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IVERMECTIN and CANCER, it has at least 15 anti-cancer mechanisms of action. Can Ivermectin Treat COVID-19 mRNA Vaccine Induced Turbo Cancers? – 9 Ivermectin papers reviewed
2ND SMARTEST GUY IN THE WORLD
This Substack recently wrote about the powerful anticancer properties of Fenbendazole: I also mentioned in passing that one of reasons Ivermectin was so viciously maligned and suppressed was that if society were taking it to cure PSYOP-19, one of the side effects would be “sudden” plummeting cancer rates, and thus BigPharma et al. went all out to destroy
Dr. William Makis MD
- 2023 Sep.23 – Man-Yuan Li et al – Ivermectin induces nonprotective autophagy by downregulating PAK1 and apoptosis in lungadenocarcinoma cells
- 2023 May – Samy et al – Eprinomectin: a derivative of ivermectin suppresses growth and metastatic phenotypes of prostate cancer cells by targeting the β-catenin signaling pathway
- 2022 Nov – Lotfalizadeh et al – The Anticancer potential of Ivermectin: Mechanisms of action and therapeutic implications
- 2022 Oct – Jian Liu et al – Progress in Understanding the Molecular Mechanisms Underlying the Antitumour Effects of Ivermectin
- 2022 Jun – Daeun Lee et al – Ivermectin suppresses pancreatic cancer via mitochondria dysfunction
- 2021 Aug – Shican Zhou et al – Ivermectin has New Application in Inhibiting Colorectal Cancer Cell Growth
- 2021 Jan – Mingyang Tang et al – Ivermectin, a potential anticancer drug derived from an antiparasitic drug
- 2019 Sep Intuyod et al – Anti-parasitic Drug Ivermectin Exhibits Potent Anticancer Activity Against Gemcitabine-resistant Cholangiocarcinoma In Vitro
- 2018 Feb – Juarez et al – The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug
2018 Feb – Juarez et al – The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug
- Satoshi Omura at the Kitasato Institute discovered Ivermectin in 1979 and was awarded a Nobel Prize in Physiology or Medicine for this discovery in 2015
- Ivermectin was FDA Approved for human use in 1987 to orally treat onchocerciasis, also known as river blindness, caused by the blackfly-transmitted parasite Onchocerca volvulus
- Ivermectin is annually taken by close to 250 million people
- most patients treated with Ivermectin have no side-effects other than those caused by the immune and inflammatory responses against the parasite, such as fever, pruritus, skin rashes and malaise
- maximum concentration in plasma is reached 4-5 h after its oral administration
- its half-life is approximately 19 h and is metabolized in the liver by the cytochrome CYP1A and CYP3A4 complexes, generating 10 metabolites, mostly demethylated and hydroxylated.
- Its excretion is mainly by feces and only 1% is excreted in the urine
- Ivermectin exerts antitumor effects in different types of cancer.
What this means Clinically:
- Chloride channel – Acute myeloid leukemia – induced cell death
- Akt/mTOR path – glioblastoma, renal cancer cell lines – inhibition of mitochondrial biogenesis or function, oxidative stress, DNA damage
- P2X7 (ICD) overexpression promotes tumor growth and metastases – ivermectin potentiates immunogenic cell death (ICD) in triple negative breast cancer cells
- PAK1 (Autophagy) – glioblastoma and ovarian cancer cell lines – Ivermectin promotes autophagy through this pathway
- WNT-TCF pathway – glioblastoma, colon cancer, melanoma – Ivermectin exerts anti-proliferative function through this pathway (possibilities to use Ivermectin to block WNT-TCF dependent cancers like breast, skin, lung)
- SIN3 Domain – breast cancer (Ivermectin acts as epigenetic modulator to alter gene expression and decrease tumor growth)
- NS3 helicase – glioma cells – Ivermectin had anti-tumor effects by acting as helicase inhibitor
In Vitro Studies:
- breast cancer, ovarian, prostate, colon, pancreas, head and neck, melanoma – inhibits cell proliferation, induction of apoptosis, autophagy, reversion of tamoxifen resistance, inhibits metastases
- glioblastoma – growth inhibition, apoptosis, and anti-angiogenesis
In Vivo Studies (done on immune deficient mice):
- acute myeloblastic leukemia – reduce tumor volume up to 70%
- glioblastoma – reduce tumor volume up to 50%
- breast cancer – reduce tumor volume up to 60%
- glioma – reduce tumor volume up to 50% (at 0.24mg/kg), however at human dose equivalent to 0.8mg/kg tumors were not detectable!
