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

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. Indeed, there are case reports published in peer review papers showing that Mebendazole can induce anti-cancer response in some aggressive cancers.

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.

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). It is labelled 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, it has been indeed shown that Fenbendazole can be 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.).

While there is more prior literature suggesting anti cancer effectiveness related to Fenbendazole, 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.).

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.
  • 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).

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

In his treatment protocol, following a discussion with one scientist from Merck animals who treated her brain cancer with Fenbendazole, Joe Tippens uses 1g granules (containing 222mg pure Fenbendazole) each day, and he is taking that 3 consecutive days. He than stops taking Fenbendazole for the next 4 days. After that he starts again, and he goes like this continuously during the year. So the drug administration is 3 days ON and 4 days OFF.

If due to any reason taking Fenbendazole for ever it’s not an option, I would at least consider taking it for 3 days, then repeat a three day course at three weeks and again at three months. This the minimum treatment schedule in my view and is inline with the rule of 3’s used when treating whipworms (Trichuris vulpis). The idea behind this treatment regime is that some warms such as Whipworms take 3 months to mature from an egg to an adult. If you kill adults at day 1, then three weeks later there will be some immature adults which will have matured, but you’ll still have eggs and larval worms present (Ref.). Nevertheless, this is the minimum regime I would use but I would probably better follow the treatment regime used by Joe Tippens (continuous 3 days ON and 4 days OFF) for 2-3 months and check if there is a response. If there is response, and tumors are shrinking I would continue, if not I would stop. Joe Tippens said he will take it for the rest of his life. He states there were no side effects for him or for over 50 people he knows taking it.

Since it has been shown that 500 mg/per person for 10 consecutive days is well tolerated in humans (Ref.), and since as discussed below the absorption of Fenbendazole in humans is poor, it may help to use from time to time a higher dose, such as 2g granules (each gram containing 222 mg pure Fenbendazole) each day, which would lead to a daily dose of 444 mg Fenbendazole.

Therefore, a suitable daily dose of Fenbendazole for longer term use may be between 220 mg (the dose that was effective for Joe Tippens) and 500mg (the dose shown tolerable in humans).

Since there are various produces for Fenbendazole under different brands, in different forms (granules, solution, capsules) and for different animals, it is best to check on the package to understand how much active ingredient (Fenbendazole) is in one gram (or ml) of the product we buy. And make sure that the daily dose of active ingredient (Fenbendazole) is somewhere between 220 mg and 500 mg.

Better to take it with or after food

Like many benzimidazoles, Fenbendazole is very poorly soluble in aqueous systems, which are found in the gastrointestinal tract, causing its low absorption to the bloodstream and thus very low bioavailability. Maximal plasma concentration levels of benzimidazoles in humans is known to be markedly increased if the substance is used immediately after a meal (Ref.1, Ref.2).

As for the case of Mebendazole, I expect another way to increase its absorption in the body is by combining it with Cimetidine (Ref.).

Add Vitamin E to possibly enable Fenbendazole effectiveness

During 2008, at the School of Medicine from Johns Hopkins University, it has been found that Fenbendazole could affect the growth of a human lymphoma cell line only when combined with vitamins (Ref.).  Supplemented vitamins included B, D, K, E, and A.

Indeed, in his treatment regime, Joe Tippens also included  the following: Tocotrienol form of Vitamin E (800IU per day, 7 days a week); Bio-Available Curcumin (600mg per day, 7 days a week), and CBD (25mg per day, 7 days a week) oil (Ref.).

The common vitamin that is both present in the supplement vitamins in the article cited above and Joe’s treatment regime is Vitamin E (800IU per day, 7 days a week). He uses a VITAMIN E (AS D-ALPHA TOCOPHEROL) complex of 400IU called Perfect E, containing:


Given that each capsule has 400UI, 2capusles/day should match Joe’s schedule.

Indeed, other studies have also shown that the combination of Fenbendazole and Vitamin E can be effective against cancer (Ref.).

Where to buy

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.


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.


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89 thoughts on “A Drug Made for Animals and Taken by Humans to Treat Cancer: Fenbendazole

    1. Since no one knows which one would be better, I would try both as toxicity is low.
      I would probably combine 1g granusles Fenbendazole/day (that is 222mg/day active component) 3days ON and 4 days OFF, and 200mg/day Mebendazole also 3 days ON and 4 days OFF. I would take them together during the same days. Also, I would take them with some oils, like Omega 3, for a better absorption.

      Kind regards,

      1. Hi Daniel

        Great and very detailed article.

        I have been diagnosed with prostrate cancer. I am based in N’Djamena, Chad. I tried to buy Fenbendazole online and it seems I require a prescription from. Veterinarian to complete the transaction. I am in New York for two weeks and would like to buy and to take it with me back. Anyway that you can assist?

            1. I managed to get Panacr c from countrysidepetsuppl web site and no prescription needed. Cost was US$ 29.93 for 3 packs by 200 grms.

  1. A great article, well detailed, as always. Thank you!
    We use mebendazol since about 1,5 years and still have some stock, but as soon as it is sold out we will try Fenbendazol. In addition it is easier to find, without prescription and cheaper !
    I was wondering already for mebendazole, but do you think can we combine them with pyrvinium, Daniel (both being anthelmintic)?

    1. Thanks for reporting Shane. Both Mebendazole and Cimetidine are drugs I like based on their anti cancer activity. I wrote about Mebendazole here https://www.cancertreatmentsresearch.com/the-over-the-counter-drug-mebendazole-acts-like-chemotherapy-but-with-virtually-no-side-effects/ As I remember, first time in my life I read about Mebendazole was on the abovetopsecret website in 2014 and it may just be your post. So, thank you very much again. Are you still taking the two?

      1. Hello Dan .. I’ve not taken them for 3 -4 years and have had regular check ups and still all clear .. just let you know I told my specialist from Christie’s hospital 4 years ago about what I’d taken and he’d never heard of them but now they are using both drugs in trails in Christie’s in conjunction with chemo at the moment so it’s looking like it’s getting the attention the drug deserves ..I’ve also helped a couple of people in my home town with them an both have had the all clear ..

        1. HI Shane, thank you. As I understand you had Ostersarcoma with mets to the lungs. The treatment you used was 100mg Mebendazole tablets 3 times a day, 200 mg cimetidine tablets 4 times a day and 50 grams of Glutamine power twice a day. Can you please let me know what was the cancer type of those who may have benefited from Mebendazole, and the dose they used? Also, could you please share the link to the trial on chemo+mebendazole at Christie’s? Thank you.

