Fenbendazole - Cure for many types of Cancer? For Dogs and People!

Phil Jayhan

New member
Recently our dog Mickey developed cancerous tumors on her hindside and through the kindness of a friend was able to have them removed. And Mickey seemed back to normal. But then after about 7 months new tumors began to grow and one of her nipples seem to be cancerous as well, So trying to find treatments for cancer I came across this drug Fenbendazole through a video of Joe Tippen and his story. An amazing story of him being cured, according to him, through Fenbendazole treatments. What's even more amazing is when I began researching this, more and more, I kept seeing in studies and Medical papers that they openly acknowledge that Fenbendazole is "highly effective at treating many cancer types." Long story short is I put Mickey on Fenbendazole treatment last week, Sunday, Monday and Tuesday. And this weeks 3 days are MTW. I have seen some positive signs already! I will post more about her treatment later, The second video is a snippet from this or another interview.






More to come...

Cheers-
Phil :)
 
Last edited:

Phil Jayhan

New member

A Drug Made for Animals and Taken by Humans to Treat Cancer: Fenbendazole

Author: Daniel S, PhD; Last update: January 31st, 2021
Original link here:

From anti-worms to anti-cancer

Previously, we discussed on this website the anti-worm drug Mebendazole (Ref.), which based on a good amount of scientific and clinical evidence, shows relevant anti cancer potential. However, as we saw, it’s not only science. Instead, there are case reports published in peer review papers showing that patinets with some aggressive cancers have experienced great response to Mebendazole. In the same article (Ref.) we explored the mechanism behind the anticancer action of Mebendazole, and found out that Mebendazole acts in a similar way as a group of chemotherapies such as Taxol. Yet, in contrast to chemotherapies, due to the way Mebendazole works, its toxicity is incomparably lower. Because of its good safety profile, the drug is an over the counter drug in most of the countries.

I specifically like the anti-worms, anti-parasites, antibiotics, antiviral drugs, as a pattern start to emerge suggesting that the origin of cancer may be related to such a trigger (e.g. viruses, parasites, etc.) in much more cases than we currently are aware of. Multiple findings and observations, that I will discuss in a different post, indicate that such triggers may initiate cancer when they land in a “fertile ground”, represented by specific genetic weaknesses combined with a compromised immune system (due to e.g. stress, lifestyle, medication, etc.). This is why, I would seriously consider using anti-worms, anti-parasites, antibiotics, antiviral drugs as a part of more comprehensive treatment approaches that could also include conventional therapies. As long as the toxicity is low, it could make sense to cycle various drugs of this type.

Recommendation: when you finish reading this post, I recommend you read also this post I recently published (September 2020): 10 Cases of Complete Remission from Advanced Cancers after using Supplements or Repurposed Drugs In this post you will find more repurposed (off-label) drugs that have been shown to induce complete remission in various cancers (published in scientific journals by clinicians and scientists from major universities and hospitals).

The anti-worm drug Fenbendazole has anti-cancer potential


In the same group of drugs as Mebendazole, a group called benzimidazoles, there is another anti-worm drug called Fenbendazole. Fenbendazole, is a drug used typically not for humans like Mebendazole, but for animals (including fish, birds and mammals). In this case, it is used to kill worms such as roundworms, hookworms, whipworms, and some tapeworms. Fenbendazole is found under various brand names such as Panacur or Safe-Guard.

I did came across this drug some years ago during my research, but only recently I was motivated to look closely at it following several e-mails from friends who shared with me the blog of a man with Small Cell Lung Cancer, who successfully treated his cancer with Fenbendazole (Ref.). On his website, Joe Tippens, not only reports his experience but also anecdotally reports being in contact with more patients experiencing benefits while using Fenbendazole, including two cases of 4th stage Pancreatic Cancer, Prostrate Cancer, Colorectal Cancer, Non-Small Cell Lung Cancer, Melanoma, Colon Cancer.

This anecdotal report would not be enough to trigger me writing this post, if I would not be convinced by the existing scientific evidence indicating the anti cancer potential connected with many of the benzimidazoles drugs. Therefore, I do believe that if Mebendazole could show relevant anti-cancer effects in humans, which it did, Fenbendazole could do it as well and hopefully even better.

In some diseases, Fenbendazole came out as more effective than Mebendazole. For example, when tested against Cryptococcus neoformans (an encapsulated fungal organism that can cause disease such as meningoencephalitis in immunocompromised hosts), it has been shown that Fenbendazole was more active than Mebendazole or other drugs against this opportunistic fungus (Ref.).

Scientific articles published during the past years, have indicated that Fenbendazole shows anti cancer effectiveness. Of these, the paper I found most relevant to specifically cite here first is a paper that was just published during 2018 in one of the most prestigious scientific magazine, that is Nature, which adds a lot of weight to the communicated message. This paper, entitled “Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways“, concludes the following:

  • “The results, in conjunction with our earlier data, suggest that Fenbendazole is a new microtubule interfering agent that displays anti-neoplastic activity and may be evaluated as a potential therapeutic agent because of its effect on multiple cellular pathways leading to effective elimination of cancer cells.”
In this paper, the authors cite potential anti cancer mechanisms associated with Fenbendazole, including disruption of microtubule function and proteasomal interference, but it was also associated with blocking the glucose uptake by cancer cells (through reducing the expression of Glut-4 transporter as well as hexokinase) and thus starving cancer cells. This means Fenbendazole could also work nicely in supporting chemotherapy and radiotherapy as well as metabolic therapies. Because of the way it works (interacting with a site on tubulin similar to colchicine but distinct from that of Vinca alkaloids), Fenbendazole will not compete with Vinca alkaloids (such as Taxol) but instead will add to the anti cancer effect of these conventional treatments similar to other benzimidazoles (Ref.).

Interestingly, when insulin stimulates glucose uptake in the cells, glucose transporter isoform 4 (GLUT4) translocates from intracellular vesicles to the plasma membrane ready to absorb glucose. This movement of GLUT4 towards the plasma membrane takes place via both rapid vibrations around a point and short linear movements (generally less than 10 microm). The linear movement seems to take place along microtubules. When disrupting the microtubules with drugs such as Fenbendazole, GLUT4 movements are disrupted as well strongly reducing insulin-stimulated glucose uptake (Ref.).

Another very interesting point coming from the Nature paper cited above is that Fenbendazole shows strong synergy when combined to DCA, a drug that I discussed earlier on this website here. So it may make very much sense to combine the two, and possibly 2DG (Ref.). Could it be that the origin of this synergy comes from the possible glutathione depletion previously observed to be related to Fenbendazole? (Ref.)
Update April 2020: A recent scientific paper suggests yet another anti cancer activity related to Fenbendazole (Ref.). In this paper, the authors suggests that drugs such as Fenbendazole reactivate p53, known as the Guardian of the Genome. p53 functions as a tumor suppressor and it’s activity is inhibited in some cancers.

