Fenbendazole: A Promising Cure for Cancer Part 2. Examining Case Reports Published by Stanford
Stanford reports on a patient who tried 4 chemo drugs, all with intolerable side effects, and the cancer continued to spread. He took fenben; cancer disappeared.
For Part 1, see this post:
The story from last week was a lot to take in, and I don’t blame anyone for being skeptical. So today I want to highlight a case report published by Stanford University titled Fenbendazole Enhancing Anti-Tumor Effect: A Case Series (linked) published in the journal Clinical Oncology Feb 10, 2021.
This case report documented three cancer patients who took FenBen.
Although I linked to this case report last week, I understand that the average person may not be equipped to weed through the technical language in scientific studies. This was a skill I had to learn slowly while working as a website writer for a venture capital medical device firm for several years—it was quite the learning curve but now I’m thankful for all the hard work I put in.
I hope that after we walk through this study, you will have a little more confidence to investigate claims for yourself instead of being at the mercy of one expert. I encourage you to open the link to the study above and follow along as we examine the claims.
Let’s examine Case 1 and then we’ll go more in-depth about what the Stanford study concluded:
Case 1: 63-year-old caucasian male
A CT scan revealed this patient had a 3 cm Renal Cell Carcinoma (RCC) on his left kidney which was surgically removed. Several months later, he had a new 5.2 cm RCC mass on his left kidney. He began treatment with 800 mg of pazopanib (chemo drug).
A follow-up CT scan showed the cancer had spread: he now had two pancreatic lesions: 1.4 cm and 2.9 cm. The side effects of pazopanib were intolerable including colitis so the patient stopped pazopanib and began cabozantinib.
The Next MRI showed the three previous masses were stable but the patient showed a new 1.1 cm iliac bone lesion.
The patient discontinued the cancer drug cabozantinib due to intolerable side effects.
One month after discontinuation, MRI showed an increase in the size of the left kidney turmor, mild decrease in 2.3 cm pancreatic head lesion, other two lesions were stable.
The patient began the third line of treatment: nivolumab.
Patient received only three total treatments of nivolumab over the course of a month due to developing severe rash and colitis. Colitis was treated with steroids. Patient discontinued nivolumab.
Patient began taking FenBen 1 gram three times per week the same month starting nivolumab at the suggestion of a friend with neck cancer.
Researchers at Stanford found after the patient took FenBen for several months (exact time not given):
Interval MRI imaging found near complete resolution of the previously noted left renal mass as well as decrease in pancreatic head/body and right posterior iliac spine lesions. Serial imaging for the past 10 months have not shown any evidence of recurrence or metastatic disease. He has continued taking FBZ without any reported side effects.
From the Discussion:
Given the complete radiologic response on only 1 month of immune checkpoint inhibitor therapy, it also seems likely that FBZ played a notable role in inducing remission. This is supported by the fact that our patient has remained in extended remission while only on FBZ for nearly a year without further administration of immune checkpoint inhibitor therapy.
Now, let’s take a look at what the researchers say about why FenBen was effective:
Let’s start with the most relevant part of the study first: its conclusion as summarized in the abstract.
FBZ [fenbendazole] appears to be a potentially safe and effective antineoplastic [antimicrobial chemotherapy] agent that can be repurposed for human use in treating genitourinary malignancies.
This conclusion is important. There are numerous anecdotal stories on the internet of how people cured cancer in nonconventional ways. And although I don’t necessarily doubt the validity of them, it’s unknown how well such cures transfer to other people’s unique cancers.
However, FenBen is different from random internet cures because of the well-documented scientific literature demonstrating that it works, at least in some cases.
Observe the first sentence under the Discussion heading:
In summary, we have three patients with different primary genitourinary [genital] tumors who demonstrated complete response after receiving FBZ therapy.
Now the technical language begins but hang with me because we’re going to work through this together. From the Discussion heading:
FBZ belongs to a class of microtubule-destabilizing agents known collectively as the benzimidazoles. The ability to disrupt microtubule polymerization to induce mitotic [cell division] arrest and promote apoptosis [cell death] is a feature shared with the vinca alkaloids [another class of chemo drugs].
Part of the reason that these studies are difficult to understand is that the writers are assuming that the audience has knowledge that the common person does not have. So here’s some background that will help you understand why Fenbendazole, a type of benzimidazole, works on cancer.
The class of cancer-fighting drugs called benzimidazoles (pronounced ben-zih-MID-a-zuls, or BZ), to which FenBen belongs, works by destabilizing a key component of the cell skeleton called the microtubule. For proper cell division, the microtubule must work correctly. If it is unstable, the cell will die when it attempts to divide. Cancer cells divide very quickly so destabilizing the microtubule can be devastating to cancer.
The dilemma with any cancer treatment is targeting the cancer cells while minimizing the disruption to normal cells. Both cancer cells and normal cells (in fact all eukaryotic, meaning non-bacterial cells) have microtubules. So wouldn’t BZs harm all the cells? Not at the same rate. Since cancer cells divide much more rapidly than normal cells, when they attempt to divide, the compromised microtubules cause cell death. Unfortunately, BZs can have negative effects on healthy cells that divide rapidly, such as hair follicles.