  2. Hello! I was just introduced to the blog by Joe last week and by no coincidence came upon your report, which I references this same Joe. I am hopeful in both of your writings. My husband was diagnosed with renal cell carcinoma in 2017, and is a patient at MD Anderson. Would Fenbendazole &Vitamin E be beneficial to someone with renal cell carcinoma? I understand your disclaimer, but can you please tell me in your best opinion if you think this could be beneficial to him. I appreciate your time and any comments you can offer. Thank you!

    1. Hi,

      the toxicity of drugs like Fenbendazole is relatively low. So I think for most patients it makes sense to try it for some time and see if there is added value. Of course I would use Fenbendazole just as an addition to other treatments, such as those provided by MD Anderson, to increase chance of positive outcome. Beyond Fenbendazole, you may like to read through this website and the forum https://www.cancertreatmentsresearch.com/community/ for other relevant options such as this one https://www.cancertreatmentsresearch.com/community/kidney-cancer/the-long-term-survival-of-a-patient-with-stage-iv-renal-cell-carcinoma-following-an-integrative-treatment-approach-including-the-intravenous-α-lipoic-acid-low-dose-naltrexone-protocol/
      On both the main web-page and the forum page there are search options where you can search for keywords such as “renal” or “kidney”.

      Kind regards,

  3. Hi Daniel,

    If we were to combine Joe’s protocol for fenbendazole with your suggestion for mebendazole then the supplements would be vitamin E, curcumin, CBD oil, cimetidine, and Omega 3. Do you have any concerns about this combination causing adverse effects, e.g. upset stomach?

    We are also considering adding another dewormer, niclosamide, based on this article:

    The article mentions that the salt form of niclosamide (niclosamide ethanolamine) is more soluble and hence may overcome the absorption problem that necessitates some of the supplements. Our hesitation about this salt form is that we cannot find any dosing information. Do you have any thoughts about this?

    Thanks much,

  4. D, did you notice the combination index of Fenbendazole and DCA from the Nature 2018 article?
    0.04? Is that even possible? There is massive massive synergy between them.
    Why has this not been more highlighted in the discussion?

    It should be of no great surprise when combining 2 anti-glycolytics that this should happen though this
    is even more extreme than I would have expected. There was also synergy with 2-DG.

    I would be interested to see if they publish formulations for FB.
    nanoFB (i.e. with chitosan perhaps)?


  5. Yes, there are likely quite a few of our old favorites that should synergize nicely with FB. It is always frustrating when we find a new path forward and the research lags behind. I was quite impressed though how strong the DCA synergy was with FB.

  6. Hi, Daniel. I am planning to try the combination of Fenbendazole and Mebendazole for my mum. But, I can’t find Panacur C at my country. Instead, I can easily find an alternative named “Quantel” in form of tablet at my place. It states containing Praziquantel PhEur 50mg and Fenbendazole PhEur 500mg.

    My question is that do you think Quantel is a suitable alternative to Panacur C in the sense that both have fenbendazole as the primary gradient? Or, it is better to use Panacur C?

    1. Dear Fung. If it contains Fenbendazole that is what you are looking for. Praziquantel is one that I like too. It is an anthelmintic used in both human and veterinary medicine. It has anticancer effects too and it was shown that Praziquantel could greatly enhance the anticancer efficacy of Taxol in various cell lines including Taxol resistant cell lines. So I see no reason why not use Quantel. Just make sure you use the normal dose. 50mg/day Praziquantel seems to be in the low dose range but please investigate yourself https://reference.medscape.com/drug/biltricide-praziquantel-342666

    1. Hi,
      good question. Bone marrow aplasia can happen for very high dose of Mebendazole (1500mg/day) Ref and so I expect that would also be the case for Fenbendazole when used in very high dose. This usually improves on stopping the medication. However, based on available info at normal dose I do not expect impact on bone marrow.
      Kind regards,

  7. Hi Daniel,
    Some people said the vitamin E badly interact with Breast cancer. However, I found some information that only the alpha tocopherol did. May I get some advise from you?

  8. Hi, We just found out 4 days ago my mom has lung cancer (mass) and lymph nodes affected as well as he in spine L5. Still awaiting biopsy to find out what kind of cells and PETSCAN. The have already told her she is stage 4 and not cureable. How would Fenbendazole work with Radiation and Chemo? They want to do Radiation on Mass right away.

  9. Hi Pnut21, sorry to hear, since they’ll likely want to do chemo you might want to check out Robert A. Nagourney M.D, he does chemosensitivity testing on bits of tumors in order to find out which chemo can be effective. He also wrote the book “Outliving Cancer”.

    1. Johan,
      So do you not think the regime that Joe Tippens used, using Fenbendazole would be ok for her to start using in conjuntions with other treatment plan?

      1. Sorry to have confused you. I know I didn’t address your question and that’s because I know very little about Fenbendazole. But since your mom just recently got her cancer dx and she hasn’t started chemo yet I wanted to let you know about this technique, chemosensitivity testing or functional profiling in order to find out how cancer cells respond when they are exposed to drugs and drug combinations. (https://www.nagourneycancerinstitute.com/cancer-faqs). A good start is half the battle!

        1. @johan: that is interesting and promising, but they ask for a large sample, about one cubic centimeter, for solid cancers. IMO cutting such a sample from a primary tumor is too risky (increase in metastasis), so a resected malignant lymph node seems the best option. I still don’t understand, from their website, how to keep the cancer cells alive, until the sample reaches their lab.

            1. @johan: thank you for the link; so you need to first order a “specimen transportation kit” from their lab; then the transport to the lab shouldn’t take too long: “within 24 – 36 hours of collection while the cells are still viable”.

          1. Ovidiu, in response to your question below, indeed that seems to be the best way to collect the sample. As for your concern about taking such a large sample of a tumor, they can also work with cancer fluids (pleural effusion/ascites).

      2. HI Pnut21, in my view, anything that may interfere with cancer cells and slows them down is good to be stop a few days before chemo and started after. Fenbendazole is part of this category so I would apply this rule. Kind regards, Daniel

  10. @Pnut21: when presenting the case, it’s better to give more accurate information, and always try to get such information from the doctors, for starters what type of lung cancer it is. You didn’t specify the size(s) and / or volume of the lung “mass”, the number of affected lymph nodes, and size of the spine metastasis (which is probably the hardest to treat). If you’ll get a biopsy sample, it would be highly recommended to test it for possibly targetable mutations. You also didn’t specify from which country you are, and if you can afford to spend money on tests and medicines, other than those done by the public health system. You also didn’t specify if your mother was smoking, or was exposed to other carcinogens. You didn’t mention any blood tests, of tumor markers commonly used to monitor lung cancer.
    About Fenbendazole, while there are some credible reports about usefulness against lung cancer, before getting a lot more information about the particular cancer patient, it’s hard to give competent advice. And since Fenbendazole has a poor and variable bioavailability in humans, it may be useful in theory, but not in practice.
    About “Radiation on Mass”, what kind of radiation? Is it stereotactic radiosurgery or something else?

