cancer or for all patients. (Completely in line with all other cancer treatments—including conventional treatment.)
Animal studies
- Several animal studies have shown promising results, where fenbendazole has inhibited the growth of various types of cancer.
Reports
- There are many reports from people who have experienced a positive effect of fenbendazole against cancer.
Limited human research
- Although there are promising results from animal studies and positive reports, many large, well-controlled clinical studies in humans have not yet been performed.
Safety profile
- Fenbendazole is not approved for the treatment of cancer in humans, and there is limited knowledge about its long-term safety profile and potential side effects. Furthermore, the production requirements for animal medications are not the same as those for human medications.
Side effects
Some of the potential side effects of fenbendazole include:
- Diarrhea
- Stomach pain
- Nausea and vomiting
- Dizziness
- Headache
- Skin rash
- Neurological problems
- Liver impact
It should be noted that this is not an exhaustive list of all possible side effects.
Interaction
Fenbendazole can also interact with other drugs, so it is important to talk to your doctor before taking it if you are taking other medications.
If you are in doubt, it can be checked here:
It every now and then appears possible to obtain Fenbendazole from Amazon.de. Instead, one might use Axolur (with Fenbendazole as the active substance), which is an over-the-counter medication in Sweden.
Antiparasitic agents
Why antiparasitic agents can have an effect on cancer cells:
Analogous (related) biological processes:
Cell division
- Both cancer cells and parasites divide rapidly, and agents that disrupt cell division can have an effect on both.
Metabolism
- Both cancer cells and some parasites have high metabolic activity to grow and divide rapidly. Agents such as Fenbendazole, Vermox, and Plaquenil can affect specific metabolic pathways that are important for both cancer cells and parasites.
Protein synthesis
- Both cancer cells and parasites produce a variety of proteins necessary for their survival and spread. Some of these proteins may have analogous structures or functions, and therefore agents that inhibit protein synthesis in parasites can also affect cancer cells.
Indirect effects
Awakening dormant immune cells
- Cancer cells are skilled at “shutting down” our immune system. Parasites can help “awaken” these dormant immune cells so they can again recognize and attack the cancer cells.
Microenvironment
- Parasites can affect the microenvironment where cancer cells are located. By removing parasites, one can change this microenvironment and make it less favorable for cancer cell growth.
Activation of the immune system
- Some parasites have an ability to stimulate and activate our immune system in a way that makes it more effective at fighting diseases, including cancer cells. Paradoxically, antiparasitic agents can thus strengthen this immune response and thereby indirectly have a cancer-suppressing effect.
Is parasitic infection then a good thing
Why do we take antiparasitic drugs but research parasites for the treatment of cancer?
It is not a contradiction. Researchers try to utilize the positive aspects of parasites without exposing humans to the negative consequences of an infection. This can be done by:
Combination treatment
- Parasites can potentially be used in combination with existing cancer treatments to increase effectiveness.
Isolating the active substances
- Researchers attempt to isolate the specific substances in parasites that have a positive effect on the immune system and develop drugs based on these substances.
Genetically modified parasites
- Work is being done to develop genetically modified parasites that only possess the desired properties and do not cause disease.
While we wait
The result of this research lies somewhere in the future. Personally, I do not dare wait for that, so I have chosen a repurposed drug in the form of Vermox (in combination with other repurposed drugs).
Note
It is important to have a nuanced understanding of parasites. While some parasites can have positive effects on our health, most parasites are harmful and can cause serious diseases. Research in this area is still in its infancy, and it is important to be critical of the information one finds.
Conclusion
There is not yet sufficient scientific evidence to recommend fenbendazole as a treatment for cancer. More studies are (as with other repurposed drugs) necessary to determine its effectiveness and safety (and no one has an economic interest in conducting such studies). That is Gemini’s opinion.
On the other hand, there are quite a few reports of people who have recovered dramatically even after stage 4 cancer. This is to an extent that there is talk of NED (No Evidence of Disease). If one is considering using fenbendazole as a complementary treatment for cancer, one should discuss the pros and cons with their practitioner.