While Fenbendazole could be relevant for many types of cancers (as also suggested by the anecdotal reports listed above and by literature on the anticancer effects of benzimidazoles drugs) prior literature has so far indicated it’s anti cancer effects in

  • Non-small Cell Lung Cancer Cells (NSCLC) (Ref.)
    • Fenbendazole inhibits the cellular proteasome function dose- and time-dependently and leads to accumulation of ubiquitylated derivatives of various cellular proteins, including p53, which, in turn, leads to apoptosis via the mitochondrial pathway
    • the cells first undergo G2/M arrest followed by apoptosis
    • Fenbendazole induced endoplasmic reticulum stress, reactive oxygen species production, decreased mitochondrial membrane potential, and cytochrome c release that eventually led to cancer cell death.
    • Update April 2020: Recently, it has been indicated that benzimidazole, including Methiazole and Fenbendazole play an important role in suppressing KRAS-mutant lung cancer cells (Ref.)
  • Lymphoma (Ref.)
  • Prostate Cancer (Ref.) and taxane-resistant prostate cancer cells (Ref.)
  • Glioblastoma (Ref.1, Ref.2)
The questions, is why I would consider using Fenbendazole, a drug used for animals, when we already have Mebendazole made for use in humans that is associated to similar anticancer mechanisms? There are three major reasons for me to do that and consider trying Fenbendazole as well:
  • First, as discussed above, in some diseases Fenbendazole was more effective than Mebendazole;
  • Second, it is known that this type of drugs is not very well absorbed in the body and the absorption may differ from person to person (Ref.). Therefore switching between different drugs with similar expected mechanisms may make sense as one of them may be better absorbed in our specific case;
  • Third, there is a good chance that the underlying anti-cancer mechanism is different for each of the drugs, even if the scientific observations suggest similar mechanisms of action (we should always remember that science represents not a complete understanding of nature, but only steps towards a better understanding).
Update December 2019: A recent study suggests that for Pancreatic Cancer, two other anti-worm drugs from the same category and used in animals, Parbendazol (brand name Verminum, Worm Guard and Helatac) and Oxibendazole, is more effective compared to Fenbendazole and Mebendazole (Ref.). While Parbendazole seems not to be on the market anymore, Oxibendazole can be found online. Here you can find this subject discussed a little more in details including discussions on what could be the relevant daily dose of Oxibendazole (Ref.).
Update September 2019: at the beginning of 2019, some months after I wrote this post, Joe’s story became viral. Here is a short interview on a TV station in US, with Joe
I am glad to see that I often addressed subjects on this website before they became known to most people.

Update May 2020: A man successfully using Fenbendazole and Artemisinin to treat his prostate cancer https://www.killingcancer.net/treatments

Fenbendazole is well tolerated in humans

Although a drug that is used for animals, according to a report available at the European Medicine Agency “Fenbendazole seems to be well tolerated in humans after oral exposure (single oral dose up to 2,000 mg/per person; 500 mg/per person for 10 consecutive days)” (Ref.)

What type and how is Fenbendazole used

Taking Panacur C granules from Merck

There are people taking it for deworming and they seem to prefer the Fenbendazole version that is meant to be used for fish (Ref.). In this case, its is used in the range of 5mg/kg/day to 10mg/kg/day. However, on his website, Joe Tippens, shows a picture of Panacur C box from Merck, sold as Canine Dewormer, containing Fenbendazole granules 22.2%. This means every gram of granules contains 222mg of pure Fenbendazole.

Dose and treatment regime

Below I discuss the dose and treatment regime but this is only visible to registered visitors. All visitors can easily register, for free, using the login options located at the right side of the page (when using a desktop) or at the bottom of the page (when using mobile), where login option via Facebook account is also available. It only takes one minute to registered on this website, while it may take much longer to collect the information addressed here.

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However, just to stay on the safe side, because of its anti oxidant properties I would not use Vit E during the chemo or radio therapy.

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Where to buy Fenbendazole

Panacure C can be found all over the world at online shops. It can be found in packages of 3 packets of 1g granules (or 222mg Fenbendazole, for small dogs) or 3 packets of 2g granules (or 444mg Fenbendazole, for adult dogs). Fenbendazole should not be confused with Flubendazole.
Note that some Fenbendazole formulations (such as solutions and paste) may contain Parabens, that can have some weak estrogenic effects. Breast and Ovarian cancer patients may wont to avoid using such formulations.

Warning! To take advantage of the fact that Fenbendazole story spread across the world like wildfire, some people have seen this as an opportunity to take financial advantage of it. As a result, there are some “supplement” web-shops selling Fenbendazole in the most clever ways. With “the best and nicest stories” around them. I will not mention the names of those, but I would advise everyone to only buy Fenbendazole that has been manufactured by a registered and known manufacturer and sold via an authentic source such as a Pharmacy. Since it’s a matter of life, we want to be 100% sure we receive what we order. Don’t forget: over the internet everyone can claim anything, like GMP-approved source, etc, to sell their products. The best way is to follow what Joe did and use the Panacur C product only.

So far, the only manufacturers that I understand can be trusted is the pharmaceutical company Merck. If you are aware of any other trusted sources, please let me know. Nevertheless, please note that regardless of the source, Fenbendazole is not manufactured for human use.

Final Note

Update December 2019: Dear reader, many visitors of this website in search for information on Fenbendazole are reading this article and after that they leave this website. However, they leave behind important value. Continue reading this website and you will find other treatments that may have the same or better potential compared to Fenbendazole, but mostly known by specialised scientists and less by other people. The same was the story of Fenbendazole. The potential behind Fenbendazole was only known by scientists, until one day, Joe Tippers with his great success and communication skills succeeded to make out of his story a viral story.

For example, see here a case report recently published in scientific literature https://www.cancertreatmentsresearch.com/a-silver-bullet-to-kill-cancer/, of a man who had stage IV cancer with many sites’s of metastasis including liver and lungs. He was not responding to conventional treatments and he was sent home to die. He treated himself at home with an unconventional treatment approach and three months after that his medical doctors report that he obtained complete remission.

And here is another recent (2018) example: (Ref) the case of a medical doctor from US with stage 4 pancreatic cancer, who next to his conventional treatment added two repurposed drugs. With that he obtained complete remission. My point is: when you find time, explore this website. I share everything for free with you. All my search for new treatment options with potential is meant to help you with more treatment ideas and all are science based.

Here is another post that you want to read that many people appreciate: A post incorporating multiple repurposed drugs and supplements into a Metabolic anti-cancer treatment strategy: https://www.cancertreatmentsresearch.com/shutting-down-the-power-house-of-cancer/

References

In vitro anti-tubulin effects of mebendazole and fenbendazole on canine glioma cells.
https://www.ncbi.nlm.nih.gov/pubmed/28078780

Benzimidazole anthelmintics have reported anti-neoplastic effects both in vitro and in vivo. The purpose of this study was to evaluate the in vitro chemosensitivity of three canine glioma cell lines to mebendazole and fenbendazole. The mean inhibitory concentration (IC50 ) (±SD) obtained from performing the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay after treating J3T, G06-A, and SDT-3G cells for 72 h with mebendazole were 0.030 ± 0.003, 0.080 ± 0.015 and 0.030 ± 0.006 μM respectively, while those for fenbendazole were 0.550  ± 0.015, 1.530 ± 0.159 and 0.690 ± 0.095 μM; treatment of primary canine fibroblasts for 72 h at IC50 showed no significant effect. Immunofluorescence studies showed disruption of tubulin after treatment. Mebendazole and fenbendazole are cytotoxic in canine glioma cell lines in vitro and may be good candidates for treatment of canine gliomas. Further in vivo studies are required.

