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
Ivermectin and cancer
Content:
- Ivermectin and cancer (scroll down)
- Antiparasitic agents compared (scroll to)
Summary of Ivermectin
Strategic purpose:
- To function as the “broad hammer” that hits the cancer’s root system (stem cells) and stops spreading. Ivermectin is used to capture cell populations that normally escape chemo and radiation and are responsible for relapse.
Mechanisms:
- Ivermectin is unique because it works on many fronts simultaneously. It shuts down the signals that cause cancer to grow (WNT and PAK-1), prevents the cell from pumping out toxins (P-glycoprotein), and makes the tumor visible to the immune system.
Role in treatment:
- Acts as the central focal point that binds the entire treatment together in a metabolic strategy. It significantly enhances the effect of other medications (such as chemo or hormone therapy) and prevents recurrence by keeping stem cells in check.
Ivermectin in a cancer strategy
Ivermectin (brand names such as Stromectol and Scabior) is originally known as an antiparasitic agent that has saved millions from river blindness. However, in modern integrative oncology, the substance has achieved status as one of the most potent “multitarget” drugs we know.
For the cancer patient, Ivermectin is interesting for one primary reason:
It breaks resistance
Standard treatment (chemotherapy and radiation) often fails over time because cancer cells learn to defend themselves. They mutate, they hide, and they pump the poison back out. Ivermectin intervenes and sabotages precisely these defensive works.
Where an agent like Plaquenil has one primary function (to stop the cleanup), Ivermectin functions as a Swiss army knife. It attacks the cancer cell from the surface, deep into the core to the stem cells, and even changes the way the immune system perceives the tumor. It is therefore an indispensable piece for patients fighting aggressive, metastatic cancer where the “standard package” is no longer sufficient.
See also Living with incurable cancer
Tip for absorption
Ivermectin is lipophilic (fat-loving). Studies show that absorption into the blood increases significantly (up to 2.5 times) if taken with a high-fat meal rather than on an empty stomach.
Attack on cancer stem cells
This is Ivermectin’s most important property and the primary reason it is used preventatively against recurrence. The problem with traditional cancer treatment is that it primarily kills cells that divide rapidly.
But in any tumor, there is a small group of cells—cancer stem cells (CSC)—that divide slowly or not at all. They function as “queens in the beehive.” Chemotherapy bounces off them because they are dormant. When the treatment is over, they wake up and create new tumors (metastases).
Cancer stem cells depend on some very specific “embryonic” signaling pathways to maintain their ability to survive—signals that the body normally only uses when a fetus is being formed. The most important ones are called WNT/Beta-catenin, Hedgehog, and Notch.
See also Block cancer signaling pathways
Ivermectin’s effect
Ivermectin has proven to be a powerful inhibitor of, in particular, the WNT signaling pathway. By blocking this signal, the stem cells lose their “instruction manual.” They lose the ability to renew themselves (self-renewal) and the ability to create new colonies. One thus attacks the disease’s very ability to reappear. Without Ivermectin (or similar substances), the root is effectively left in the ground. [6, 11]
Stop the invasion
A less known but vital mechanism is Ivermectin’s ability to block the enzyme PAK-1 (p21-activated kinase 1).
For a cancer cell to spread from, for example, the breast to the bones, it must be able to change shape and move through the tissue. PAK-1 functions as the cell’s “motor” in this process. It is a key enzyme that controls the cell’s skeleton and its ability to invade new tissue. Over 70% of all cancers (including breast, lung, and pancreatic cancer) have overactive PAK-1, which drives aggressive growth.
Ivermectin’s effect
Ivermectin inhibits PAK-1 effectively. Without this enzyme, the cancer cell becomes “paralyzed.” It loses the ability to move and invade surrounding tissue, which significantly reduces the risk of metastases markantly. [2]
Blocking resistance
This point can be the difference between whether your other medicine works or not. One of the main reasons cancer treatment fails is that cancer cells develop Multi-Drug Resistance (MDR).
Specifically, the cancer cell forms many small pumps in the cell membrane called P-glycoprotein (P-gp). These pumps function like a bilge pump on a boat. That is, as soon as chemotherapy or other drugs enter the cell, P-gp physically pumps them out again before they can do damage. This is why a tumor can shrink initially, only to suddenly grow again despite treatment.
Ivermectin’s effect
Ivermectin physically binds to these pumps and blocks them completely.