See also The parasite’s path to cancer
See also Mebendazole inhibits the spread of cancer
See also Repurposed Drugs
See also Cancer treatment based on the Mitochondrial Stem Cell Connection
See also No medicine – Plan B
To be continued…
Links
Interaktioner (søg på præparater) (Interaktionsdatabasen, Lægemiddelstyrelsen) (Interaktionsdatabasen, Danish Medicines Agency)
Fenbendazole, Ivermectin and Mebendazole for Breast Cancer Success Stories – 37 Case Reports (The Medical Adviser, June 2025)
- Relevance: Several peer-reviewed articles and case studies suggest that Fenbendazole, Ivermectin, and Mebendazole may play an important role in the treatment of stage 4 breast cancer. Research shows that these substances have different anti-cancer mechanisms that can be effective against cancer cells. Specific studies include a protocol for Ivermectin, as well as investigations of Fenbendazole and Mebendazole in relation to breast cancer and metastases.
Get busy living (Joe Tippens’ website. Pioneer in the use of Fenbendazole for cancer treatment)
mycancerstory.rocks (Joe Tippens’ Facebook page for users)
Fenbendazole for Cancer (Internal)
Fenbendazole as a Potential Anticancer Drug (National Library of Medicine)
What My Patients are Asking (Breast Cancer Treatment)
Oral Fenbendazole for Cancer Therapy in Humans and Animals (PubMed)
Page created: July 1, 2024, Last revised October 26, 2024
d. 01.07.24, Senest revideret d. 26.10.24
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What you read on Jeg har Kræft is not a recommendation. Seek competent guidance.
Antiparasitic drugs – compariso
Short summary of differences and similarities
Although several antiparasitic agents are being investigated for their effect against cancer, they work in widely different ways:
Mebendazole:
- Destroys the cancer cell’s internal “skeleton” (microtubules) to stop cell division. Among the drugs mentioned here, it is the one most extensively studied in clinical trials.
Fenbendazole:
- Also destroys the cell’s “skeleton” but is additionally believed to create metabolic stress. It has a strong anecdotal history.
Niclosamide:
- Interrupts the cell’s energy supply while simultaneously blocking its growth signals.
Ivermectin:
- Creates internal stress in the cell and prevents it from pumping out chemotherapy, which can counteract resistance.
Hydroxychloroquine:
- Blocks the cell’s “recycling system” (autophagy), causing it to succumb to its own waste.
The point is that these different mechanisms allow for strategic combinations where cancer can be attacked from multiple angles simultaneously to achieve a stronger effect.
Antiparasitic agents compared
One of the most promising areas within complementary and experimental cancer treatment is repurposed drugs. A particularly interesting group consists of antiparasitic agents. Many of these substances have proven to possess potent anticancer properties, but it is crucial to understand that they do not all work the same way. Their attacks on cancer cells are widely different.
Below is a comparison of the most discussed substances and their unique mechanisms of action to provide a clear overview of their individual strengths and potential.
Mebendazole (Vermox)
- Main mechanism: Destruction of microtubules (the cell’s scaffolding)
- Mebendazole’s primary and most well-documented effect is a disruption of the cancer cells’ internal skeleton. The substance, which belongs to the benzimidazole family, works by binding to the protein tubulin and preventing it from assembling into microtubules. This effectively stops cell division (mitosis) and leads to cell death. Mebendazole is also the benzimidazole that has been the subject of the most formal clinical investigations, especially in connection with aggressive brain tumors (glioblastoma), where it has been tested as a supplement to standard chemotherapy.
- Characteristics: A direct, physical attack on the cell’s structure. It is the benzimidazole most extensively studied in human clinical trials.
See also links at the bottom of this article
Fenbendazole
Main mechanism: Destruction of microtubules (the cell’s scaffolding).
- Fenbendazole shares the same core mechanism as mebendazole, namely destroying the cancer cells’ microtubules and thereby stopping cell division. Its popularity, however, is driven more by preclinical studies (laboratory and animal trials) as well as strong patient reports and compelling anecdotal evidence.
Secondary mechanisms:
- In addition to the microtubule effect, research indicates that fenbendazole has a unique ability to stress the metabolism of cancer cells by blocking their sugar uptake. Certain studies also indicate that it can reactivate the tumor-suppressor gene p53.
Characteristics:
- Characterized by having a strong anecdotal history and a research focus on its ability to create metabolic stress.
See also links at the bottom of this article
Niclosamide
Niclosamide takes a completely different approach, which is primarily metabolic and signal-oriented.