Impairment of the Ubiquitin-Proteasome Pathway by Methyl N-(6-Phenylsulfanyl-1H-benzimidazol-2-yl)carbamate Leads to a Potent Cytotoxic Effect in Tumor Cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436308/

In recent years, there has been a great deal of interest in proteasome inhibitors as a novel class of anticancer drugs. We report that fenbendazole (FZ) (methyl N-(6-phenylsulfanyl-1H-benzimidazol-2-yl)carbamate) exhibits a potent growth-inhibitory activity against cancer cell lines but not normal cells. We show here, using fluorogenic substrates, that FZ treatment leads to the inhibition of proteasomal activity in the cells. Succinyl-Leu-Leu-Val-Tyr-methylcoumarinamide (MCA), benzyloxycarbonyl-Leu-Leu-Glu-7-amido-4-MCA, and t-butoxycarbonyl-Gln-Ala-Arg-7-amido-4-MCA fluorescent derivatives were used to assess chymotrypsin-like, post-glutamyl peptidyl-hydrolyzing, and trypsin-like protease activities, respectively.

Non-small cell lung cancer cells transiently transfected with an expression plasmid encoding pd1EGFP and treated with FZ showed an accumulation of the green fluorescent protein in the cells due to an increase in its half-life. A number of apoptosis regulatory proteins that are normally degraded by the ubiquitin-proteasome pathway like cyclins, p53, and IκBα were found to be accumulated in FZ-treated cells. In addition, FZ induced distinct ER stress-associated genes like GRP78, GADD153, ATF3, IRE1α, and NOXA in these cells. Thus, treatment of human NSCLC cells with fenbendazole induced endoplasmic reticulum stress, reactive oxygen species production, decreased mitochondrial membrane potential, and cytochrome c release that eventually led to cancer cell death.

This is the first report to demonstrate the inhibition of proteasome function and induction of endoplasmic reticulum stress/reactive oxygen species-dependent apoptosis in human lung cancer cell lines by fenbendazole, which may represent a new class of anticancer agents showing selective toxicity against cancer cells.

Unexpected antitumorigenic effect of fenbendazole when combined with supplementary vitamins. https://www.ncbi.nlm.nih.gov/pubmed/19049251

Diet containing the anthelminthic fenbendazole is used often to treat rodent pinworm infections because it is easy to use and has few reported adverse effects on research. However, during fenbendazole treatment at our institution, an established human lymphoma xenograft model in C.B-17/Icr-prkdcscid/Crl (SCID) mice failed to grow. Further investigation revealed that the fenbendazole had been incorporated into a sterilizable diet supplemented with additional vitamins to compensate for loss during autoclaving, but the diet had not been autoclaved.
To assess the role of fenbendazole and supplementary vitamins on tumor suppression, 20 vendor-supplied 4-wk-old SCID mice were assigned to 4 treatment groups: standard diet, diet plus fenbendazole, diet plus vitamins, and diet plus both vitamins and fenbendazole. Diet treatment was initiated 2 wk before subcutaneous flank implantation with 3 x 107 lymphoma cells. Tumor size was measured by caliper at 4-d intervals until the largest tumors reached a calculated volume of 1500 mm3.

Neither diet supplemented with vitamins alone nor fenbendazole alone caused altered tumor growth as compared with that of controls. However, the group supplemented with both vitamins and fenbendazoleexhibited significant inhibition of tumor growth. The mechanism for this synergy is unknown and deserves further investigation. Fenbendazoleshould be used with caution during tumor studies because it may interact with other treatments and confound research results.

Effects of fenbendazole and vitamin E succinate on the growth and survival of prostate cancer cells

We describe antitumor activities of vitamin E succinate (VES), an anti-oxidant and fenbendazole (FBZ), a commonly used veterinary anthelmintic. We used VES and FBZ, at low concentrations, singly and in combination, to test their inhibitory effects on proliferation of human and mouse prostate cancer cells in vitro. Administered alone, FBZ inhibited proliferation faster than VES in both mouse and human prostate cancer cell lines and a synergistic effect between both was also observed. Apoptosis was the likely mechanism for the observed effect. These drugs may deserve to be tested for their efficacy in the control of prostate cancer using in vivo models.

Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme. https://www.ncbi.nlm.nih.gov/pubmed/21764822

Glioblastoma multiforme (GBM) is the most common and aggressive brain cancer, and despite treatment advances, patient prognosis remains poor. During routine animal studies, we serendipitously observed that fenbendazole, a benzimidazole antihelminthic used to treat pinworm infection, inhibited brain tumor engraftment. Subsequent in vitro and in vivo experiments with benzimidazoles identified mebendazole as the more promising drug for GBM therapy. In GBM cell lines, mebendazole displayed cytotoxicity, with half-maximal inhibitory concentrations ranging from 0.1 to 0.3 µM.

Mebendazole disrupted microtubule formation in GBM cells, and in vitro activity was correlated with reduced tubulin polymerization. Subsequently, we showed that mebendazole significantly extended mean survival up to 63% in syngeneic and xenograft orthotopic mouse glioma models. Mebendazole has been approved by the US Food and Drug Administration for parasitic infections, has a long track-record of safe human use, and was effective in our animal models with doses documented as safe in humans. Our findings indicate that mebendazole is a possible novel anti-brain tumor therapeutic that could be further tested in clinical trials.

Identification of selective therapeutic agents for metastatic prostate cancer by phenotype-based screening http://www.dtic.mil/dtic/tr/fulltext/u2/a545657.pdf

Background: As with many solid tumors, the prognosis for prostate cancer patients worsens when tumors metastasize to distant organs, such as the bone. Current chemotherapy is relatively limited for metastatic prostate cancer. Methods: We utilized a screening method consisting of multiple panels of highly metastatic and less metastatic prostate cancer cells to identify compounds that selectively target metastatic prostate cancer cells but not on less metastatic and normal prostate epithelial cells. Selected drugs from a library of 1120 FDA-approved drugs were then tested for their ability to improve the survival of mice in a highly aggressive Dunning rat prostate carcinoma lung metastasis model, and for anti-tumor activity on paclitaxel-resistant and experimental bone lesion of prostate tumors. To improve the bioavailability of agents for systemic administration, we utilized a modified micelle preparation as well as nanoparticle (PLGA-PEG)-based formulation.

Results: We identified fenbendazole, fluspirilene, clofazimine, niclosamide and suloctidil, which showed selective cytotoxicity on metastatic prostate cancer cells in vitro and in vivo. Such selectivity could explained by differential induction of apoptosis. Upon improvement in bioavailability, fenbendazole and albendazole significantly extended the survival of metastases bearing mice, and the extension of lifespan by albendazole was equivalent or greater than that provided by paclitaxel. These drugs were active in taxane-resistant tumors and in the bone microenvironment, two clinical conditions of men with advanced prostate cancer. Conclusion: Metastatic tumor cells differ in their responses to certain drug classes. Albendazole shows promise as a potential adjunct to standard therapy in patients with metastatic prostate cancer.