    1. I apologize, at the time I wrote that I gave what info I had. Today biopsy results came back and we were told she has grandular cancer of the lungs, non small cell, adenocarcenoma, stage 4.She will see the radiation oncologist hopefully next eeeek.

      1. @Pnut21: no need to apologize, to you this is new, and probably very stressful. Just remember to get as much useful information as possible, and share it when you ask for advice. From the oncologist you could find out which mutation tests are paid by the public health. In LUAD (lung adenocarcinoma), the most common mutations (determined from the biopsy sample, while it’s still fresh) are Kras, EGFR, ALK, Braf, Her2, etc. Common blood markers for LUAD are CEA (carcinoembryonic antigen), CYFRA21-1, NSE, CA 19-9, CA 125, etc. The oncologist should ask to perform such blood marker tests, since they are relatively cheap, and keep testing again the one which seems the most relevant, in order to monitor disease progression between CT scans.
        It would be helpful if you tried to answer some of the questions in my previous post. I suppose you have the CT scan, and interpretation of it.

  11. Having a low level prostate cancer, slowly rising psa of 4.6 , decided to try fenbendazole, sourcing from Safeguard Horse Dewormer, my question is about my plan to take this daily and not the alternating 4 on 3 off schedule that Joe Tippens has used …. my question is there a downside to every day use, aside the expense ? My layman theory is it will be more effective against cancer if used daily. I will also use a complex vitamin E supplement, will skip the CBD for now.
    Thanks for this well researched page, kanzanc.

  12. Interesting. I also found more info from files
    Fenbendazole products.pdf)
    at the facebook page
    which is devoted to fenbendazole.
    ——————–The dosage Joe took was 222mg of fenbendazole for 3 days on
    and 4 days off weekly. Joe was advised this to ensure optimal liver functioning. Some people do take it
    everyday for the first 2 weeks then drop down to the recommended 3-4 regime. Dosages up to 300mg
    have proven to be well tolerated.———————–

  13. Hi Daniel – have been fascinated by your article – having just read Joe Tippens account of his self-medicating with Fenbendazole.
    I have inoperable stage 4 bowel (colon) cancer, metastasised to my peritoneum. Had 8 rounds of chemo last year, drug free since then.

    I ordered 3 months worth of the Fenbendazole but have a problem with starting it straight away.

    Are you able to tell me whether having had an auto-immune disease (Sarcoidosis, in my lungs, 20 years ago, leaving them scarred) means I should not jump in right away? There is pitifully little research into Sarcoidosis, so I suspect the answer to this may be unknown. Can you help?

    Many thanks.

    1. Thank you Harrio. Auto immune reactions are based on up regulating glycolysis and MCT transporters. Using glyco inhibitors and MCT inhibitors should work against auto immune reactions. Fenbendazole seems to be also a GLUT inhibitor which means it should down-regulate glycolisis. So from this point of view Fenbendazole should help against auto-immune reactions. Adding MCT inhibitors such as Quercetin could further help to minimize potential auto-immune reactions. Kind regards, Daniel

  14. Daniel, Thank you for helping those of us who are in very difficult situations. Our special needs daughter has been diagnosed with Stage 4 liver cancer (after3 years of trying to find out what was wrong!!)! She is tube fed and weighs 60 lbs. at 30 years of age. My question is how we could give her the Fenbendazole and what dosage you would recommend? We fully understand that you are not recommending this medicine but we are most interested in it because she is not improving and we feel that we should try it. Thank you so very much for your work and compassion to help others. ❤️⭐️ janice

    1. Thank you Janice. I am so sorry you have to go through this. Regarding the dose, the rule that I always used was to start with 25% of the target dose and if everything is good move step by step (e.g. in 4-5 steps) to the target dose. The target daily dose is mentioned in the article above. Giving it via the tube is new to me but if I would have to give it via this route, I would probably buy the solution (Fenbendazole is found under different brands in different forms: granules, solution, capsules) or otherwise mix the granules with water. Adding fatty foods will help the absorption of Fenbendazole. Janice, have you considered trans arterial chemo embolisation (TACE) to treat the liver?
      If not, please see the following:

  15. Hello.
    I am a 6.5 years liver cancer fighter. My first OP was in April 2013. It was an HCC as big as my fist.
    Then follow 3 more times surgery in the next 3 years. Until today I got 5 microwave ablatations and 17 Tace(mitomycin) by Prof Vogl in Frankfurt.
    In my opinion from all natural ways Im doing, the high dose rectal and hyperbar ozone therapy was the best way for me. The last 1 year Im in stable disease.
    2 weeks ago Im on the fenben protocol includes Gamma E, B1 and DCA.
    I give you more Informations until it works.
    By the way, 3 years ago I have got 13 Infusions 3BP don’ t helped me.
    I think 3bp only works in tace. But no one in germany will do this. Prof Vogl only gives chemo tace.
    I am so sorry for my bad englisch.

    1. Hi Andre,

      Thank you so much for sharing the info with us. Your English is very good and today, with Google translator, there are fortunately no more language barriers. 17 TACE sounds like a lot indeed. It’s great that you can have access to prof Vogl’s treatments. Is this covered by the German insurance?

      Nice to know that you think and feel Ozone helps and 3BP did not help you. I think depending on tumor (size, location) and other know (such as dose, time, etc.) and unknown variables, 3BP helps some and do not hep others. 3BP TACE is good for some and not good for others. Same with IV. It’s an experimental treatment with important anti-cancer potential and the humanity still needs to understand how to use it in the best way.

      This may explain why 3BP was not effective enough in your case:
      “Therefore, therapeutic strategies should focus on both targets, glycolysis and mitochondrial OXPHOS. Even though some studies reported that mitochondrial OXPHOS is also one of 3-BP targets[185], 3-BP has been mainly demonstrated to be the most potent glycolytic inhibitor among various types of inhibitors. However, including our studies, the results of in vivo studies that have used human HCC cell lines did not exhibit complete remission, but showed only partial remission after 3-BP treatment[18,19,43-70]. One reason why 3-BP did not completely suppress tumor growth might be the low efficiency to suppress mitochondrial OXPHOS, the lactate shuttle, and high redox potential in cancer cells. To overcome the weakness of glycolytic inhibitors, the inhibitors to target mitochondrial OXPHOS and other involved mechanisms such as the suppression of ROS production, might be effective when used simultaneously with glycolytic inhibitors as a combination treatment.”