Main mechanism: Metabolic collapse (energy blockade)
- Niclosamide acts as an “uncoupler” in the cancer cell’s power plants, the mitochondria. It simply short-circuits the process that produces energy (ATP), leading to an immediate and fatal loss of energy in the cell. Simultaneously, massive oxidative stress is created (via ROS production), further damaging the cell.
Secondary, but crucial mechanism: Signaling sabotage
- Beyond the energy blockade, niclosamide’s great strength is its ability to simultaneously inhibit a wide range of central signaling pathways that cancer cells depend on (Wnt, STAT3, mTOR, NF-κB). This hits not only growth but also the otherwise resilient cancer stem cells.
Characteristics:
- A dual attack that both removes the cell’s fuel and interrupts its internal communication.
See also links at the bottom of this article
Ivermectin
Ivermectin is again different from those mentioned above, working broadly on several systems related to cell stress and transport.
Main mechanism: Induction of oxidative stress and ion imbalance
- Like niclosamide, ivermectin can create high levels of oxidative stress (ROS) that are toxic to the cancer cell. It is also believed to affect ion channels in the cell membrane, disrupting the fragile electrical balance the cell maintains.
Secondary, but crucial mechanism: Inhibition of transport pumps
- One of the main causes of chemoresistance is that cancer cells develop pumps (such as P-glycoprotein) that actively push chemotherapy back out of the cell. Ivermectin has been shown to block these pumps. This means it can make resistant cancer cells sensitive to chemotherapy again, as the poison now remains inside the cell.
Characteristics:
- Creates internal stress and prevents the cancer cell from “pumping” out toxins.
See also links at the bottom of this article
Hydroxychloroquine (Plaquenil)
This drug, which is an antimalarial agent, has a very specific and unique mechanism.
Main mechanism: Blocking autophagy (the cell’s recycling station)
- Autophagy is a survival mechanism where the cell breaks down and recycles its own damaged parts to obtain energy and building blocks under pressure (e.g., during chemotherapy). Hydroxychloroquine blocks this process. The result is that the cancer cell cannot “clean up” after itself, leading to an accumulation of toxic waste inside. This makes the cell significantly more vulnerable and can push it toward cell death, especially when it is already stressed by other treatments.
Characteristics:
- Prevents the cancer cell from “eating itself” to survive pressure.
See also links at the bottom of this article
Artemisinin (and derivatives)
Main mechanism: Iron-activated cell death via free radicals
- Artemisinin, originally a Nobel Prize-winning drug for malaria, has a highly effective and specific mechanism of action. Cancer cells need large amounts of iron to divide rapidly, and they therefore have a much higher concentration of iron than normal, healthy cells. The artemisinin molecule contains a special chemical structure (an endoperoxide bridge) that reacts violently when it comes into contact with iron. This reaction creates an explosion of unstable and highly damaging molecules called free radicals (specifically Reactive Oxygen Species, ROS). This internal “bomb” of oxidative stress destroys the cancer cell’s membranes, proteins, and DNA from within, forcing it into cell death. The process has similarities to a specific type of cell death called ferroptosis (iron-dependent cell death).
Access in Denmark:
- The pure, most potent substance artesunate (a derivative) is a prescription drug in Denmark, while the plant Artemisia annua is typically sold as a dietary supplement.
Characteristics:
- Functions as a “Trojan horse” that exploits the cancer cell’s own iron dependency to create a targeted internal explosion.
See also links at the bottom of this article
Overview
| Drug | Primary Mechanism of Action | Unique Characteristics |
| Mebendazole | Destruction of microtubules | Attacks the cell’s “skeleton.” Most studied in clinical trials. |
| Fenbendazole | Destruction of microtubules | Attacks the cell’s “skeleton.” Strong anecdotal history. |
| Niclosamide | Metabolic collapse (energy blockade) | Removes cell fuel and sabotages signaling pathways. Poor absorption. |
| Ivermectin | Induction of oxidative stress / Inhibition of pumps | Creates internal stress and counteracts chemoresistance. |
| Hydroxychloroquine | Inhibition of autophagy | Prevents the cell’s “recycling system” from working. |
| Artemisinin (and derivatives) | Iron-activated formation of free radicals (ROS) | Exploits high iron content in cancer cells to create oxidative stress. |
Conclusion
The clear conclusion is that there is no single “antiparasitic” effect against cancer. Each substance represents a unique angle of attack that exploits different vulnerabilities in the cancer cell’s complex machinery. This diversity opens the door for intelligent combination treatments, where a tumor can be hit from several sides simultaneously. In the long run, a deeper understanding of these mechanisms can lead to more tailored treatment, where the choice of a repurposed drug is based on the specific biochemical profile of the individual tumor. The potential lies not in a single “miracle cure,” but in the strategic use of an entire arsenal of different, rediscovered “keys,” each of which can unlock a new door in the cancer cell’s defense.
