Index for Fenbendazole

Index for Fenbendazole

References after the book:

Above header image: Left Image Before fenbendazole treatment showing large mass left kidney with extension into renal vein (red arrows). Right image after 5 months of fenbendazole mass has resolved (green arrow) . Courtesy of: Chiang, R. S., et al. “Fenbendazole enhancing anti-tumor effect: a case series.” Clin. Oncol. Case Rep 4 (2021): 2-5.

Renal Cell Carcinoma Successful Treatment with Fenbendazole
Chiang, R. S., et al. “Fenbendazole enhancing anti-tumor effect: a case series.” Clin. Oncol. Case Rep 4 (2021): 2-5.

The following Renal Cell Carcinoma Case Report comes from a 63 yr old man with metastatic kidney cancer, that spread to his pancreas, lungs, inferior vena cava, and bone. He tried immunotherapy but it was unsuccessful and it also was not tolerated well. Given six months to live, he learned about fenbendazole. He took 222 mg for 3 consecutive days followed by 4 days off. Within 2 months of taking fenbendazole, the largest mass in the kidney was gone and the other tumors shrank considerably. By 5 months, all the tumors were gone. This Case Report was also written up in a medical journal providing more much detail. This case report is from a substack entitled: “Fenbendazole Can Cure Cancer”. This case report was also published in a medical journal as a case report (see below in comments)…

Kang, Kyung-Sun, and Da-Hyun Kim. “Fenbendazole induces cell cycle arrest in colorectal cancer cells and patient-derived colon cancer organoids.” Cancer Research 82.12_Supplement (2022): 2313-2313.

Colorectal cancer is one of leading cause of cancer-related deaths. Therefore, there have been various attempts to cure the cancer by developing new efficient anti-cancer therapy in addition to surgical resection and chemotherapy. In this study, we investigated the effects of fenbendazole, an anti-helminthic drug, both colon cancer cells and patient-derived colon tumor organoids. Notably, we employed 3D tumor organoid models because 2D-cultured cell lines were not able to recapitulate the physiology of solid tumors. We first observed that treatment of fenbendazole to colon cancer cells induced apoptosis within 24 hours, which was extended for a long-term. We revealed that fenbendazole markedly suppressed proliferation rate via cell cycle arrest. Cell cycle progression is elaborately regulated by multiple genes, such as cyclins and cyclin-dependent kinases (CDKs). From a screening of cell cycle-related factors, we found that the protein levels of CDK1 phosphorylated at Tyr15 and cyclin B1 which was known to regulate M phase transition, were drastically downregulated when the tumor cells were exposed to fenbendazole. Next, colorectal tumor-bearing mouse model was established using AOM/DSS. Oral administration of fenbendazole into the mouse not only reduced the number of tumor cells but also lowered tumor grades. Overall, our study suggested a possibility that fenbendazole could be applied for anti-cancer therapy by targeting cell cycle arrest…

Fenbendazole Index for the Book:

p. 13
Joe Tippens’s Fenbendazole Story: Joe
Tippens was diagnosed with non-smallcell
lung cancer with extensive metastatic
disease and sent home to hospice with
a projected three months to live. An old
friend, a veterinarian, suggested he take a
dog de-wormer drug called Fenbendazole.
Three months after starting the drug, his
PET scan, done at MD Anderson Cancer
Center in Houston was completely clear
of cancer. I had the pleasure of meeting
and briefly chatting with Joe at the Annie
Appleseed meeting February 2020. Joe
Tippens has a large Facebook group where
thousands of cancer patients share stories.

Synergy Combination of DCA and Fenbendazole
The anti-cancer activity of the antiparasitic
drug fenbendazole (FZ) was found to be
“strongly synergistic” with DCA. FZ increased
P53 protein, which translocated to the mitochondria,
resulting in a mitochondrial celldeath
pathway. FZ inhibited glucose uptake,
reduced lactate levels, and reduced HK2 activity.
Dr. Nilambra Dogera et al. write (2018) :

We evaluated the effect of FZ in combination
with the microtubule targeting drug
taxol, glycolytic inhibitor 2 deoxyglucose
[2DG] and dichloroacetate [DCA] – a pyruvate
dehydrogenase kinase inhibitor which
acts by shifting the metabolism towards
glucose oxidation over glycolysis…. there
was a strong synergism by FZ and DCA.