      Here is some relevant info shared by J, https://www.cancertreatmentsresearch.com/case-report-hepatocellular-carcinoma-hcc-successfully-managed-with-tace/#comment-7833

      Yes, Andre, please share with us anything that you learn and you think may help others. Thanks a lot and if you have questions please let me/us know.

      Kind regards,

      1. D, here is one that just came out that might help to amp up 3-BP.

        For me, the 3-BP era of cancer medicine really started with the melanoma patient. Injecting 50-100 mg liver TACE 3-BP and seeing a tumor shut-down (as with the liver patient) really is not that overly impressive. There are lots of other agents that could be effective in similar circumstances.

        Yet, Injecting 2 mg/kg IV of unformulated 3-BP in saline and seeing the truly massive tumor response with the melanoma patient was overwhelmingly shocking to me. It was almost magical! Even the animal experimental results with systematic 3-BP administration seemed somewhat cautious about suggesting that this would be of help in humans.

        The straight 3-BP only gave about a 50% knockdown on LDH with the melanoma patient. Then they added in the paracetamol and LDH went to zero! I almost freaked out! That was truly truly shocking. When I posted this result on several cancer forums, at first they did not get it. They misread the figure. They thought there was only a slight 20-50% response. When I clarified that the tumor was essentially completely deactivated, the forum webmasters were absolutely furious with me and I was banned from a few of these forums because of it.

        Obviously injecting straight 3-BP in saline would now be thought fairly close to insanity and the original researchers are pushing towards more realistic formulations such as liposomal 3-BP etc, though the article with the melanoma patient certainly captured widespread interest in 3-BP. There are not many anti-cancer medicines that spring to mind that have such overwhelming anti-cancer effects as seen in the melanoma patient article and yet have almost no side effects.

        The first article cited above moves the 3-BP glutathione story another step forward. This time they do a dual combo with BSO shutting down gutathione and auranofin shutting down thioredoxin. This has me excited! the melanoma patient had a truly massive response when they added in the paracetamol to the 3-BP. Yet, this trick probably would not work for all patients. Some patients probably would have the thioredoxin backup cycle to counter 3-BP. Imagine what might happen if the dual combo shut down glut and thio and then you came in with 3-BP. Wow! Would be nice if they add a nanoformulations for knocking down glut and thio.

        1. Dear J,

          Thank you for your great comments and references. This reference is indeed very relevant to amp up not only 3BP but also 2DG, chemo and radio.

          I totally agree, the 3BP era for us started with the publication of the case in Egypt, that also gave us indication about the safety dose/time. That was a great reference point. Although some may consider close to insanity using experimental treatments such as 3BP, I still think that makes sense. What is insanity is not to make careful steps when stepping into uncharted territories.

          I also very much agree and expect that the effectiveness of 3BP will strongly be affected by the inhibition of anti-oxidants, based on what we have seen when my wife was using 3BP – ALA was essentially cancelling its anti cancer effect even when used a few days after.

          Your post here makes me want to write a post on this subjects as it is very relevant and less discussed in our discussion group here, that is ” inhibition of redox metabolism in cancer”. I promise I will do that soon, after finishing a family visit.

          Some of the points to be addressed:
          – reduction/inhibition of glutathione production
          – reduction/inhibition of thioredoxin production
          – reduction/inhibition of cysteine import via e.g. Sulfasalazine https://www.cancertreatmentsresearch.com/cancer-addiction-to-cystinecysteine-another-piece-in-the-puzzel/
          – reduction of cysteine ingestion via the Methionine Restricted diet https://www.ncbi.nlm.nih.gov/pubmed/30725411
          – combination of the above with glycolisis inhibitors and conventional theraphies

          Again, thanks a lot for the inspiring reference and words.

          Kind regards,

  16. Daniel, I am new to this blog having recently of using Fenbendazole for use as a treatment for cancer. This January my son as diagnosed with small cell lung carcinoma with metastasis to the liver, sacrum and hip bone and brain. He has had 4 treatments of chemo (carboplatin and etoposide) and immunotherapy (aterzolizumab) with on going treatments of immunotherapy every 3 weeks. He has also received radiation on his-lung, back, hip and brain. His pet scans have shown a slight improvement. He was also diagnosed with MS almost 5 years ago. He was on Texfidera, but was taken off once he started the chemo and immunotherapy treatments.
    My question to you is. Do you think he will benefit by taking the Fenbendazole. And if so, How is it taken and What amount is given? Any help or direction you can give us would be greatly appreciated.
    Thank you,
    Angela B.

    1. HI Angela,

      I am very sorry to hear about your son? What age is him? If he is an adult, the doses mentioned in the article above should be in-line with what the adults are using. For patients between 2 and 17, I discussed here how to calculate the dose vs. the dose for adults https://www.cancertreatmentsresearch.com/tips-on-treatments-a-list-to-be-constantly-updated/ If you need help with the calculation, please let me know and will do that for you.

      Kind regards,

  17. Hi Daniel, I have found your Blog very informative and helpful. I have stage 4 ADPA which is a very rare Adenocarcinoma. Started in a finger and then Axilliary Node, then mets to one lung. Within 3 months of surgery (lung re section) several more tumors showed up in the same lung, plus one in a buttock. After 3 sessions of chemo (Paclitaxel and Carboplatin) a CT scan showed mixed results, the smaller nodes were stable, the larger increased by 20%+. So my Oncologist is now trialling 4 sessions of Doxorubicin. In between this I read J Tippens blog and started to use Panacur c which I was able to obtain from an American supplier. (I reside in New Zealand and its not available here) I use it in combo with Vit A, VitD3,Vit C, Turmeric,Green tea extract,Rei-shi super mushrooms and Resveratol. I am unable to obtain CBD oil in NZ but am seeking a prescription to import 3 months supply from Canada. I also had a CT scan several days ago, and will get the results at my next Oncology visit( in 3 days) so am hoping for a better result, maybe its too early to see a result from the Fenbendazole? This is most likely my only chance to hold this cancer from faster progression, I have been given 3 to 4 months if the treatment is not helpful. Would you have any suggestions that may be helpful in my quest. Many thanks, Patrick.