- colon cancer – reduce tumor volume up to 85%
- median dose employed was equivalent to 0.4 mg/kg in humans from 10 to 42 days (oral, intraperitoneal or intra-tumoral)
- the in vitro and in vivo antitumor activities of Ivermectin are achieved at concentrations that can be clinically reachable based on the human pharmacokinetic studies done in healthy and parasited patients
2019 Sep Intuyod et al – Anti-parasitic Drug Ivermectin Exhibits Potent Anticancer Activity Against Gemcitabine-resistant Cholangiocarcinoma In Vitro
- Ivermectin studied on cholangiocarcinoma cells that were chemo resistant (gemcitabine)
- Ivermectin inhibited cancer cell proliferation and colony formation in a dose and time dependent manner(!)
- Ivermectin caused S-phase cell cycle arrest and cell death
- Conclusion: “Ivermectin might be useful as an alternative treatment for cholangiocarcinoma, especially in patients who do not respond to chemo.”
2021 Jan – Mingyang Tang et al – Ivermectin, a potential anticancer drug derived from an antiparasitic drug
- specific mechanism of IVM-mediated cytotoxicity in tumor cells is unclear; it may be related to the effect of IVM on various signaling pathways
- IVM seems to induce mixed cell death in tumor cells
- Ivermectin selectively inhibits the proliferation of tumors at a dose that is not toxic to normal cells and can reverse the MDR (multi-drug resistance) of tumors.
- In healthy volunteers, the dose was increased to 2 mg/kg, and no serious adverse reactions were found
- Unfortunately, there have been no reports of clinical trials of IVM as an anticancer drug
- large number of research results indicate that IVM affects multiple signaling pathways in tumor cells and inhibits proliferation, IVM may cause antitumor activity in tumor cells through specific targets
- Ivermectin regulates the tumor microenvironment, inhibits the activity of tumor stem cells and reduces tumor angiogenesis and tumor metastasis.
- It has become increasingly clear that Ivermectin can induce a mixed cell death mode involving apoptosis, autophagy and pyroptosis depending on the cell conditions and cancer type.
- Ivermectin can enhance the sensitivity of chemotherapeutic drugs and reduce the production of resistance. Therefore, IVM should be used in combination with other drugs to achieve the best effect
2022 Jun – Daeun Lee et al – Ivermectin suppresses pancreatic cancer via mitochondria dysfunction
- Poster presentation from South Korea
- Ivermectin was combined with gemcitabine in pancreatic cancer
- Ivermectin-gemcitabine combination inhibited pancreatic cancer cell proliferation via G1 arrest of cell cycle
- in vivo experiments showed ivermectin-gemcitabine significantly suppressed tumor growth of pancreatic cancer compared with gemcitabine alone
- Conclusion: “Ivermectin could be a potential antitumor drug for the treatment of pancreatic cancer”
2021 Aug – Shican Zhou et al – Ivermectin has New Application in Inhibiting Colorectal Cancer Cell Growth
- Colorectal cancer is 3rd most common cancer worldwide, lacks effective therapy
- Ivermectin tested on colorectal cancer cell lines
- Ivermectin dose-dependently inhibited colorectal cancer growth
- promoted cell apoptosis
- promoted total and mitochondrial ROS production (reactive oxygen species)
- induced colorectal cancer cell S-phase arrest
- Conclusion: Ivermectin might be a new potential anticancer drug therapy for human colorectal cancer
2022 Oct – Jian Liu et al – Progress in Understanding the Molecular Mechanisms Underlying the Antitumor Effects of Ivermectin
- PAK1 (Autophagy) – Ivermectin, acts as PAK1 inhibitor and inhibits growth of breast cancer, ovarian cancer, glioblastoma and NF2tumors and involved in cell death in Nasopharyngeal carcinoma and melanoma.