An Overview of Tubulin Inhibitors That Interact with the Colchicine Binding Site
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667160/

Tubulin dynamics is a promising target for new chemotherapeutic agents. The colchicine binding site is one of the most important pockets for potential tubulin polymerization destabilizers. Colchicine binding site inhibitors (CBSI) exert their biological effects by inhibiting tubulin assembly and suppressing microtubule formation. A large number of molecules interacting with the colchicine binding site have been designed and synthesized with significant structural diversity. CBSIs have been modified as to chemical structure as well as pharmacokinetic properties, and tested in order to find a highly potent, low toxicity agent for treatment of cancers. CBSIs are believed to act by a common mechanism via binding to the colchicine site on tubulin. The present review is a synopsis of compounds that have been reported in the past decade that have provided an increase in our understanding of the actions of CBSIs.

Exacerbation of Acetaminophen Hepatotoxicity by the Anthelmentic Drug Fenbendazole (Ref.)

Fenbendazole is a broad-spectrum anthelmintic drug widely used to prevent or treat nematode infections in laboratory rodent colonies. Potential interactions between fenbendazole and hepatotoxicants such as acetaminophen are unknown, and this was investigated in this study. Mice were fed a control diet or a diet containing fenbendazole (8-12 mg/kg/day) for 7 days prior to treatment with acetaminophen (300 mg/kg) or phosphate buffered saline. In mice fed a control diet, acetaminophen administration resulted in centrilobular hepatic necrosis and increases in serum transaminases, which were evident within 12 h.

Acetaminophen-induced hepatotoxicity was markedly increased in mice fed the fenbendazole-containing diet, as measured histologically and by significant increases in serum transaminase levels. Moreover, in mice fed the fenbendazole-containing diet, but not the control diet, 63% mortality was observed within 24 h of acetaminophen administration. Fenbendazole by itself had no effect on liver histology or serum transaminases.

To determine if exaggerated hepatotoxicity was due to alterations in acetaminophen metabolism, we analyzed sera for the presence of free acetaminophen and acetaminophen-glucuronide. We found that there were no differences in acetaminophen turnover. We also measured cytochrome P450 (cyp) 2e1, cyp3a, and cyp1a2 activity. Whereas fenbendazole had no effect on the activity of cyp2e1 or cyp3a, cyp1a2 was suppressed. A prolonged suppression of hepatic glutathione (GSH) was also observed in acetaminophen-treated mice fed the fenbendazole-containing diet when compared with the control diet.

These data demonstrate that fenbendazole exacerbates the hepatotoxicity of acetaminophen, an effect that is related to persistent GSH depletion. These findings are novel and suggest a potential drug-drug interaction that should be considered in experimental protocols evaluating mechanisms of hepatotoxicity in rodent colonies treated with fenbendazole.

The Benzimidazole-Based Anthelmintic Parbendazole: A Repurposed Drug Candidate That Synergizes with Gemcitabine in Pancreatic Cancer (Ref.)

Pancreatic cancer (PC) is one of the most lethal, chemoresistant malignancies and it is of paramount importance to find more effective therapeutic agents. Repurposing of non-anticancer drugs may expand the repertoire of effective molecules. Studies on repurposing of benzimidazole-based anthelmintics in PC and on their interaction with agents approved for PC therapy are lacking. We analyzed the effects of four Food and Drug Administration (FDA)-approved benzimidazoles on AsPC-1 and Capan-2 pancreatic cancer cell line viability.
Notably, parbendazole was the most potent benzimidazole affecting PC cell viability, with half maximal inhibitory concentration (IC50) values in the nanomolar range. The drug markedly inhibited proliferation, clonogenicity and migration of PC cell lines through mechanisms involving alteration of microtubule organization and formation of irregular mitotic spindles. Moreover, parbendazole interfered with cell cycle progression promoting G2/M arrest, followed by the emergence of enlarged, polyploid cells. These abnormalities, suggesting a mitotic catastrophe, culminated in PC cell apoptosis, are also associated with DNA damage in PC cell lines. Remarkably, combinations of parbendazole with gemcitabine, a drug employed as first-line treatment in PC, synergistically decreased PC cell viability. In conclusion, this is the first study providing evidence that parbendazole as a single agent, or in combination with gemcitabine, is a repurposing candidate in the currently dismal PC therapy.

Benzimidazoles Downregulate Mdm2 and MdmX and Activate p53 in MdmX Overexpressing Tumor Cells (Ref.)

Tumor suppressor p53 is mutated in about 50% of cancers. Most malignant melanomas carry wild-type p53, but p53 activity is often inhibited due to overexpression of its negative regulators Mdm2 or MdmX. We performed high throughput screening of 2448 compounds on A375 cells carrying p53 activity luciferase reporter construct to reveal compounds that promote p53 activity in melanoma. Albendazole and fenbendazole, two approved and commonly used benzimidazole anthelmintics, stimulated p53 activity and were selected for further studies. The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins. We also observed a reduction of cell viability and changes of cellular morphology corresponding to mitotic catastrophe, i.e., G2/M cell cycle arrest of large multinucleated cells with disrupted microtubules.

In summary, we established a new tool for testing the impact of small molecule compounds on the activity of p53 and used it to identify the action of benzimidazoles in melanoma cells. The drugs promoted the stability and transcriptional activity of wild-type p53 via downregulation of its negative regulators Mdm2 and MdmX in cells overexpressing these proteins. The results indicate the potential for repurposing the benzimidazole anthelmintics for the treatment of cancers overexpressing p53 negative regulators.

Drug library screen reveals benzimidazole derivatives as selective cytotoxic agents for KRAS-mutant lung cancer. (Ref.)

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancer (NSCLC). Mutations in KRAS are detected in 30% of NSCLC cases, with most of them occurring in codons 12 and 13 and less commonly in others. Despite intense efforts to develop drugs targeting mutant KRAS, no effective therapeutic strategies have been successfully tested in clinical trials. Here, we investigated molecular targets for KRAS-activated lung cancer cells using a drug library. A total of 1271 small molecules were screened in KRAS-mutant and wild-type lung cancer cell lines.

The screening identified the cytotoxic effects of benzimidazole derivatives on KRAS-mutant lung cancer cells. Treatments with two benzimidazole derivatives, methiazole and fenbendazole-both of which are structurally specific-yielded significant suppression of the RAS-related signaling pathways in KRAS-mutated cells. Moreover, combinatorial therapy with methiazole and trametinib, a MEK inhibitor, induced synergistic effects in KRAS-mutant lung cancer cells. Our study demonstrates that these benzimidazole derivatives play an important role in suppressing KRAS-mutant lung cancer cells, thus offering a novel combinatorial therapeutic approach against such cancer cells.