As these are medications, it is naturally essential to discuss their use with your healthcare provider.
See also Metabolic strategy – block signaling pathways by cancer type – chart overviews
If you are in doubt about interaction, it can be checked here:
See also Repurposed Drugs
See also No medicine – Plan B
Se også The parasite’s path to cancer
Links
Ivermectin:
Ivermectin, a potential anticancer drug derived from an antiparasitic agent (Science Direct, 2021)
- Relevance: This article provides a broad overview of the many proposed anti-cancer mechanisms for ivermectin. It mentions, among other things, the effect on Hippo, Akt/mTOR, and WNT signaling pathways, which supports the drug’s versatility.
The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT-TCF pathway responses in human cancer (EMBO Molecular Medicine, 2014)
- Relevance: A very specific study confirming that ivermectin is an effective blocker of the WNT signaling pathway, which is a fundamental and often overactive signaling pathway in many cancers, including colorectal and breast cancer.
- Relevance: An animal study shows that the drug ivermectin has a strong anti-cancer effect on non-small cell lung cancer (NSCLC). The study concludes that ivermectin works by blocking the central growth signaling pathway (EGFR/PI3K/AKT/mTOR), leading to increased cell death and inhibited tumor growth.
Ivermectin and Cancer: Exploring the Potential Link (Williams Cancer Institute, 2023)
- Relevance: Ivermectin has potential as a cancer treatment by inhibiting tumor growth, inducing apoptosis, strengthening the immune system, and preventing angiogenesis. These mechanisms may supplement existing therapies, but further clinical research is necessary. Overall, Ivermectin opens new possibilities for the development of innovative cancer treatments.
Ivermectin, a potential anticancer drug derived from an antiparasitic drug (Science Direct, 2021)
- Relevance: Ivermectin, an antiparasitic macrolide, has shown promising potential as a cancer treatment by inhibiting tumor cell proliferation and promoting apoptosis through multiple signaling pathways. This opens possibilities for clinical use of ivermectin as an anti-neoplastic agent. Further research is needed to realize this potential in cancer treatment.
Fenbendazole:
Fenbendazole, Ivermectin and Mebendazole for Breast Cancer Success Stories – 37 Case Reports (The Medical Adviser, June 2025)
- Relevance: Several peer-reviewed articles and case studies suggest that Fenbendazole, Ivermectin, and Mebendazole may play an important role in the treatment of stage 4 breast cancer. Research shows that these substances have different anti-cancer mechanisms that can be effective against cancer cells. Specific studies include a protocol for Ivermectin, as well as investigations of Fenbendazole and Mebendazole in relation to breast cancer and metastases.
- Relevance: Fenbendazole can kill both common cancer cells and the difficult cancer stem cells in cervical cancer by disrupting the cells’ growth cycle. It stopped tumor growth in animal models without weight loss, in contrast to chemotherapy, and resulted in full survival in those treated. These results make fenbendazole a promising treatment choice against cervical cancer.
Transcriptome analysis reveals the anticancer effects of fenbendazole on ovarian cancer: an in vitro and in vivo study (PubMed, 2024)
- Relevance: Fenbendazole can inhibit the growth and promote the death of ovarian cancer cells by disrupting the cell cycle and causing mitotic catastrophe. It was also shown to reduce tumor growth in mice, suggesting it could become a promising treatment for ovarian cancer. These results open possibilities for new therapies against this serious disease.
Mebendazole:
Albendazole and Mebendazole as Anti-Parasitic and Anti-Cancer Agents: an Update (PubMed, 2021)
- Relevance: Albendazole and mebendazole are broad-spectrum deworming medications that block microtubules and have shown promising anti-cancer effects in vitro and in vivo. They can be used against parasitic infections and potentially as cancer treatment, but long-term use can cause side effects like liver damage. Mebendazole is currently more popular in cancer trials due to albendazole’s toxicity.