- Apoptosis (Caspase Dependent) – Ivermectin induces apoptosis in glioblastoma, chronic myeloid leukemia cells, also breast cancer, ovarian cancer.
- Immunogenic Cell Death (ICD – P2X7 signaling) – ivermectin induces cell death in triple negative breast cancer.
- YAP1 Inhibition – hepatocellular and cholangiocarcinoma, colorectal cancer, ovarian cancer, gastric cancer – ivermectin exerts anti-tumor effects
- WNT Path (cancer progression – differentiation, metastasis, cell senescence, tumor initiation, tumor growth) – Ivermectin inhibits this path – inhibits colon cancer and lung cancer, ivermectin also limits formation of cancer stem cells.
- TF3 Path – ivermectin stimulates apoptosis of melanoma cells.
- RNA Helicase Inhibition – ivermectin inhibits cell invasion and proliferation of glioma cells
- SID Peptide (SIN3A/B) – Ivermectin inhibits breast cancer progression, also restores tamoxifen sensitivity
- Akt/mTOR inhibition – Ivermectin inhibits mitochondrial respiration – glioblastoma, CML leukemia (some cancers like breast, leukemia and lymphoma are more metabolically active and depended on mitochondria – more responsive to ivermectin inhibition)
- ivermectin is an angiogenesis inhibitor
- ivermectin has anti-mitotic activity
In humans, toxicity of ivermectin is very low, no serious adverse reactions have been found in healthy volunteers at dose up to 120 mg (~2 mg/kg) (Reference: GuzzoCA, FurtekCI, PorrasAG, et al. Safety, tolerability, and pharmacokinetics of escalating high doses of ivermectin in healthy adult subjects. J Clin Pharmacol. 2002;42(10):1122–1133.)
2023 May – Samy et al – Eprinomectin: a derivative of ivermectin suppresses growth and metastatic phenotypes of prostate cancer cells by targeting the β-catenin signaling pathway
- Ivermectin (derivative) inhibits prostate cancer cell viability, migration capacities
- Ivermectin induces apoptosis, autophagy (via ROS)
- Ivermectin downregulates expression of cancer stem cell markers
- Conclusion: Ivermectin has tremendous potential to target metastatic prostate cancer cells and provides new avenues for therapeutic approaches to advanced prostate cancer
2023 Sep.23 – Man-Yuan Li et al – Ivermectin induces nonprotective autophagy by downregulating PAK1 and apoptosis in lung adenocarcinoma cells
- Ivermectin was studied on lung adenocarcinoma cells
- Ivermectin strikingly impeded colony formation and viability of cancer cells, along with cell proliferation, caused apoptosis and enhanced autophagy
- Ivermectin efficiently suppressed cellular growth of lung adenocarcinoma cells in vivo among nude mice
Ivermectin exerts anti-cancer effects through at least 15 different pathways proven in the medical literature, both in vitro and in vivo!
(You get a nice summary of these 15 pathways from the 2021 paper by Mingyang Tang et al.)
First, let’s quickly summarize the anti-cancer mechanisms (a quick summary can be found in 2022 paper by Loftalizadeh et al):
- Ivermectin induces tumor cell death: apoptosis, autophagy, pyroptosis
- Ivermectin inhibits tumor initiation and tumor progression (via WNT inhibition, YAP1 inhibition)
- Ivermectin inhibits tumor growth and proliferation (via Akt/mTOR inhibition, MAPK inhibition)
- Ivermectin stops cancer cell migration, invasion and metastasis (via PAK1 inhibition – seen in 70% of all cancers, EMT inhibition, RNA Helicase inhibition)
- Ivermectin causes cancer cell mitochondrial dysfunction (inhibits mitochondrial biogenesis, increases reactive oxygen species selectively only in cancer cells)
- Ivermectin regulates tumor microenvironment (to inhibit tumor growth and progression, via P2X7 path, ICD – mediates immunogenic cell death)
- Ivermectin inhibits cancer stem cells (which are responsible for tumor initiation, progression and recurrence)
- Ivermectin inhibits tumor angiogenesis (tumor blood vessel creation)
- Ivermectin has anti-mitotic activity (interacts with mammalian tubulin)
- Ivermectin is an epigenetic regulator of cancer to inhibit cancer progression (alters gene expression to inhibit cancer progression, SIN3A, EMT)
- Ivermectin can overcome tumor multidrug resistance
What cancers can Ivermectin treat?