    1. Dear Patrick,

      Thank you for your comment and question. I am sorry you have to go through this and hope that soon you will start to be better and better.

      Regarding conventional treatment I checked Aggressive Digital Papillary Adenocarcinoma and as you probably know, this is a short summary:
      – Surgery: if possible this is the best counventional treatment approach
      – Radio and chemo: according to this paper (Ref.)
      o all of the cases reported in literature lead to little or no improvement with no obvious benefit
      o there is no agreed standardization of the use of adjunctive chemotherapy or regimens, but agents used before and reported in the literature include cisplatin, gemcitabine, 5-FU, mitomycin, adriamycin, thiotepa, fluoxymesterone, carboplatin, paclitaxel, docetaxel, and VP-16

      Therefore, based on the above, if the doctor is going to try Doxorubicin, I would do the best to use approaches that could support Doxorubicin and try to increase the chance for effectiveness. Next to that I would add other treatment options that may add extra chances. I would also try Fenbendazole indeed.

      While I do not know many details regarding the tumor size, exact location, history, etc, here are some ideas that may be relevant:
      1. ADPA shows tumor overexpression of FGFR2 indicating that targeting the fibroblast growth factor (FGF)/FGF receptor axis might be a promising treatment for ADPA and probably for the overall group of sweat gland carcinomas. https://onlinelibrary.wiley.com/doi/full/10.1111/bjd.17446
      Example of drugs and supplements that interfere with FGF/ FGFR are listed in the Tble 1 of the following paper https://iris.unibs.it/retrieve/handle/11379/477703/37957/2016%20review%20Pharmac%20Res.pdf (or https://www.ncbi.nlm.nih.gov/pubmed/27013279)
      Of these, some that I consider most relevant are Tranilast, Celecoxib, Thalidomide, Curcumin, EGCG, Resveratrol. All have been shown to inhibit FGF. To make sure I address well FGF, I would use two drugs and two supplements, e.g. Celecoxib + Tranilast or Thalidomide and Curcumin+EGCG
      2. If the tumor is at the surface, I would also consider making solutions for topical administration such as that described here https://www.cancertreatmentsresearch.com/3-bromopyruvate/
      Whenever I would use a new substance, I would only apply on a very small portion of the skin to test the reaction. Other substances can also be mixed with e.g. 70% DMSO for topical applications.
      3. There are multiple intravenous treatments discussed on this website that may help, such as Salinomycin https://www.cancertreatmentsresearch.com/salinomycin/, Diflunisal https://www.cancertreatmentsresearch.com/diflunisal-2/, 3BP https://www.cancertreatmentsresearch.com/3-bromopyruvate/, Taurolidine https://www.cancertreatmentsresearch.com/taurolidine/, Curcumin https://www.cancertreatmentsresearch.com/curcumin-an-universal-cancer-treatment/, 2DG https://www.cancertreatmentsresearch.com/a-new-approach-to-improve-effectiveness-of-cancer-therapies-is-getting-ready-to-begin-human-trials/
      All can be accessible for anyone who really wants them and who has a medical trained person that is willing to help with administering them. However, they should be treated with care as they are experimental therapies, yet with high chance of anti cancer activity.
      Of these intravenous therapies, one of the easiest to implement that may help increase the effectiveness of chemo is 2DG https://www.cancertreatmentsresearch.com/a-new-approach-to-improve-effectiveness-of-cancer-therapies-is-getting-ready-to-begin-human-trials/ 2DG for intravenous admin is available at German pharmacies and if you have a doctor who is willing to help I can connect him with an academic team from US that will help him for free with relevant info for implementation of this treatment. Usually it’s given after chemo for 2 days via an infusion pump (in the same way as 5-FU chemo is given to patients).
      4. Fenbendazole and any other drug and supplement that is expected to reduce tumor activity should be stop about 3 days before chemo day, and start again during the chemo day
      5. Fasting before chemo may help reduce the side effects of Doxo and may help increase it’s effectiveness
      6. Combining glucose absorption inhibitors such as those discussed here https://www.cancertreatmentsresearch.com/glucose-absorption-inhibitors-to-inhibit-tumor-growth/ with mitochondria inhibitors such as those discussed here https://www.cancertreatmentsresearch.com/a-list-of-mitochondria-inhibitors/ may help. Of these, one combination could be Canagliflozin with Metformin
      When using more drugs, you can always check the interaction between the drugs here https://reference.medscape.com/drug-interactionchecker?src=google besides discussing that with doctors
      7. You can also contact Care Oncology Clinic and consider starting up this drug cocktail including Metformin, Doxycycline, Statin and Mebendazole https://www.cancertreatmentsresearch.com/drug-cocktail-that-could-double-the-average-survival-time/
      8. Doxorubicin that you are using is a weak basis, which means that there is a high chance for Doxo to be deactivated by the acidity around the tumor before getting into the tumor as discussed here https://www.cancertreatmentsresearch.com/ph-cancer-a-top-treatment-strategy/
      In order to minimize this chance, I would use strategies that would be alkalize the body. Some obvious ways to do that are using Sodium Bicarbonate, or Basentabs https://www.pascoe.de/en/products/detail/basentabs-ph-balance-pascoe.html prior to chemo. In addition, using proton pump inhibitors such as Omeprazole (this is easy to get) may help. I discussed this in more details here https://www.cancertreatmentsresearch.com/ph-cancer-a-top-treatment-strategy/ Chloroquine (an anti-malaria drug) combined with Omeprazole may further help increase effectiveness of chemos such as Doxorubicin https://www.ncbi.nlm.nih.gov/pubmed/16495919 https://www.ncbi.nlm.nih.gov/pubmed/29225688 I wrote some more words about Chloroquine here https://www.cancertreatmentsresearch.com/chloroquine-hydroxychloroquine/

      I hope these ideas help.

      Kind regards,

      1. Hi Daniel, Just completed my appointment with the Oncologist, and was informed re the CT scan results. He was surprised with the mixed results again, larger lung Tumor only increased in size by 1mm, two of the smaller lung tumors also shows a very small size increase, the 4th tumor decreased. He has decided to cease the Doxorubicin and will start a three weekly treatment of Oxaliplatin and Capecitabine, the Capecitabine taken in 4 x 500grm Tablets x twice daily for 2 weeks on one week off. At this time he has also applied to get me into a Car T Cell trial in Melbourne Australia. This may be difficult to achieve as Australian residents will obviously have first preference. My Oncologist tells me there have been some excellent results with Car T Cell therapy on solid tumors. I would be interested to see what you think on this? Also do you think it is ok to continue with the Fenbenzadole during the Oxaliplatin treatments. The other meds I will now be taking are Domperidone 10mgs x 3 daily (as required) and Loperamide (as req) x 4 daily. I also discussed the possibility of trialling 2-DG (Metrononic) but he believes this would be better done in a clinic where treatment can be administered and monitoring for possible side effect is covered. In his opinion this would not be undertaken by medical professionals in NZ. He would be ok with me going to Germany or elsewhere for treatment ( 2-DG), but as our family finances have already been stretched to the limit by treatment and tumor profiling cost this is not a good option. Many thanks, Patrick.