Consequence:
- When the “bilge pump” is stopped, the level of medication inside the cancer cell rises sharply. This means that a dose of chemotherapy or other medicine that was previously ineffective suddenly becomes lethal to the cancer cell. Ivermectin “locks the door” so the poison stays inside. [4]
There are certain chemo agents where the use of Ivermectin can be decidedly dangerous. See the section Safety and Precautions.
Immune effect
Many aggressive tumors are “cold.” This means they have built a microenvironment that makes them invisible to the body’s killer cells (T-cells). For the patient, this is fatal as the immune system stands passively on the sidelines.
Ivermectin has the ability to induce a special form of cell death called Immunogenic Cell Death (ICD). When a cancer cell dies from Ivermectin, it doesn’t just quietly implode. It releases danger signals (the molecules ATP and HMGB1) to the surroundings.
This is equivalent to sending up a distress flare from the cancer tissue. It attracts the immune system’s cells, which suddenly can “see” the tumor and begin to attack it. In this way, Ivermectin helps convert a cold tumor into a “hot” tumor, which is crucial for long-term survival. [3]
Synergy with other agents
In a metabolic strategy, Ivermectin never stands alone. Its ability to block pumps and signaling pathways makes it the perfect “partner” for other substances in a combination treatment.
Synergi with Plaquenil
This is a classic “hammer and anvil” combination. Ivermectin damages the cancer cell (via ICD and microtubule stress). Normally, the cell would attempt to repair the damage by eating itself (autophagy). But if one simultaneously takes Plaquenil, autophagy is blocked. The cell is attacked (by Ivermectin) and deprived of the possibility of repair (by Plaquenil). This leads to metabolic collapse. [5]
Synergi with hormone therapy (Tamoxifen/ Letrozol)
In breast cancer, many develop resistance to anti-estrogen treatment over time. Ivermectin can restore sensitivity by downregulating the signaling pathway STAT3, which is often the cause of resistance.
This makes the hormone treatment effective again and thus extends its lifespan. [1]
Synergi with Fenbendazol
Both Ivermectin and Fenbendazole/Mebendazole attack the cancer cell’s structure, but in different ways. Fenbendazole/Mebendazole hit the microtubules (the skeleton) very specifically, while Ivermectin hits the signals and the pumps. Together, they create massive stress that is difficult for the cell to adapt to.
Safety and precautions
Although Ivermectin has been given in billions of doses against parasites with few side effects, cancer treatment often requires higher doses over longer periods. This requires respect for the substance.
Blood-brain barrier (MDR1 gene)
Ivermectin should work in the body but be kept out of the brain. This normally happens automatically via a barrier. However, some people have a genetic variation in the MDR1 gene that makes the barrier leaky. If Ivermectin enters the brain, it can cause neurological symptoms such as dizziness, balance problems, and in rare cases, seizures. Always start low to test your tolerance.
Interactions
Ivermectin can increase the effect of blood-thinning medication (such as Warfarin/ Marevan). This should be closely monitored. Since Ivermectin affects the liver, one should be cautious with alcohol and other liver-straining substances at the same time.
Warning
Critical interaction with chemotherapy:
- Because Ivermectin blocks P-glycoprotein (the “bilge pump”), it can violently increase the concentration of certain types of chemotherapy—such as Etoposide and Taxanes—in the blood. If the body is prevented from excreting the chemo, it can lead to an unintended overdose that can destroy bone marrow and cause life-threateningly low blood counts. If you are in active chemo treatment, the use of Ivermectin requires extreme caution.
Interactions (search for preparations) (Interaktionsdatabasen, Danish Medicines Agency) [10]
Research
Breast cancer
Extensive data, including case reports, indicates effectiveness against metastatic breast cancer. Particularly triple-negative breast cancer (TNBC), which is difficult to treat, shows sensitivity to Ivermectin because this form of cancer is highly dependent on the WNT signaling pathway and PAK-1 to grow. [1]
Lung cancer
A new study from 2025 in animal models shows that Ivermectin can effectively slow the growth of non-small cell lung cancer (NSCLC). The study concludes that Ivermectin works by blocking the central growth signaling pathway EGFR/PI3K/AKT, leading to increased cell death. [7]
Colorectal cancer
Over 90% of all cases of colorectal cancer are driven by mutations in the WNT signaling pathway. Since Ivermectin is a specific WNT inhibitor, it is theoretically one of the most promising agents for this specific cancer type. [6]
Conclusion
For the cancer patient seeking ways outside the system’s standard offerings—or where standard offerings are exhausted—Ivermectin represents a strategically important option. It is not merely a “pill against parasites.”