Update August 24th, 2019: several months after I wrote this article, the story of Joe Tippens made the news, and after that it went viral. Following that, some Facebook groups have been created where people are discussing the use of Fenbendazole against cancer. Here is one such group https://www.facebook.com/groups/429159131252194/ (Fenbendazole for Cancer Group)

Drug repurposing and relabeling for cancer therapy: Emerging benzimidazole antihelminthics with potent anticancer effects
https://www.sciencedirect.com/science/article/abs/pii/S0024320520309413

Origin of drug and radio-refractory clones, cancer stem-like cells, and rapid angiogenesis and metastasis are among the primary concerns that limit the efficacy of anticancer treatments, emphasizing the urgency of developing new therapeutics. Factors like high attrition rates, huge investments, patients’ heterogeneity, and diverse molecular subtypes have challenged the rapid development of anticancer drugs. Treatment with repurposing pleiotropic benzimidazole antihelminthics, like mebendazole, albendazole, and flubendazole has recently opened a new window, owing to their easy access, low cost as a generic drug, and long track record of safe use in the human population. This review highlights the outcomes of preclinical and clinical studies of these drugs as a potent anticancer agent(s) conducted in the last two decades. Substantial preclinical studies, as well as limited clinical trials, suggest noteworthy anticancer potency of these pleiotropic benzimidazoles, particularly as potent microtubule disrupting, anti-angiogenic, and anti-metastatic agents, inhibitors of the immune checkpoint, hypoxia-inducible factor, epithelial-mesenchymal transition, cancer stemness, and multidrug resistance protein 1, and inducers of apoptosis and M1 polarization. These anticancer effects are attributed to multiple action points, including intrinsic apoptosis, canonical Wnt/β-catenin, JAK/STAT-3, JNK, MEK/ERK, and hedgehog signaling pathways. The effective anticancer properties of mebendazole, albendazole, and flubendazole either alone or synergistically with frontline drugs, warrant their validation through controlled clinical trials to use them as promising avenues to anticancer therapy.

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This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.

Please read an extended version of the Disclaimer here: https://www.cancertreatmentsresearch.com/?page_id=1794
 
Last edited:

Phil Jayhan

New member
Just when you thought it couldn't get any better, comes along Mebendazole. I haven't even gotten around to trying this as I just began my treatment of my Dog Mickey with Fenbendazole and thus far it actually is leaning on the side of promising. Her fever has remained normal since just after her first 3 treatments last week, and the general distress she was in has abated as well. Her cancerous nipple which was dangling low and had a cherry red small grape sized mass at the end has actually for the first time since it appeared, started to draw back up into or towards her body and barely dangles low at all any more. She has more energy then she did when we first got her 2.5 years ago. (She was a rescue dog)

The drug Mebendazole is made for people. But Fenbendazole is safe for humans as well as animals. As long as people do some basic research they will discover that they can only dose themselves 3 days a week, with 4 days off, to avoid liver toxicity. Also Mebendazole has the same distinct warning about dosing. 3 days on 4 days off as far as I can see. Again liver toxicity. I have learned that 2 of the 3 major things Fenbendazole does is it repairs our P53 gene believe it or not. And it is our P53 gene which makes our T cells and killer T cells which fight against bacterial, viral invaders as well as cancerous growths. The 2nd thing it does is that it inhibits the tumors ability to process glucose, effectively killing any tumor.

I am trying to make this thread a one stop shop for people where they can obtain enough knowledge to make a choice as well as a springboard for their own personal research. Many people who come to this thread might not have very much time left and I want it to be clear, concise and packed with relevant knowledge, easy to find. Ok, below is the article on Mebendazole.

Cheers-
Phil (y)


____________________________________________________________________________


POSTED ON APRIL 25, 2017 BY DANIEL

Mebendazole: A Cancer Fighting Drug We Find at the Supermarket


Original link here:

Background:
Yes, in the European countries Mebendazole can be found on the supermarket shelves.
Mebendazole is an anthelmintic drug that has been used since the early 1970s to treat a range of parasitical worm infections, including threadworm, tapeworms, roundworms, and other nematode and trematode infections in humans and domestic animals (Ref.). The drug is among those on the World Health Organization’s list (WHO) (Ref.).

Mebendazole became and remained one of my preferred drugs since I learned about it at the beginning of 2014. This was mainly due to the multiple strong points that are defining Mebendazole. Those strong points are:

  • it has high potential for serious effectiveness against cancer supported by both
    • a large number of scientific publications (Ref.) and
    • clear case reports in humans, where, Mebendazole alone was effective in inducing cancer regression, in cancer patients with adrenal cancer (Ref.) and colorectal cancer (Ref.), not responding anymore to conventional treatment methods
  • it has nearly no side effects, and due to this reason
  • it is an over the counter drug in most of the countries, which means there is no need for a doctor prescription
  • and on top of all, it is a very cheap drug
  • available virtually anywhere and everywhere.


The first website where I came across Mebendazole discussion was, I think, this one: http://www.abovetopsecret.com/forum/thread822776/pg1 I was happy to see in 2014, just a few months latter after I studied Mebendazole intensively and became convinced about its anti cancer relevance, a paper has come out from one of my favorite Anti Cancer Foundation, i.e. Anticancer Fund, consolidating a good amount of research and proposing Mebendazole as a re-purposed drug against cancer. Here is that nice paper published in 2014: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096024/ By that time, we were already using it.

Before and after the publication of the above paper by Anticancer Fund, there were multiple relevant scientific papers published around Mebendazole and multiple discussions, triggering me to start writing about Mebendazole. Interestingly and amazingly, in 2016, a drug company has decided to charge 200x higher price for Mebendazole (thanks to Helga, a reader of this website I learned about this) (Ref.). Fortunately, it seems that in the US there is still available a powder form that is cheap. Alternatively, it can anyway be ordered online as discussed below in the “Source” section. This was another point when I wanted to write about Mebendazole. Today, finally, I succeeded to write this post, triggered again by another publication coming from US Oncology center and School of Medicine, suggesting the re-purposing of Mebendazole as a replacement for Vincristine chemotherapy for the treatment of Brain tumors (Ref.).
Credit photo: https://valelab.ucsf.edu/research/microtubules/

While many of the constant readers of this website already know Mebendazole, I hope the article will help the awareness of new readers.
Indeed, Mebendazole, alone or combined with chemo, has been shown to be effective against multiple forms of cancer cells, such as:

  • adrenal cancer (Ref.1, Ref.2)
  • colon cancer (Ref.1, Ref.2)
  • brain cancer, medulloblastoma, glioblastoma (Ref.1, Ref.2, Ref.3, Ref.4)
  • melanoma (Ref.1, Ref.2, Ref.3)
  • head and neck squamous cell carcinoma (HNSCC) (Ref.)
  • cholangiocarcinoma or bile duct cancer (Ref.)
  • gastric cancer (Ref.)
  • breast cancer (Ref.)
  • lung cancer (Ref.1, Ref.2)
  • ovarian (Ref.)
  • leukemia (Ref.) acute myeloid leukemia (AML) (Ref.)
  • pancreatic cancer (Ref.)
  • fibrosarcoma (Ref.)
A study, showed a high level of activity against leukaemia, colon cancer, CNS and melanoma cell lines, with lesser activity in breast, ovarian, renal and NSCLC lines (Ref.).