- The top 5 COVID-19 mRNA Vaccine Induced Turbo Cancers are: lymphomas, brain cancers, breast cancers, colon cancers and lung cancers (signals also seen in leukemias, hepatobiliary cancers, testicular cancers, sarcomas and melanomas)
- Ivermectin has been shown to kill these cancer cells (in vitro or in vivo):
- breast cancer, especially triple negative breast cancer which is often seen in COVID-19 mRNA Vaccinated women and has the worst prognosis.
- glioblastoma and gliomas (glioblastomas are often seen in COVID-19 mRNA Vaccinated individuals)
- leukemias, both AML and CML (these are the most aggressive and quickly lethal mRNA Turbo Cancers)
- colorectal cancer (Stage 4 Colon cancers common in COVID-19 mRNA vaccinated)
- hepatobiliary cancers: hepatocecullar carcinoma, cholangiocarcinoma, pancreatic cancer (major signal with COVID-19 mRNA Vaccines)
- lung cancer (Stage 4 lung cancers in COVID-19 mRNA Vaccinated)
- melanoma (definite signal in COVID-19 mRNA vaccinated)
- renal cell cancer (possible signal with mRNA Turbo Cancers) and urothelial carcinoma
- ovarian cancer (possible signal with mRNA Turbo Cancers)
- gastric cancer
- prostate cancer (possible signal with mRNA Turbo Cancers)
- Nasopharyngeal cancer
There is almost no literature on Ivermectin and lymphomas which are probably the most common COVID-19 mRNA vaccine turbo cancers – this must be investigated.
What dose of Ivermectin to treat COVID-19 mRNA Vaccine Turbo Cancer?
- Guzzo et al published a paper in 2022 on the “Safety, tolerability, and pharmacokinetics of escalating high doses of Ivermectin in healthy adult subjects”
- The highest dose tested to be safe with no side effects, was 2 mg/kg.
- Max concentration in plasma is 4 hours after oral intake
- Half life is 18 hours
- Dr.David E. Scheim PhD, Blacksburg VA also wrote an interesting article on Ivermectin Safety in Sep.7, 2021 (Source)
- Several studies have shown that Ivermectin’s anti-cancer effects are DOSE-DEPENDENT (higher dose = better response)
Warning: not to be taken as medical advice – hypothetical situation: if I was faced with a COVID-19 Vaccine Induced Turbo Cancer or an advanced stage cancer, I would be looking at an Ivermectin dose of 2mg/kg orally, daily or every two days.
Also mentioned is a “High Dose Ivermectin” regimen of 2mg/kg per day for a doctor with Stage 4 Gallbladder cancer, taken for over a year, with visual side effects for a few days initially which resolved.
Also described is a case of enlarged Prostate suspicious for cancer, and a 5 week Ivermectin 45mg/day regimen that dropped PSA from 89.1 to 10.9 with resolution of nocturnal urinary frequency. For a 100kg man, that is a dose of 0.45mg/kg, significantly lower than the 2 mg/kg safe dose published by Guzzo et al.
The article describes a cancer patient with a neck tumor and lung metastases on a High Dose Ivermectin regimen of 2.45mg/kg daily.
I believe that it is a reasonable hypothesis that COVID-19 mRNA Vaccine Turbo Cancer patients could benefit from High Dose Ivermectinregimens, such as 2mg/kg and we urgently need more research to be done in this area.
(mRNA Vaccine Induced Turbo Cancers such as leukemias, glioblastomas, breast cancers (including triple negative), colon cancers, hepatobiliary cancers, lung cancers, melanomas, renal cell cancers, ovarian cancers, prostate cancers – as there is already evidence in the literature)
Yesterday the Expose published an article [above] which highlighted just a few of the various diseases that were found to be potentially caused by parasites, including cancers. A recent review of nine published research papers by Doctor William Makis further supports the views in the article, but Dr Makis is more qualified to say “it is a reasonable hypothesis that COVID-19 mRNA Vaccine Turbo Cancer patients could benefit significantly from anti-parasitic drugs.”