It is one of the few agents capable of hitting the cancer’s “root system” (stem cells) and simultaneously breaking the resistance that makes chemotherapy ineffective. By blocking the WNT signaling pathway, stopping the cell’s pumps, and making the tumor visible to the immune system, Ivermectin tips the balance in favor of the patient. In a metabolic cocktail, Ivermectin is often the factor that makes the difference between stagnation and regression of the disease.
Interactions (search for preparations) (Interaktionsdatabasen, Danish Medicines Agency)
See also Ivermectin’s immunotoxic effect
See also Metabolic strategy – block signaling pathways by cancer type – chart overviews
See also The parasite’s path to 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
[1] Novel Drug Combo Shows Promise Against Triple-Negative Breast Cancer (City of Hope, 2021)
- Content: An article from a recognized cancer research center describing research into Ivermectin. It confirms that the substance shows promising results against aggressive Triple-Negative breast cancer by attacking the cancer cells in a new way.
[2] Ivermectin, a potential anticancer drug derived from an antiparasitic agent (Science Direct, 2021)
- Content: A broad overview of the many anti-cancer mechanisms for Ivermectin. The article reviews the effect on signaling pathways such as Hippo, Akt/mTOR, and WNT, as well as the stabilization of microtubules.
[3] Ivermectin And Cancer: Exploring The Potential Link (Williams Cancer Institute, 2023)
- Content: A review from an institute working with intratumoral treatments, describing Ivermectin’s ability to create “hot” tumors via immunogenic cell death (ICD).
[4] Ivermectin reverses the drug resistance in cancer cells (PubMed, 2019)
- Content: A key study for understanding Ivermectin as supportive treatment. It documents the substance’s ability to block the P-glycoprotein pump, which prevents cancer cells from spitting chemotherapy and other medication back out.
[5] Ivermectin induces autophagy-mediated cell death (Bioscience Reports/PubMed, 2019)
- Content: Research showing how Ivermectin not only slows growth but can actively induce cell death and autophagy. This makes it ideal to combine with an autophagy inhibitor like Plaquenil for maximum stress on the cancer cell.
[6] The river blindness drug Ivermectin inhibits WNT-TCF pathway responses (EMBO Molecular Medicine, 2014)
- Content: A fundamental study confirming that Ivermectin blocks the WNT signaling pathway. Since WNT is a main driver in colorectal and breast cancer, among others, this study is central to the substance’s use against cancer stem cells.
[7] Targeting EGFR/PI3K/AKT/mTOR and Bax/Bcl-2/caspase3 pathways with ivermectin (PubMed/ScienceDirect, 2025)
- Content: An animal study showing strong effect against non-small cell lung cancer (NSCLC). The study concludes that Ivermectin works by blocking the central growth signaling pathway EGFR/PI3K/AKT, leading to increased cell death and inhibited tumor growth.
[8] Ivermectin: Uses, Dosage, Side Effects, Warnings (Drugs.com, 2025)
- Content: Detailed and updated information on side effects, dosages, and contraindications. An important source for checking the safety profile and interactions before starting.
[9] Albendazole and Mebendazole as Anti-Parasitic and Anti-Cancer Agents (PubMed, 2021)
- Content: A comprehensive review containing important comparative data on the mechanisms of action for the entire group of antiparasitic agents in oncology. The article explains how these substances (just like Ivermectin) work by blocking the cell’s skeleton (microtubules) and inhibiting glucose uptake.
[10] Interaktioner (search for preparations) (Interaktionsdatabasen, Danish Medicines Agency)
- Content: Official Danish database for checking medication combinations.
[11] Targeting the Mitochondrial-Stem Cell Connection in Cancer Treatment: A Hybrid Orthomolecular Protocol (Journal of Orthomolecular Medicine, 2024)
- Content: The article introduces a “hybrid protocol” combining repurposed drugs and supplements. The purpose is specifically to hit cancer stem cells by cutting off their energy supply in the mitochondria, supporting the metabolic approach where Ivermectin is a central piece.
Page created: December 12, 2025
To be continued…
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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
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What you read on Jeg har Kræft is not a recommendation. Seek competent guidance.