Based on all the research available, I would expected the highest chance of effectiveness of Mebendazole, against

  • adrenal cancer,
  • colon and colo-rectal cancer,
  • brain cancer,
  • melanoma and
  • leukemia
and possibly
  • pancreatic cancer and
  • lung cancer
However, given the low cost, limited to now side effects, its availability and potential, I would still try it for the other cancer types (next to other treatments), specifically for the aggressive cancer types. Based on the above results, the other potentially responsive tumor types seem to be those of
  • ovarian,
  • breast,
  • bile duct,
  • gastric.
Note: other anthelmintic drugs have also been shown to present strong anti cancer effects, but their main anti cancer mechanisms may be different. Of the anthelmintic category, Albendazole is one of my other favorites due to its unique anti cancer mechanism (to be discussed elsewhere) but that comes with some liver toxicity. Albendazole has been indicated to be effective against, e.g. ovarian cancer (Ref.). Here is a study suggesting that of the existing repurposed drugs, antiparazite medication is one of the most effective group of drugs against cancer, after typical anti neoplastic drugs (Ref.).

The ever growing evidence that anti parasitic medication is effective against cancers may also trigger medical doctors and researchers look at cancer from other perspectives, e.g. cancer as a parasitic disease, a perspective which so far has been only discussed outside the mainstream medicine. Here is an example that consolidated such a perspective http://jeffreydachmd.com/2016/05/cancer-as-a-parasitic-disease/ I think, successful researchers have to always keep their mind open, ready to consider new perspectives proposed by others and even better connect the available “dots” to generate new perspectives. As we will discuss further, the only drawback with Mebendazole is that due to its absorption which can be different in different patients, the results may vary from patient to patient.

According to recent research, Mebendazole may inhibit Multi Drug Resistence (MDR) transporters (Ref.). These are the transporters used by cancer cells to push out chemotherapies in order to survive during chemo treatments. Therefore, using Mebendazole during chemo treatments may lead to increase effectiveness of the conventional therapies.

Case Reports in Humans:
Besides all the studies in the lab indicating the effectiveness of Mebendazole against various cancer types, below are two published scientific case reports that are clear and coming from trust-able sources. In both cases, Mebendazole has been applied after the patients were not responding anymore to conventional therapies. The medical doctors have decided to use Mebendazole following scientific results from various research groups suggesting Mebendazole may be effective for those cancer types. This indeed, was the case. The results were extremely promising:

Mebendazole monotherapy and long-term disease control in metastatic adrenocortical carcinoma https://www.ncbi.nlm.nih.gov/pubmed/21454232
Here is a PDF version available.

A 48-year-old man with adrenocortical carcinoma had disease progression with systemic therapies including mitotane, 5-fluorouracil, streptozotocin, bevacizumab, and external beam radiation therapy. Treatment with all chemotherapeutic drugs was ceased, and he was prescribed mebendazole, 100 mg twice daily, as a single agent. His metastases initially regressed and subsequently remained stable. While receiving mebendazole as a sole treatment for 19 months, his disease remained stable. He did not experience any clinically significant adverse effects, and his quality of life was satisfactory. His disease subsequently progressed after 24 months of mebendazole monotherapy.
My comments: as discussed in the article, the patient received only 200mg Mebendazole each day. That to me is the lowest daily dose and according to multiple sources the dose could be further increased with no issues. In addition, Mebendazole is known to be poorly absorbed in the body and there are ways to increase its absorption. All these will be further discussed in the “Dose and Application” section below, but the point is that while the medical doctors authors of this article have my highest regards, in the future higher dose can be used to try increase Mebendazole effectiveness.

Drug repositioning from bench to bedside: tumour remission by the antihelmintic drug mebendazole in refractory metastatic colon cancer. https://www.ncbi.nlm.nih.gov/pubmed/24160353
Here is a PDF version available.

A patient with refractory metastatic colon cancer was treated with MBZ at the standard anthelmintic dose of 100 mg twice daily. The patient experienced no subjective adverse effects at all from the drug and computerized tomography evaluation after six weeks of therapy showed near complete remission of the metastases in the lungs and lymph nodes and a good partial remission in the liver. At this stage, the liver enzymes AST and ALT were found elevated up to five and seven times above upper limit of normal and mebendazole was temporarily stopped and then reintroduced at half dose. Liver enzymes slowly decreased and the patient still reported no adverse effects from mebendazole. The disease was stable at a new CT, confirming the response observed earlier.

My comments: Since Mebendazole is not associated with hepatic dysfunction (Ref.) and since the daily dose used here is on the very low side, I suspect the elevation of AST and ALT was due to the tumor lysis.

Mechanism:
The primary anti cancer mechanism is related to the depolymerization of tubulin in human tumor cells caused by Mebendazole, inhibiting mitotic spindle formation, and therefore inducing mitotic arrest and apoptosis. This is a mechanism similar to that one I already described in details in the post on Griseofulvin: https://www.cancertreatmentsresearch.com/decide/ so I will not discuss again, here, the details of the mechanism.

Indeed, Mebendazole has been shown to cause mitotic arrest in parasitic cells as early as 197o’s (e.g. Ref.). As a reference for the reader, at some level, Mebendazole acts similar to microtubule dynamic inhibiting chemotheraphies such as microtubule-stabilizing (e.g., paclitaxel, docetaxel) or microtubule-destabilizing (e.g., vinblastine, vincristine, nocodazole, colchicine) agents (Ref.)
Mebendazole has been found to work against tumors via other mechanisms as well:

  • angiogenesis inhibition (Ref.) MBZ may inhibit the action of VEGFR-2 by binding to it (Ref.)
  • inactivates Bcl-2 and activates caspases to promote apoptosis in cancer cells, and the release of cytochrome c, which has also been shown to trigger apoptosis in malignant cells (Ref.). Here is how Bcl-2 fits into the picture (Ref.).
  • hedgehog inhibitor (Hh) (Ref.) Here is how hedgehog fits into the picture (Ref.). The hedgehog (Hh) signaling pathway is activated in many types of cancer and therefore presents an attractive target for new anticancer agents. Hedgehog ligands or markers of downstream pathway activity have been detected in melanomas, lung cancers, ovarian cancers, adrenocortical cancers and colorectal cancers (Ref.), which are all responsive to Mebendazole, as discussed above. Interestingly, among other Hedgehog inhibitors that have previously identified are also drugs that interact with microtubules, including vinblastine, vincristine, and paclitaxel (Ref.). Itraconazole, that I previously discussed in a different post is also a hedgehog inhibitor: https://www.cancertreatmentsresearch.com/itraconazole/ So there may be a connection between hedgehog inhibition and microtubule dynamics inhibition.
  • based on the fact that ultra low dose microtubule inhibiting chemotherapy is known to activate the immune system, (https://www.cancertreatmentsresearch.com/ultra-low-dose-taxol/) it has been proposed that Mebendazole could do the same (Ref.) Update 2020 August: here is a recent paper suggesting immune activation due to ERK mediated immune cell activation (Ref.)
Interestingly, Mebendazole is not toxic against normal cells. Researchers speculated a defect in at least one mitotic checkpoint function in tumor cells leading to their higher sensitivity to Mebendazole (Ref.).

Update November 2017: Here is an article, published this month, presenting a diagram with Mebendazole’s anti cancer mechanisms known so far: https://www.tjpr.org/admin/12389900798187/2017_16_10_32.pdf

Side effects:
In general, the drug is well tolerated but some people may present adverse effects and may have to discontinue. Here is the product description https://www.janssen.com/canada/sites/www_janssen_com_canada/files/product/pdf/ver11192014cpm.pdf

At high dose, it has been found to possibly induce bone marrow suppression in patients chronic liver disease (Ref.) That reverted to normal after the drug was stopped. There are rare reports of reversible alopecia, urticaria, rash, gastro-intestinal upset, leukopenia, and neutropenia in some patients treated with high-dose MBZ (Ref.)