One anti parasitic drug in particular, Fenbendazole, however, has not been sanctioned for human use by the FDA, but despite lacking “official” approval, it is cheap, safe and more importantly, there is substantial documented evidence indicating its anti-cancer properties.
Following his review of the papers, Dr. Makis says that “there is extensive evidence of anti-cancer effects in the published literature, both in vitro and in vivo, and this is not a controversial medication, as it has been made out to be.” and he “would like to see clinical trials with either Mebendazole or Fenbendazole.”
As a follow up from yesterday’s article on Parasites, I believe that the content of the review from Dr. Makis would be of interest to our readers, and perhaps beneficial to many people, I sincerely hope it reaches those who may need to see it. The article therefore it has been republished below in it’s entirety.
FENBENDAZOLE and CANCER – at least 12 Anti-Cancer mechanisms of action. Not approved by FDA. Cheap. Safe. Kills aggressive cancers. Why no Clinical Trials? Nine research papers reviewed.
Dr. William Makis MD | Substack
2023 Jun – Movahedi et al – Repurposing anti-parasite benzimidazole drugs as selective anti-cancer chemotherapeutics
- Benzimidazole drugs (including Fenbendazole) have widely been used as anti-helminth agents in both human and/or livestock since the 1960s
- These drugs have rapidly become more popular than previous medications due to superiority in terms of efficacy, toxicity and application
- Benzimidazole drugs are considered as non-toxic anti-helminth agents in humans and livestock. Acute toxicities are rarely reported for these drugs.
- Neither chronic adverse effects in dogs and rats treated with very high dosages, nor irritation, carcinogenicity or teratogenicity in treated rats and rabbits have been observed
- Two major mechanisms of action:
- 1. antimitotic activity (inhibition of tubulin polymerization by binding to tubulin sites of rapidly dividing cells (leads to cell cycle arrest)
- 2. disrupt cell metabolic processes by inducing oxidative stress
- Result: induce apoptosis (cell death) of rapidly proliferating parasites and cancer cells!
- These drugs inhibit tumor proliferation and growth
- many new benzimidazole derivatives have been developed for the treatment of cancers such as colon cancer, breast cancer, lung cancer, chondrosarcoma and leukemia
- Furthermore, new benzimidazole derivatives have demonstrated high capability for overcoming drug resistance
- benzimidazole drugs exhibit anti-metastatic effect through inhibiting cell migration and invasion
- benzimidazole drugs also suppress telomerase reverse transcriptase (TERT) expression, whose activation is associated with metastasis
- benzimidazole drugs are potent in targeting cancer stem cells and preventing tumor recurrence.
- benzimidazole drugs are also found to prevent the radiation-induced transformation of cancer cells into radiation-resistant cells, and furthermore sensitize some drug-resistant cells.
- Clinical trials are ongoing for cancer therapy with benzimidazole drugs.
- For example, clinical study of mebendazole as adjuvant treatment for colon cancer is in Phase 3 (NCT03925662)
- and mebendazole in combination with other antiprotozoal agents including albendazole for neoplasm therapy is in Phase 2 (NCT02366884).
- Three Phase 1 clinical trials are also ongoing for mebendazole and brain tumors (NCT02644291, NCT01729260, NCT0183787862).
- THERE ARE NO CLINICAL TRIALS WITH FENBENDAZOLE
- low water solubility of benzimidazole drugs impedes their clinical applications
- nano-formulations are being created to improve bioavailability
- benzimidazole drugs are also being combined with other chemotherapeutics, such as paclitaxel, trametinib, gemcitabine and methoxyestradiol, to enhance the anti-cancer treatment efficacy.
- benzimidazole drugs have also sensitized tumor cells to radiation therapy
2023 Apr – Chi-Son Chang et al – Anti-cancer effect of fenbendazole-incorporated PLGA nanoparticles in ovarian cancer
- ovarian cancer is the deadliest gynecological cancer
- nanoparticles deliver poorly soluble drugs
- fenbendazole, an anti-parasitic drug was examined due to its anti-cancer effects: ability to interfere with microtubule polymerization, block cell cycle progression, increase p53 protein stability and induce apoptosis.