        1. Hi Patrick,

          Regarding your question on Car T Cell therapy, my general opinion is that new/experimental therapies, especially those in the immune modulation space, should be used only when no other options are available. That is because the humanity is still at the very beginning in terms of understanding how the immune system can be controlled, while marketing of the involved companies it’s way ahead of that.

          Kind regards,

          1. Thank you for your reply Daniel, My Oncologist is attempting to enroll me in a Car T Cell trial in Melbourne Australia. This is if the current Chemo is not effective, it will be the final option for me. He did outline the possible serious side effects of Car T Cell therapy, and told me that there have been a number of deaths believed to be caused by this treatment. Although I seem to be tolerating Chemo well and he is surprised that my level of general fitness and wellbeing (under the circumstances) has not declined, he still believes I do not have many months left. I am continuing with the Fenbenzadole combined with the herbals suggested. Regards…Patrick

            1. Hi Patrick,
              It doesn’t matter what that oncologist believes, just don’t allow his beliefs to become yours. Your belief can be to become healthy again, this way your mind can work towards that goal. My father-in-law is alive 16years after he was given 6 months (glioblastoma). You are not an average of some statistic.

              All the best,


              PS. Here’s a list of supplements, you might want to consider adding some to your regimen:

              Artemisinin: 200 – 500 mg once or twice a day on an empty stomach or 2 hours after last meal, and with cod liver oil for better absorption. Intermittent dosing (4-5 days on/2-3 days off) 6 up to 24 months. Alternative: Artesunate
              Honokiol: 1-3 gr/day in 2 or 3 divided doses. Honokiol+Magnolol>95% or HonoPure
              D-limonene: 0.5-3gr/day, in divided doses.
              Ursolic acid: 0,5- 1gr/day divided in 2 doses (breakfast,dinner). Take with some coconut oil for better absorption. 4 week cycles (4 weeks On/1 or 2 weeks Off).
              Allicin: therapeutic amounts of stable Allicin in the bloodstream can be obtained by taking a supplement called Allimed.
              Citric Acid: 0.05 to 0.1g/kg/day with water and with meals (in 2 or 3 divided doses).
              IP6: 500mg – 18 g/day
              Turky Tail: Trametes or Coriolus Versicolor, 4 g twice daily.
              Panax Ginseng: 800-2000mg/day (in divided doses, morning, afternoon).
              C-phycocyanin: 0.8-1.6 gr/day in 2 or 3 divided doses or 4-8 g Spirulina/day (Spirulina is about 20% C-phycocyanin by weight.)
              Jiaogulan: 5-20mg/kg/day (1 kg =2.20462 lb) in 4 week cycles (4 weeks On/1 or 2 weeks Off). Take between meals. Rich source of dammarane-type saponins
              Modified Citrus Pectin
              Bovine Tracheal Cartilage

              One strategy is to rotate/alternate supplements. To combine various supplements add one at a time, start with the lowest possible dose and gradually increase if no side effect is observed

              Here are some things you could do with diet:

              *Foods that kill cancer stem cells (CSC): 6-Gingerol(Ginger), Epigallocatechin-3-gallate(Green Tea), Curcumin(Turmeric), β-Carotene(Carrot), Delphinidin(Berries), Baicalein(Chinese Skullcap), Isothiocyanates(Cruciferous vegetables), Linalool (Mint), Lycopene(Tomato), Parthenolide(Feverfew), Perylill alcohol( Mint, Cherry, Lavender), Ursolic acid(Thyme, basil, oregano), Withaferin A (ashwagandha), Resveratrol(Grapes, plums, berries), Silibinin(Milk Thistle), Quercetin(Capers, onion), Vitamin D3(Fish, egg yolk, cod liver oil), Piperine(Black pepper), Guggulsterone (Myrrh Gum), Flavanoids

              *Cholesterol-Lowering Foods: some cancer cells are vulnerable to cholesterol -> eat foods rich in soluble fiber: Beans, Oats, Berries (BOB). Hawthorne berries. Flax seeds. Green tea.

              *Sugar restriction: Eliminate all processed and artificial sugars. Fruits are allowed but choose fruits with strong anticancer properties.

              *Glycolysis inhibition: Turmeric, Graviola, Cardamom Spice, Ginger, Quercetin, Resveratrol, Apigenin, Citric acid

              *Reduce lactate levels: magnesium supplements (best taken with food in evening), Top 10 List of High Magnesium Foods, nettles(extract, tea), lemon juice (citric acid), Green tea (extract), Saffron, KD

              *The ketogenic diet(KD): eating a low-carb diet will cause the body to start burning fat(ketones) instead of sugar(glucose).

              *Time Restricted Eating

              *Inhibit glutamine uptake: green tea (egcg), ashwagandha, peppers

              *Increase NK cell activity: reduced lactate levels improve NK cell activity, enzymatically modified rice bran, blueberries, Brolico(this is a supplement), melatonin(as a supplement, also in foods like pistachios, lentils) Panax ginseng, cardamom & black pepper (work synergistically) Turkey Tail, Active Hexose Correlated Compound, zinc(1 hour before breakfast or before lunch), Modified citrus pectin{study}.

              *Eating enzyme-rich foods and adding an oral enzyme preparation (in between meals) to your diet plan might be very helpful at eliminating cancer cells.

              *Limit the metabolic flexibility of cancer: rhubarb (extract, tea)→Metformin enhances the effects of emodin, berberine

              As you can see it’s fairly simple to implement a combination or all strategies combined. The KD could be done intermittently, for example, a few days once a month.

        2. Hello Patrick,
          I have contacted PeterMac about their Anti-Lewis Y Chimeric Antigen Receptor-T Cells (LeY-CAR-T) in Patients With Solid Tumours (LeY-CAR-T) – is this the one you are interested in?.