Let’s examine the next sentence:
Proposed mechanisms for FBZ’s anti-tumor properties include inhibition of proteasomal activity, p53 activation, cytotoxicity via tubulin disruption, and downregulation of glycolytic enzymes crucial for cancer cell survival.
What does “the inhibition of proteasomal activity” mean?
A proteasome is a protein complex inside a cell that is responsible for removing damaged proteins and recycling them.
When the proteasome activity is inhibited, the cell will fill up with damaged and misfolded proteins, eventually leading to cell death. (By the way, studies have shown that fasting increases proteasomal activity in normal cells. See my post on autophagy.)
FenBen delivers “differential sensitivity.” This means that because cancer cells are much more metabolically active than normal cells, they require much higher rates of protein turnover for growth and division. This makes them significantly more sensitive to proteasome inhibition than a healthy cell. Therefore, the inhibition of proteasomal activity can wreak havoc on a cancer cell while doing only minimal damage to normal cells. (As a side note, if you intermittently fast while taking FenBen, this makes your normal cells more resilient to proteasomal inhibitors because of increased autophagy. Furthermore, since cancer cells hog enormous amounts of glucose, they can potentially starve or have greatly slowed growth when little glucose is available during the fast. "The vulnerability of cancer cells to nutrient deprivation and their dependency on specific metabolites are emerging hallmarks of cancer. Fasting or fasting-mimicking diets (FMDs) lead to wide alterations in growth factors and in metabolite levels, generating environments that can reduce the capability of cancer cells to adapt and survive and thus improving the effects of cancer therapies." From a study published in the journal Cancer titled "Fasting and Cancer.")
What is P53 activation?
P53 is the name of a cancer-fighting gene that is often mutated in people with cancer. FenBen appears to signal mutant P53 to act like wild type (non-mutated) P53. This is important because, "The ability of p53 to induce apoptosis [cell death] in cancer cells is believed essential for cancer therapy."
What is cytotoxicity via tubulin disruption?
This statement is digging a little deeper into the original statement that FenBen disrupts the microtubules necessary for cell division. Here, the researchers are pointing out that the tubulins within the microtubules are the exact object that FenBen attacks, and this disruption causes the cancer cell to die when it attempts to divide.
What is the downregulation of glycolytic enzymes?
Glycolysis simply means using glucose (sugar) for fuel. Glycolysis is a main metabolic pathway that provides a source of energy and building blocks for cancer cell growth and proliferation.
There are various enzymes that are necessary for glycolysis to occur. FenBen downregulates or inactivates those enzymes making the cancer unable to process glucose for fuel.
Note: the article published in the journal Nature titled “Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways” outlines the same pathways as the Stanford study.
By way of reminder, Nature is possibly the world’s most prestigious scientific journal. If you still have doubts about FenBen, please click on the article above and read it.
Here’s the last sentence of the discussion from the Stanford case studies:
Altogether, our findings show microtubule disruption, p53 stabilization, and interference with glucose metabolism as collective underlying mechanisms of FZ induced preferential elimination of cancer cells both in vitro [in a petri dish] and in vivo [in a living organism].
Putting It All Together
The challenge that any chemo drug faces is that cancer has an incredible ability to adapt to whatever you throw at it. There are dozens of cancer drugs that perform similar functions to those four cancer-fighting pathways outlined above, but to be effective, they need to do all four at once. If a cancer drug’s main function is to downregulate the enzymes used in glycolysis, then the cancer will often quickly adapt and find a different way to utilize glucose for energy. However, it’s much more difficult for cancer to adapt to four different pathways attacking it at once. Another consideration is how well the drug targets the cancer cell without disrupting the normal cells; in other words, how well differentiated its functions are. The better they target cancer cells, the fewer side effects.
Many people are surely thinking: why am I spreading the news about this FenBen story when our country spends $500 billion/year on cancer research? Surely all that money means that the standard cancer clinics have access to the very best cures and technologies ever available to mankind. Think of all the scientists in all the labs and all the money for research they have. Why talk about a dog dewormer? It’s just silly.
I have only one reason: because when you go and read the FenBen testimonials, the majority of them are from people who first tried traditional chemo and it didn’t work. They were told to call hospice. FenBen was their last resort. Furthermore, I have yet to read about any side effects of FenBen. Remember the Stanford study says: “No side effects from FBZ were reported.”
I did this little thought experiment in my head that went like this: what if FenBen had some potentially negative side effects? Then, if I spread the news, I would risk not only seeming like a nutcase to some people but actually hurting some people. What if FenBen, had say, one-tenth the side effects of common chemo treatments? Instead, it’s the chemo treatments that have all the side effects. FenBen appears to have few.
Unfortunately, the cost to get a new drug FDA-approved can be up to $2.8 billion, so the company footing the bill needs the profits of the sale to offset this cost. Since FenBen is long off patent, it costs only $15/tube. But perhaps a philanthropist could foot the bill for FDA approval? After he saves the Blue Bird, maybe Elon can throw his money at something even more helpful.
For those with doubts about FenBen’s effectiveness after reading this, I encourage you to contact the corresponding author of the Stanford case report directly, Ryan S. Chang, from the Department of Medicine at Stanford University Medical Center at sandrysri@stanford.edu.