MBZ is contraindicated during pregnancy, due to its potential anti-angiogenesis properties.
In the event of accidental overdose, abdominal cramps, nausea, vomiting and diarrhea may occur (Ref.).

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Dose and Administration:
One of the challenge with Mebendazole administrations is its low bioavailability which leads to only 20% absorption. The mebendazole plasma concentration-time profiles differed considerably between patients receiving 10 mg/kg Mebendazole; elimination half-lives ranged from 2.8-9.0 h, time to peak plasma concentration after dosing ranged from 1.5-7.25 h and peak plasma concentrations ranged from 17.5 to 500 ng/ml. (Ref.) Such doses are indeed in the plasma level reported to achieve anti cancer effects in the lab. Hoewever, as it can be seen the distribution of plasma level is wide so not everyone will reach high plasma level of Mebendazole.

Therefore, to address the challenge related to reaching a high level of mebendazole plasma level, which on one hand is due to the bad absorption and on the other hand due to a strong first pass metabolism in the liver, the following actions can be taken:

  • administer with a fatty meal (Ref.)
  • long term administration (Ref.)
  • increased dose may increase the absorption (Ref.)
  • given with Cimetidine (another of my preferred anti cancer drugs) (Ref.) will reduce its metabolism in the liver. Cimetidine can be found as an over the counter drug on eBay but should be used with care when combined with chemo as it will increase the plasma level of some of the chemos.
The low bioavailability is also probably why its side effects are very limited. Mebendazole is rapidly metabolized to less toxic metabolites by the liver, and this could be another reason for its low toxicity (Ref.). Increasing the plasma level with the strategy mentioned above, may also bring some side effects, so have an eye on that.

According to the literature, some people may absorb better Mebendazole compared to other, that may also lead to different effectiveness of Mebendazole in different people.

In the two successful case reports referenced above, the patients have used the minimum dose typically used against worms, i.e. 100mg 2x/day.
This, to my opinion is on the low side of the dose but could be the starting dose. A high dose, but still feasible, according to a World Health Organisation reference (Ref.) cited by the Anticancer Fund (Ref.), could be up to of 40–50 mg/kg/day for at least 3–6 months. This seems to be the long-term treatment of cystic echinococcosis. Another reference in terms of max dose still feasible is that used for alveolar echinococcosis, where 40–50 mg/kg/day is used with treatment for at least two years, and possibly longer for patients with inoperable disease (Ref.).
Based on the above, a person of 50kg could use up to 2.5g Mebendazole for months to years. Actually, this website pointed out a discussion on Inspire website where a caregiver said a brain cancer patient accessing a clinical trial at John Hopkins Hospital was “taking 2500mg in the morning, 3000 mg in the afternoon & evening.” (Ref.)

That is really a huge dose. Indeed, there was a clinical trial at John Hopkins Hospital, involving Mebendazole for Brain cancer gave it at 3x500mg/day with meals, on a 28 day cycle (Ref.). I haven’t found yet the results reported.

Following the above discussions, I would take the daily dose split into two, during or just after breakfast and dinner, if possible together with Cimetidine 400mg 2x/day. I would always start with a low dose Mebendazole and go up step by step to the target dose. If the target dose is very high, I would split that in 3x/day. Also, please note that in the clinical trail they did not used Cimetidine. And since Cimetidine may very much increase the plasma level of Mebendazole (some say by 50%), in case we use that I would make sure the target dose is lower than what was used at John Hopkins Hospital. Janssen Pharma product descriptions states the following regarding the dose: “In controlled safety studies, humans have received from 100 to 1200 mg of mebendazole daily for up to 14 days with no reported side effects.” (Ref.)

Update Nov 2019:

Here are two clinical trials on Mebendazole:

Although a dose of 50 mg/kg/day seems very high, here is a man reporting that his son takes a very high dose of mebendazole as a part of a clinical trial, using 4.5g/day without significant side effects (Ref.).

Update July 2020: Here is a nice old article discussing the following:

“Mebendazole levels were measured in our patient 1 (Table). To the best of our knowledge, previous reports of side effects have not included data on these levels; such measurements, however, may be important because of the drug’s erratic intestinal absorption and possible dose-related toxic effects. Fasting levels measured in 22 patients receiving 16 to 48 mg/kg/day ranged from undetectable to 300 ng/mL.6 Only 19% of the levels exceeded 75 ng/mL, and levels did not correlate with dosages.6 Our first patient’s random and fasting levels were 147 to 239 ng/mL. High levels have also been reported in a patient with cholestatic jaundice, presumably reflecting decreased hepatic metabolism, the primary route for elimination of mebendazole.1 In our two patients and in the two previous patients described with neutropenia,45 either extensive liver replacement by cysts or underlying liver disease was noted and may have predisposed to high levels of mebendazole or its metabolites.7” https://pubmed.ncbi.nlm.nih.gov/6842806/
This demonstrated the need to do our best to increase the blood levels of Mebendazole by increasing its absorption (taking it with fats) and lowering its metabolism (with Cimetidine/Tgamet).
Source:
The brand name is Vermox, Benda, etc. sold as a solution or tablet. I prefer the tablet version. Those tablets come in 100mg or 500mg version. I prefer the 500mg version and cut them in pieces if lower dose is required.

Mebendazole is available at many pharmacies in many countries, online and over the counter. Here is an example of a version that is available over the counter at a super market in the Netherlands: https://www.kruidvat.nl/kruidvat-anti-worm-mebendazol-100mg-tabletten/p/1023933 . In this case 6x100mg tablets costs 3 euro.

Another option is to buy from eBay or from sites like this one: http://smartproduct4u.com/?ref=285 many of which are coming from Thailand.
Finally, if there is no other option or would like to go the low cost version, we can buy it from China, via Alibaba, at a cost of about 200 euro/kg if I remember correctly. But that is powder version. Btw, just think about this: 200 euro for 1000g in China vs. about 800.000 euro for 1000g in USA, after the price increase initiated by a US drug company last year. Imagine the gross profit on this one. How can, we, the society accept something like this???