- However, fenbendazole has low water solubility and poor bioavailability which are major obstacles to its clinical application as an anti-cancer agent
- Nanoparticles were loaded with fenbendazole to increase bioavailability
- Results: natural form of fenbendazole significantly decreased cell proliferation of both chemosensitive and chemoresistant ovarian cancer cells
- But in vivo (xenograft mouse models), only the nanoparticle fenbendazole formulation showed anticancer effects.
2023 Mar – Semkova et al – Redox-mediated Anticancer Activity of Anti-parasitic Drug Fenbendazole in Triple-negative Breast Cancer Cells
- fenbendazole was tested on triple negative breast cancer cells, three different types including a highly metastatic type
- Results: the highly metastatic breast cancer cells were more vulnerable to fenbendazole induced oxidative stress
2023 Mar – Haebeen Jung et al – Differential cytotoxic effects of fenbendazole on mouse lymphoma EL-4 cells and spleen cells
- fenbendazole was tested on a mouse lymphoma cell line vs normal spleen cells
- purpose of this study was to investigate the cytotoxic effects of fenbendazole on normal cells of the spleen, which is a major reservoir of immune cells
- fenbendazole increased cell death of lymphoma cells but not of normal spleen cells
- fenbendazole induced reactive oxygen species in lymphoma cells but not normal spleen cells
- fenbendazole induced G2/M cell cycle arrest in lymphoma cells, not spleen cells
- Conclusion: fenbendazole has anticancer effects on lymphoma cells but minimal toxicity on normal spleen cells.
2022 Sep – Deokbae Park et al – Anti-cancer effects of fenbendazole on 5-fluorouracil-resistant colorectal cancer cells
- Benzimidazole anthelmintic agents have been recently repurposed to overcome cancers resistant to conventional therapies.
- fenbendazole was tested on chemo resistant colorectal cancer cells
- Results: fenbendazole significantly induces apoptosis as well as cell cycle arrest at G2/M phase on both colorectal cells and chemo resistant colorectal cancer cells.
- Benzimidazole is historically known to bind beta-tubulin, disrupt microtubules, and arrest cell division
- Benzimidazole is also known to activate p53 and p21 but decrease mutant p53 expression
- in colorectal cancer cells: fenbendazole is presumed to activate p53-mediated apoptosis by increasing p53 expression(!), and partly necrosis, autophagy and ferroptosis
- in chemo-resistant colorectal cancer cells: fenbendazole triggers apoptosis without affecting p53 expression, apoptosis was partly induced by Beclin-1, and further augmented by ferroptosis
- 6 mechanisms of action: (cell cycle arrest G2/M, activate p53-mediated apoptosis, autophagy, necroptosis, ferroptosis, Beclin-1 mediated apoptosis)
2022 Jan – Li-wen Ren et al – Benzimidazoles induce concurrent apoptosis and pyroptosis of human glioblastoma cells via arresting cell cycle
- fenbendazole was tested against glioblastoma cancer cells
- 1. fenbendazole dose-dependently suppressed DNA synthesis
- 2. fenbendazole inhibited cell migration and invasion of GBM cells
- 3. fenbendazole also dose-dependently induced the GBM cell cycle arrest at the G2/M phase via the P53/P21/cyclin B1 pathway.
- 4. fenbendazole triggered pyroptosis of GBM cells (pyroptosis is a form of programmed cell death) through the NF-κB/NLRP3/GSDMD pathway
- 5. fenbendazole induced mitochondria-dependent apoptosis of GBM cells
- 6. flubendazole inhibited tumor growth of glioblastoma in vivo in a dose dependent manner (in a nude mouse U87 cell xenograft model)
- Conclusion: “Taken together, our results demonstrated that benzimidazoles might be promising candidates for the treatment of GBM.”
2020 Aug – Deok-Soo Son et al – The Antitumor Potentials of Benzimidazole Anthelmintics as Repurposing Drugs
- Benzimidazole anthelmintics have broad-spectrum action to remove parasites both in human and veterinary medicine
- Due to their low cost and high efficacy, benzimidazole anthelmintics have been used throughout the world since their introduction in the 1960s
- Benzimidazole anthelmintics are well-tolerated without severe side effects, and their decades of use provide a basis for safety in humans.