          1. Hello Johan,
            Can I ask if your post to Patrick of June 14, 2019 AT 3:47 AM – is it specifically to treat glioblastoma multiforme (GBM)?
            Thank you

            1. Hi Raymond, no it isn’t specific to GBM, I’ve posted about that on another thread.

          2. Hello Westie, yes this is the trial that my oncologist is attempting to enrol me in. I have not yet had a response to indicate success in joining the trial. Here is hoping.

    2. Hi Patrick,
      Since you’re already using VitC and Green Tea you might want to consider adding lysine to that mix.
      There are studies that show the anti- mets potential of adding lysine to catechins:

      There could also be anticancer benefit of taking vitamin K in addition to vit C

      There’s a product from NZ that combines VitC, K and lysine:
      CK3 Liposomal Vitamin C
      Vitamin C in combination (at 100:1) with K3 and lysine

      Since you’re using turmeric potential synergies could be obtained from combinations with green tea, which you’re already taking, Berberine, Boswellia.


      1. Thank you for your assistance and suggestions Johan, I will certainly purchase the Vit C combo from Bushlore and add it to the daily intake. Regards…Patrick

      2. thank you for the info and assistance Johan. I have today added Boswellia extract and Bioperine to my regime. Will try and remove all refined sugar .. with a sweet tooth it will take time. Regards Patrick

  18. Daniel….I too am fascinated by this article. Background: Feb 11, 2019. Husband (56, nonsmoker) has NSCLC adenocarcinoma, mets to 1 lymph node, rib, 5 bones in pelvic area, plural effusion. Positive for EFGR and TP53. On targeted therapy Tagrisso 80mg. Have added the COC protocol since May 26th. We have scans scheduled for tomorrow (6/14). I would like your thoughts on adding Fenbendazole to his protocol. We feel that the Mebendazole is not enough. Question: To your knowledge with adding Fenbendazole to the COC protocol and the Tagrisso, would there be any concerns to worry about…..liver?, kidneys?, anything else? If we did add it, what would your recommendation be with dosage…how much, how often? In your opinion, would you add the rest of Joe’s protocol with the COC protocol and Tagrisso? I am FOCUSED on keeping my husband alive and well. My mother was diagnosed with NSCLC two days after my husband, stage 1. She had surgery for removal of 20 percent of lung. Developed complications after surgery and passed away……if I only knew one month ago what I know now, she could have still been with us. Please know how much people like us appreciate your willingness to share your information!!! Bless You!

    1. Dear Crystal,

      thank you so much for your kind words. I am glad that you find the information shared here useful.

      Indeed using Fenbendazole for NSCLC may be a very good idea. Here is a very recent paper (June 2019) by National Cancer Center Research Institute from Japan stating the same:
      Drug Library Screen Reveals Benzimidazole Derivatives as Selective Cytotoxic Agents for KRAS-Mutant Lung Cancer

      Answering your questions:
      – I do not expect major toxicity from Fenbendazole – the Statin included in the COC protocol has a higher (liver) toxicity. I do not expect any major interaction between Fenbendazole and those you mentioned. However, whenever you introduce a new drug, always start with a lower dose and move to the target dose in a few to several steps. For example, if the target dose is 1g, I would start with 250mg and next day move to 500mg, followed by 750mg and finally 1g, if no special reaction is observed.
      – Regarding the dose and admin strategy, I would use the same as Joe, i.e. 1g granules (containing 222mg Fenbendazole) each day, 3 days ON and 4 days OFF (please see the details in the article above and if you still have questions please let me know). The three additional supplements used by Joe are easy to access and cheap and taken in low dose, so I would add them.

      I am so sorry to hear about your dear mom and now the challenges with your dear husband. I very much hope that the treatment approach you are implementing will help and push the tumors away. Whenever you come across other relevant treatments/info please share them on this website so that we could help others as well. Blesses to you too!

      Kind regards,

  19. Hallo Daniel.
    Ja, die Tace bezahlt meine deutsche Versicherung. Ich hatte vorgestern die 18 Tace bei Prof Vogl. Es geht mir aber gut.
    Meine Biopsie sagte das ich keine p53 gene habe sondern im Übermaß cd34.
    Macht es dann überhaupt Sinn wenn ich das fenben protocol nehme? Oder wäre mebendazol das bessere Medikament. Fenben soll ja p53 stark hemmen.
    Vielen dank lieber Daniel.
    Grüße, Andre

  20. Sorry To bother you. My name is Weber I live in Rio de Janeiro, Brazil. I am a carrier of prostate cancer with bone metastasis. My bone metastasis is very advanced, I want to know if fenbendazole can help me to stop the advanced of bone metastasis. Can I use the oral solution? Do you know other person, besides Joe, who succeeded using fenbendazole?

    1. Dear Weber,

      I am so sorry to hear about your challenges. I hope you will be better soon.

      Fenbendazole could be a relevant option that is easy to access and implement. In addition to that you may want to have a look at the following:

      1. Drugs and Supplements relevant to prostate cancer:
      Here you will find a list of supplements that are very relevant to prostate cancer.

      2. Post on Zinc as a cancer treatment relevant to Prostate cancer https://www.cancertreatmentsresearch.com/unlocking-zincs-potential-to-fight-cancer/ – this needs to be combined with Quercetin in order to be effective – Quercetin is an extract from onion that can be found as supplement online and is taken between 1g and 3g/day

      3. If you have a doctor willing to help you with giving 2DG metronomic, with or without chemo, please let me know and I will connect your doctor with the academic team in US to support him with info on that https://www.cancertreatmentsresearch.com/a-new-approach-to-improve-effectiveness-of-cancer-therapies-is-getting-ready-to-begin-human-trials/

      4. As shown by Don https://www.cancertreatmentsresearch.com/a-visitor-story-healing-from-stage-4-prostate-cancer-with-fasting-and-juicing/ diet is very relevant in cancer, specifically for prostate cancer. In this case, next o avoiding sugar, I would specifically avoid fats (cholesterol is the basis for hormones), and red meat (as it contains higher amounts of glutamine which is highly relevant for prostate cancer cells).

      5. Supplements that are very relevant for Prostate cancer are Prostasol and Nutrition 2000 – both are acting as ADT (some of the people with whom I am in contact used them and saw positive results)

      6. Basentabs supplements found at online shops in Europe are also very good against prostate cancer.

      7. Another approach that may help for prostate cancer is discussed here https://www.cancertreatmentsresearch.com/reduce-cholesterol-in-cancer-cells-to-fight-cancer/

      8. Some years ago I was in contact with a cancer scientist and prostate cancer patient who was managing his PSA with 3BP (he was taking it orally mixed in water as discussed here https://www.cancertreatmentsresearch.com/3-bromopyruvate/). He also stated that he had good results with DCA https://www.cancertreatmentsresearch.com/dichloroacetate-dca-treatment-strategy/

      9. ALA+HCA may be also a relevant strategy for prostate cancer https://www.cancertreatmentsresearch.com/another-weak-spot-of-many-cancer-cells-atp-citrate-lyase-inhibition/

      I hope this helps. If you have questions, please let me know.