Other clinics recommending Mebendazole:
Care Oncology Clinic in London, UK: http://careoncologyclinic.com/ They usually seem to give to their patients a combination of drugs including Sratin + Metformin + Doxycycline + Mebendazole. Here is an article explaining in details the price, activity and vision of this clinic http://www.telegraph.co.uk/wellbeing/health-advice/crowdfunding-cure-cancer/

References:
Mebendazole monotherapy and long-term disease control in metastatic adrenocortical carcinoma https://www.ncbi.nlm.nih.gov/pubmed/21454232
Repurposing Drugs in Oncology (ReDO)—mebendazole as an anti-cancer agent https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096024/
Mebendazole, a well-known anti-helminthic drug in wide clinical use, has anti-cancer properties that have been elucidated in a broad range of pre-clinical studies across a number of different cancer types. Significantly, there are also two case reports of anti-cancer activity in humans. The data are summarised and discussed in relation to suggested mechanisms of action. Based on the evidence presented, it is proposed that mebendazole would synergise with a range of other drugs, including existing chemotherapeutics, and that further exploration of the potential of mebendazole as an anti-cancer therapeutic is warranted. A number of possible combinations with other drugs are discussed in the Appendix.
Repositioning of the anthelmintic drug mebendazole for the treatment for colon cancer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825534/
Sixty-eight compounds were defined as hits with activity in both of these cell lines (<40 % cell survival compared with control) at 10 μM drug concentration. Analysis of chemical similarity of the hit compounds revealed several distinct clusters, among them the antiparasitic benzimidazole group. Two of these compounds, mebendazole (MBZ) and albendazole (ABZ) are registered for human use. Data from the NCI 60 cell line panel revealed only modest correlation between MBZ and ABZ, indicating differences in mechanism of action. This was further supported when gene expression signatures were compared in the CMAP database; ABZ ranked very low when MBZ was used as the query signature. Furthermore, MBZ, but not ABZ, was found to significantly interact with several protein kinases including BCR–ABL and BRAF. Analysis of the diagnosis-specific activity of MBZ showed activity in 80 % of the colon cancer cell lines in the NCI 60 panel. Three additional colon cancer cell lines and three cell models with non-malignant phenotypes were subsequently tested, confirming selective colon cancer activity of MBZ. MBZ seemingly has repositioning potential for colorectal cancer therapy.

Repurposing the antihelmintic mebendazole as a hedgehog inhibitor https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297232/

The hedgehog (Hh) signaling pathway is activated in many types of cancer and therefore presents an attractive target for new anticancer agents. Here we show that mebendazole (MBZ), a benzamidazole with a long history of safe use against nematode infestations and hydatid disease, potently inhibited Hh signaling and slowed the growth of Hh-driven human medulloblastoma cells at clinically attainable concentrations. As an antiparasitic, MBZ avidly binds nematode tubulin and causes inhibition of intestinal microtubule synthesis. In human cells, MBZ suppressed the formation of the primary cilium, a microtubule-based organelle that functions as a signaling hub for Hh pathway activation. The inhibition of Hh signaling by MBZ was unaffected by mutants in the gene that encodes the Hh pathway signaling protein SMO, which are selectively propagated in cell clones that survive treatment with the Hh inhibitor vismodegib. Combination of vismodegib and MBZ resulted in additive Hh signaling inhibition. Because MBZ can be safely administered to adults and children at high doses over extended time periods, we propose that MBZ could be rapidly repurposed and clinically tested as a prospective therapeutic agent for many tumors that are dependent on Hh signaling.
Combination of Manumycin A and Mebendazole in Human Breast Cancer Cell Lines, a PhD thesis from 2010 https://uh-ir.tdl.org/uh-ir/bitstream/handle/10657/166/HADDADIN-.pdf?sequence=2

An article on Mebendazole, on a nice website of a breast cancer patient: https://magiccocktailquest.wordpress.com/2015/06/08/mebendazole/
Mebendazole is unique among tubulin-active drugs in activating the MEK–ERK pathway https://www.nature.com/articles/s41598-020-68986-0
We recently showed that the anti-helminthic compound mebendazole (MBZ) has immunomodulating activity in monocyte/macrophage models and induces ERK signalling. In the present study we investigated whether MBZ induced ERK activation is shared by other tubulin binding agents (TBAs) and if it is observable also in other human cell types. Curated gene signatures for a panel of TBAs in the LINCS Connectivity Map (CMap) database showed a unique strong negative correlation of MBZ with MEK/ERK inhibitors indicating ERK activation also in non-haematological cell lines. L1000 gene expression signatures for MBZ treated THP-1 monocytes also connected negatively to MEK inhibitors. MEK/ERK phosphoprotein activity testing of a number of TBAs showed that only MBZ increased the activity in both THP-1 monocytes and PMA differentiated macrophages. Distal effects on ERK phosphorylation of the substrate P90RSK and release of IL1B followed the same pattern. The effect of MBZ on MEK/ERK phosphorylation was inhibited by RAF/MEK/ERK inhibitors in THP-1 models, CD3/IL2 stimulated PBMCs and a MAPK reporter HEK-293 cell line. MBZ was also shown to increase ERK activity in CD4+ T-cells from lupus patients with known defective ERK signalling. Given these mechanistic features MBZ is suggested suitable for treatment of diseases characterized by defective ERK signalling, notably difficult to treat autoimmune diseases.

Drug repurposing and relabeling for cancer therapy: Emerging benzimidazole antihelminthics with potent anticancer effects https://www.sciencedirect.com/science/article/abs/pii/S0024320520309413

Origin of drug and radio-refractory clones, cancer stem-like cells, and rapid angiogenesis and metastasis are among the primary concerns that limit the efficacy of anticancer treatments, emphasizing the urgency of developing new therapeutics. Factors like high attrition rates, huge investments, patients’ heterogeneity, and diverse molecular subtypes have challenged the rapid development of anticancer drugs. Treatment with repurposing pleiotropic benzimidazole antihelminthics, like mebendazole, albendazole, and flubendazole has recently opened a new window, owing to their easy access, low cost as a generic drug, and long track record of safe use in the human population. This review highlights the outcomes of preclinical and clinical studies of these drugs as a potent anticancer agent(s) conducted in the last two decades. Substantial preclinical studies, as well as limited clinical trials, suggest noteworthy anticancer potency of these pleiotropic benzimidazoles, particularly as potent microtubule disrupting, anti-angiogenic, and anti-metastatic agents, inhibitors of the immune checkpoint, hypoxia-inducible factor, epithelial-mesenchymal transition, cancer stemness, and multidrug resistance protein 1, and inducers of apoptosis and M1 polarization. These anticancer effects are attributed to multiple action points, including intrinsic apoptosis, canonical Wnt/β-catenin, JAK/STAT-3, JNK, MEK/ERK, and hedgehog signaling pathways. The effective anticancer properties of mebendazole, albendazole, and flubendazole either alone or synergistically with frontline drugs, warrant their validation through controlled clinical trials to use them as promising avenues to anticancer therapy.

Disclaimer:
This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.
Please read an extended version of the Disclaimer here: https://www.cancertreatmentsresearch.com/?page_id=1794

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ADRENAL CANCER, ANGIOGENESIS INHIBITORS, BRAIN CANCER, COLON CANCER, COLORECTAL CANCER, LEUKEMIA, MELANOMA, MITOSIS INHIBITORS, SYNTHETIC 80 COMMENTS
 

Ruby Gray

New member
Thanks Phil! There is a huge amount of credible technical information here to study.
If, as many studies have found, neoplasms are in at least some instances a bodily response to microbes, parasites etc, then these drugs stand a very good chance of being effective in treatment of them.
That they are safe, readily available and inexpensive, is a huge advantage.
Certainly well worth studying this more.
I hope Mickey makes a full and spectacular recovery!
 

alpha77

Member
What was the dog fed and was he possibly for longer times exposed to either EMF / RF or EF fields? Note EF fields are generated by "normal" wiring too especially if not properly installed or have "dirty electricity". Rf is ofc from wireless devices / smartphones / routers / antennas etc. EMF is the magnetic component of EF (eg. microwave oven). Where did the dog sleep for example anything above mentioned near him?
 
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