- Benzimidazole anthelmintics selectively bind to β-tubulin of parasitic worms, causing their immobilization and death
- In addition to being antiparasitic agents, benzimidazole anthelmintics are known to exert anticancer activities which are summarized (also see image at start of article):
- disrupts microtubule polymerization
- inhibits cancer cell viability
- inhibits cancer cell migration and invasion
- induces apoptosis and autophagy
- increased cell cycle (G2/M) arrest
- induces differentiation and senescence
- inhibits angiogenesis
- reduces colony formation and inhibits stem-ness in cancer cells
- inhibits drug resistance and sensitize cells to conventional chemo
- blocks glucose transport and impairs glucose utilization
- Benzimidazole anthelmintics have been shown to inhibit cell viability in a variety of cancer cell lines, appearing as a promising medication:
- breast cancer
- glioma & glioblastoma
- lung cancer
- hepatocellular carcinoma
- urothelial cancer
2020 Jun – Yong Han et al – Involvement of reactive oxygen species in the anti-cancer activity of fenbendazole, a benzimidazole anthelmintic (leukemia)
- In this study, we investigated whether Fenbendazole has anti-cancer activity in HL-60 cells, a human leukemia cell line
- fenbendazole significantly decreased the metabolic activity of leukemia cells
- fenbendazole decreased the mitochondrial membrane potential of leukemia cells in a concentration-dependent manner
- fenbendazole increased apoptosis and necrosis of leukemia cells
- Conclusion: fenbendazole exerts anti-cancer activity against leukemia cells, in part, via ROS production (reactive oxygen species)
2018 Aug – Dogra et al – Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways
- Fenbendazole is known to have a high safety margin and most species tolerate it very well
- Fenbendazole targets microtubules in human NSCLC Lung cancer cells
- Fenbendazole treatment results in early G2/M block accompanied by cell death
- Tumour cell lines with wild-type p53 show enhanced sensitivity to Fenbendazole induced apoptosis
- Inhibition of glucose uptake by Fenbendazole sensitizes cancer cells to undergo apoptosis
- Fenbendazole effectively inhibits colony formation of human NSCLC Lung Cancer cells in culture
- In Vivo: Fenbendazole suppresses tumor growth
- Fenbendazole possesses a unique ability to induce p53 to a considerably high level (!)
- Conclusion: Altogether, our findings show microtubule disruption, p53 stabilization and interference with glucose metabolism as collective underlying mechanisms of Fenbendazole induced preferential elimination of cancer cells both in vitro and in vivo.
Ivermectin is FDA approved.
Fenbendazole is NOT approved for human use by Food and Drug Administration (FDA) and European Medicines Agency (EMA). It is available as a veterinary medication.
Fenbendazole is part of a larger group of drugs known as benzimidazoles, which are anthelmintic drugs (i.e., drugs that kill parasitic worms). Another benzimidazole is mebendazole, which can be prescribed to humans with certain parasitic infections.
Mebendazole (Vermox) is FDA approved for human use, but it’s significantly more expensive.
Why is Fenbendazole so popular? The Story of Joe Tippens and his terminal Stage 4 Small Cell Lung Cancer
Joe Tippens Cancer Protocol:
- Fenbendazole 222mg per day with food (originally 3 days on, 4 days off)
- Curcumin 600mg per day
- CBD Oil: 25mg sublingually per day
- Vitamin E: 800IU per day
Dr. Tom Rogers MD (Performance Medicine – Knoxville, TN) Suggests Several Protocols utilizing Fenbendazole which are interesting:
ACTIVE CANCER TREATMENT – For active cancer, take one capsule of Fenbendazole (444 mg) daily. Some people recommend you take one day off a week. Note: I think I would just take Sundays off. Again, you’re not supposed to develop a tolerance to this, but taking a little break is probably a good idea. To improve the protocol , take CBD oil (25mg) 1-2 drops every night before sleep. To strengthen the protocol take Curcumin (600mg) twice a day with food. To support the liver, take Milk Thistle (250mg) twice a day with food. Note: Fenbendazole should be taken with or after a meal to improve absorption.
COMPLEMENTARY CANCER TREATMENT – Take one capsule of Fenbendazole (222mg) every day, once a day after a fatty meal; Curcumin (600mg) one capsule, two times a day after breakfast and lunch; CBD oil (25mg) 1-2 drops under the tongue every day before sleep.