      Kind regards,

  21. Hello Daniel,

    Some worrying finding on Mebendazole (MBZ) and Fenbendazole (FBZ) – which seems to increase IL-8 expression significantly.

    IL-8 is an important proangiogentic factor when it comes to formation of liver mets from various cancers.

    The reason for my interest is my friend have had growth of liver mets (new) after start of FBZ and MBZ.
    Also my friend started Clindamycin which can be a problem too in regards of angiogenesis.

    Kindly let me know your thoughts.

    Thank you

    1. Dear Raymond,

      Thank you so much for your good question. I read the article you shared here and other related references and at this point my opinion is the following:

      1. While on Fenbendazole there is not enough info to make a detailed statement, benzimidazoles such as Mebendazole are known to induce liver toxicity but that is rare and when that happens it takes place in a higher dose range and for longer term usage. Examples that are discussed in the article you cited are:
      – “Bekhti and Pirotte (1987) described a case of acute hepatocellular injury in a patient treated with MBZ 600 mg/day for echinococcosis.”
      – “Seitz et al. (1983) and Junge and Mohr (1983) reported MBZ-induced hepatic injury, and the liver biopsy of the patient revealed hepatocytic necrosis and portal inflammation with eosinophils during long-term (49–60 days) and high-dose (2–3.5 g/day) therapy with MBZ.”

      2. When this rare event is induced, the paper you cited suggests it may be due to a release of IL-8 and TNFa triggered by benzimidazoles. I agree that even if inflammatory events at the liver happen only in rare cases and at high doses, we should be aware of that, specifically when dealing with liver mets.

      3. While I would keep in mind the above, regarding the possible release of IL-8, for most of the patients and at a normal dose I would not be worried of possible pro-angiogenesis effects induced by benzimidazoles. There is actually literature suggesting they have anti angiogenesis action https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096024/ Of course this is theory, but beyond theory we have a case report published in the literature, where Mebendazole showed strong anti cancer action. That was in a patient with a large and highly active adrenal cancer which is known to depend strongly on angiogenesis. And Mebendazole alone succeeded to stop the tumour growth and even reduce that.
      In addition, this more recent article on benzimidazoles (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5881671/) reports some results that are contradictory to the results from the article you cited.
      Here are a few more articles addressing the immune modulation mechanism by Mebendazole:

      In conclusion, I think it’s a good idea for the cancer patients with liver mets to be extra careful when using benzimidazoles. Nevertheless, please note that there is a report on a cancer patient with liver mets experiencing partial remission of the liver mets while on Mbendazole https://www.cancertreatmentsresearch.com/the-over-the-counter-drug-mebendazole-acts-like-chemotherapy-but-with-virtually-no-side-effects/#comment-4142

      Kind regards,

  22. Dear Daniel,

    In my recent FoundationOne test, the Genomic Findings for NSCLC Stage IV are:-

    #MET exon 14 splice site (2888-18_2888-7del12)
    #MDM2 amplification
    #MLH1 Q537
    #TP53 E285K

    I am currently on the 2nd line TKI: Capmatinib (INC280) to treat MET exon 14. I had progression on the 1st line TKI: Cabozantinib, hence TP53 pop up as a new finding (in resistance).

    Do you know of any inhibitors that can be used to target MDM2 amplification, MLH1 Q537, TP53 E285K ?

    Thank you sincerely for your help.

    1. Dear Raymond,

      Expressions like these will be up and down as a function of time and cell population. This is why I prefer to consider treatment angles that are more constant, and this is why I often discuss the metabolic angle. However, answering your question on MDM2, here is a list of references indicating several FDA approved drugs that may be relevant, including those like Mebendazole/Fenbendazole:

      – MBZ appears to be effective through p53-dependent and independent pathways. For example, in lung cancer cell lines, it was found that MBZ treatment caused post-translational p53 stabilization and the downstream expression of p21 and MDM2 http://ecancer.org/journal/8/full/443-repurposing-drugs-in-oncology-redo-mebendazole-as-an-anti-cancer-agent.php

      – Identification of FDA-approved drugs that computationally bind to MDM2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3448857/

      – Benzimidazoles Downregulate Mdm2 and MdmX and Activate p53 in MdmX Overexpressing Tumor Cells https://www.mdpi.com/1420-3049/24/11/2152/pdf-vor

      – Nitroxoline induces cell apoptosis by inducing MDM2 degradation in small‐cell lung cancer https://onlinelibrary.wiley.com/doi/full/10.1002/kjm2.12051

      Kind regards,

      1. Dear Daniel,

        Thank you sincerely for your most valuable feedback – it is most valued and appreciated.
        I will study them and discuss with the doctor and see what he says.

        As always, with gratitude,

      2. @Daniel: Nitroxoline is unlikely to be effective (at least alone) against NCSLC, since it has a short half-life in blood, and concentrates in urine. My experience with it (7 years ago) is that the common dose of 600 – 800 mg / day is tolerable, but gives a bit of liver damage, which is manageable. I believe a half dose (300 – 400 mg / day) should be well tolerated long term, and usable as part of an anti-angiogenic regimen.

  23. Hi Daniel

    We purchase Panacur from an ag store for our horses, which is a paste. However, I did a search tonight on duckduckgo.com and am finding that there are several sites which carry the canine wormer. Just a thot for those who are having probs getting a hold of the product.

    Any chance the paste could be used as well? Also, if someone is using multiple modalities, will the Panacur C continue to work as stated, or will there be a conflict between the various modalities?

    Thanks for your time, in advance.


    1. Hi BlueLinen,

      Thank you for your question and sharing the info.

      As long as the same amount of active ingredient is used (in this case Fenbendazole) It should not matter what product is used. However, it may be some difference of bioavailability in humans depending on whether it is a solution, paste or any other type. Since these products are made for animal use, we do not have references on the use in humans and their bioavailability depending on product type. This is why, if possible, I would stick with the approach/type/brand used by Joe and described above, as it seems that worked for some. Regardless of the band, I would also try to add some fats in order to increase the chance for absorption (this type of drugs is not so well absorbed as also discussed in the post on Mebendazole).

      Kind regards,

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