- Relevance: Mebendazole and paclitaxel have a synergistic effect on inhibiting proliferation and microtubular structures in oral tongue squamous cell carcinoma (OTSCC) by inhibiting the PI3K/AKT signaling pathway. The combination increases apoptosis markers and may be a promising treatment for OTSCC. Further research is needed to confirm their clinical potential.
In vitro evaluation of lipidic nanocarriers for mebendazole delivery to improve anticancer activity (PubMed, 2024)
- Relevance: Mebendazole nanostructures (MBZ-NLCs) are stable and contain a larger portion of the active substance than standard forms. They are ten times more effective against cancer cells and can prevent the movement of cancer cells in laboratory experiments. The results suggest that mebendazole nanostructures could become a good treatment for lung cancer, but more tests in the body are needed.
Plaquenil:
- Relevance: A new study shows that the substance 2-BFI (an imidazoline I2-receptor agonist) significantly enhances the cell-killing effect of the autophagy inhibitor hydroxychloroquine (HCQ) against colorectal cancer cells. The combination works by creating increased oxidative stress and disrupting cancer cell metabolism and survival mechanisms.
Malaria Drug Could Combat Chemotherapy-Resistant Head and Neck Cancers (UPMC, 2022)
- Relevance: This is an easy-to-understand summary of a study that shows a concrete example of how hydroxychloroquine is used to overcome chemo-resistance. It explains how the substance can “re-sensitize” cancer cells so that chemotherapy works again.
Repurposing Drugs in Oncology (ReDO)—chloroquine and hydroxychloroquine as anti-cancer agents (PubMed, 2017)
- Relevance: Chloroquine (CQ) and hydroxychloroquine (HCQ) have potential as anti-cancer treatment, especially in combination with standard therapies. They affect both cancer cells and the tumor microenvironment through autophagy inhibition and modulation of signaling pathways such as p53 and CXCR4-CXCL12. Further clinical studies are necessary to optimize dosing and treatment regimens.
Niclosamide:
- Relevance: This study identified 35 genes, including CDK1 and TTK, as important targets in ovarian cancer, which often develops resistance to treatment. NSC765690 (MCC22) was found to be a promising niclosamide analog with strong activity against both targets, which may help overcome chemotherapy resistance. The results show a data-driven approach to developing new therapies for ovarian cancer.
Niclosamide Treatment Suppressed Metastatic, Apoptotic, and Proliferative Characteristics of MDA-MB-231 Cancer Stem Cells (PubMed, 2025)
- Relevance: This study showed that niclosamide effectively induces apoptosis and stops the cell cycle in aggressive triple-negative breast cancer-CSCs in a 3D model. The treatment reduced metastasis- and resistance-related genes as well as EMT markers, which may improve treatment effectiveness against cancer. The results suggest that niclosamide can increase CSC sensitivity and prevent tumor recurrence.
Pharmacological advances and therapeutic applications of niclosamide in cancer and other diseases (PubMed, 2025)
- Relevance: Niclosamide is an FDA-approved drug with potential in cancer treatment, especially against resistant ovarian cancer, by modulating cell proliferation and apoptosis. New formulations and nanotechnology improve bioavailability, strengthening its therapeutic possibilities. It shows promising versatility in the treatment of cancer, viral infection, and inflammatory diseases.
- Relevance: NHC, an improved form of niclosamide, shows increased solubility and potential as a treatment for colon cancer. The analysis confirms that NHC is more effective than NES, and metabolomics as well as 16S rRNA investigate its mechanism. This may open new possibilities for niclosamide-based cancer treatment.
Antitumor activity of niclosamide-mediated oxidative stress against acute lymphoblastic leukemia (PubMed, 2024)
- Relevance: Niclosamide was shown to be able to inhibit growth and induce apoptosis in acute lymphoblastic leukemia (ALL) by increasing reactive oxygen species and activating TP53. It has potential as a new treatment to improve response and extend survival in ALL patients. These results indicate that niclosamide could become a promising therapeutic agent against ALL.
In General:
Targeting the Mitochondrial-Stem Cell Connection in Cancer Treatment: A Hybrid Orthomolecular Protocol (Journal of Orthomolecular Medicine)
Interactions (search for preparations) (Interaktionsdatabasen, Danish Medicines Agency)
Page created: July 1, 2024, Last revised July 2, 2025
❤
What you read on Jeg har Kræft is not a recommendation. Seek competent guidance.