CANCER RELAPSE PREVENTION – Taking Fenbendazole for active cancer and cancer relapse prevention, take one capsule (222 mg) three times a week, once a day after a fatty meal.In addition, take Curcumin (600mg) one capsule/two times a day after breakfast and lunch, Milk Thistle, and CBD Oil (25mg) 1-2 drops under the tongue everyday before going to sleep. Note: Have your doctor follow and check liver and kidney function tests. It’s easy, cheap, and you can get this at any doctor’s office.
CANCER PREVENTION (prophylactic) – Those that have had genetic tests and know they’re really prone to getting cancer can take Fenbendazole prophylactically. Take one capsule (222 mg) 3 times a week, once a day after a fatty meal. Then no Fenbendazole for four days. Repeat for 10 weeks and then take 10 weeks off; Curcumin (600 mg) one capsule two times a day after breakfast and lunch; CBD oil (25mg) 1-2 drops under the tongue every day before sleep. Continue that regimen indefinitely.
Fenbendazole is not that controversial when you consider the scientific evidence objectively.
Fenbendazole has at least 12 proven anti-cancer mechanisms in vitro and in vivo:
- disrupts microtubule polymerization (major mechanism)
- induces cell cycle (G2/M) arrest
- blocks glucose transport and impairs glucose utilization by cancer cells (major)
- increases p53 tumor suppressor levels (major)
- inhibits cancer cell viability (mTOR)
- inhibits cancer cell migration and invasion (EMT pathway)
- induces apoptosis
- induces autophagy
- induces pyroptosis and necrosis
- induces differentiation and senescence
- inhibits tumor angiogenesis
- reduces colony formation and inhibits stem-ness in cancer cells
- inhibits drug resistance and sensitizes cells to conventional chemo as well as radiation therapy
A very similar drug in the same family as Fenbendazole is FDA approved: Mebendazole, and it is in several Clinical Trials right now for brain cancers and colon cancers.
So why are there no Fenbendazole Clinical Trials for Cancer?
The answer seems rather obvious: it’s very cheap, it’s safe and it seems to be very effective.
Fenbendazole is not going to make anyone rich, and in cancer treatments, that is a non-starter.
What about COVID-19 mRNA Vaccine Induced Turbo Cancers?
Fenbendazole shows in vitro and/or in vivo activity against these cancers:
- breast cancer (including triple negative breast cancer – which is seen in COVID-19 mRNA Vaccinated individuals with Turbo Cancer)
- lymphomas (these are the most common COVID-19 mRNA Vaccine Turbo Cancers and there is more evidence for Fenbendazole with Lymphomas than with Ivermectin)
- leukemias (most aggressive COVID-19 mRNA Vaccine Turbo Cancers)
- glioblastomas and gliomas (extremely aggressive COVID-19 mRNA Vaccine Turbo Cancers)
- lung cancer (NSCLC) (strong signal for COVID-19 mRNA Vaccine Turbo Cancers)
- hepatocellular carcinoma (signal for COVID-19 mRNA Vaccine Turbo Cancers)
- rhabdomyosarcomas (possible signal for COVID-19 mRNA Vaccine Turbo Cancers, sarcomas in general are on the rise)
- ovarian cancers
- urothelial cancers
Although the anti-parasitic Fenbendazole is not FDA approved for human use, there is extensive evidence of anti-cancer effects in the published literature, both in vitro and in vivo, and this is not a controversial medication, as it has been made out to be.
Fenbendazole has an excellent safety profile and its close relative, Mebendazole is FDA approved, and it’s undergoing several Clinical Trials for Cancer Treatments in the US right now, including colon cancers and brain cancers.
I believe that it is a reasonable hypothesis that COVID-19 mRNA Vaccine Turbo Cancer patients could benefit significantly from either Mebendazole or Fenbendazole and I would love to see urgent clinical trials with both.
Source – FENBENDAZOLE and CANCER – at least 12 Anti-Cancer mechanisms of action. Not approved by FDA. Cheap. Safe. Kills aggressive cancers. Why no Clinical Trials? Nine research papers reviewed. – Dr. William Makis MD