96) Dogra, Nilambra, Ashok Kumar, and Tapas
Mukhopadhyay. “Fenbendazole acts as a moderate
microtubule destabilizing agent and causes cancer
cell death by modulating multiple cellular pathways.”
Scientific reports 8.1 (2018): 1-15.


p 252
Synergy of Chloroquine with Mebendazole

In 2019, Dr. So Jung Sung et al. reported that
the autophagy inhibitor chloroquine synergizes
with mebendazole, dramatically augmenting
anti-cancer efficacy. (93)
One might expect similar synergy with
fenbendazole, another microtubule inhibitor
structurally similar to mebendazole in the
“azole” drug family. Fenbendazole is a veterinary
antiparasitic drug that has been repurposed
as an anti-cancer drug. (94)

p. 252
The Joe Tippens Story

The Joe Tippens story has created considerable
interest in fenbendazole as an anti-cancer
agent. I had the pleasure of meeting Joe
Tippens at the 2020 Annie Appleseed meeting
in West Palm Beach, Florida. Joe Tippens
grew up on a ranch in western Oklahoma,
and was a healthy, successful venture capitalist
until 2016, when he was diagnosed with a
left-lower lobe asymptomatic lung mass that
proved to be small-cell lung cancer with spread
to mediastinal nodes. In September 2016, Joe
underwent chemotherapy and left lung radiotherapy
at MD Anderson Cancer Center. By
December 2016, the left lung mass was gone,
yet the cancer was now disseminated widely
with metastatic disease. His doctors offered
him a clinical trial of Keytruda® (an immune
checkpoint inhibitor) and sent him home, with
the understanding of a poor prognosis and a
three-month life expectancy. Upon returning
home, Joe received a telephone call from an old
friend, a large-animal veterinarian in western
Oklahoma, who told Joe about fenbendazole, a
canine dewormer, and suggested he had nothing
to lose and should try it. In January of 2017,
Joe started the fenbendazole (222 grams per
day 3 days a week), which was available online
without a prescription at a number of pet medicine
online shops. Joe added curcumin (600
mg/day), tocotrienol and tocopheral vitamin
E (800mg/day) and “broad spectrum” CBD oil
(1–2 droppers/day). In May of 2017, a repeat
PET scan was completely clean, showing “no
evidence of disease.”

Joe writes that when his MD Anderson doctor
saw the PET scan, the doctor scratched his
head and replied:
We don’t quite know what to make of this
as you are the only patient in the clinical
trial with this kind of response. [Read the
Joe Tippens story at www.mycancerstoryrocks.



p 298
Some anti-cancer drugs (such as fenbendazole) depend on
a functioning P53.

p 314
Chapter 24 Mebendazole and Fenbendazole

p. 317
Fenbendazole Microtubule Agent
and Glycolysis Inhibitor
The benzimidazole drug family includes
mebendazole, albendazole, flubendazole and
fenbendazole, all antiparasitic drugs of similar
structure. All use microtubule inhibition as the
main mechanism of action. A number of very
effective chemotherapy drugs (taxanes and
vinca alkaloids) also target the microtubule
system of the cancer cell. Disrupting microtubule
activity blocks the spindle formation
needed for cell division and blocks cell division
in metaphase (a phase in mitosis), causing cell
death (apoptosis).

p 318

Fenbendazole is effective at low micromolar
concentrations and is remarkably safe for animals
and humans, resulting in relatively mild
changes in the microtubule structure of cancer

In 2018, Dr. Nilambra Dogra et al. studied
the effects of fenbendazole (FZ) on a NSCLC
(non-small-cell lung cancer) cell line in vitro
and in vivo mouse xenografts and make this
favorable conclusion:
FZ [Fenbendazole] … is a safe and inexpensive
anthelmintic drug possessing an
efficient antiproliferative activity…. potent
growth-inhibitory activity…. moderate
affinity for mammalian tubulin and exerts
cytotoxicity to human cancer cells at micromolar
concentrations. Simultaneously, it
caused mitochondrial translocation of p53
and effectively inhibited glucose uptake,
mRNA expression of GLUT transporters
as well as HK2 [hexokinase 2]—a key
glycolytic enzyme that most cancer cells
thrive on. It blocked the growth of human
xenografts in nu/nu mice model when mice
were fed with the drug orally…. potential
therapeutic agent because of its effect
on multiple cellular pathways leading to
effective elimination of cancer cells. (48)
Treatment of the NSCLC lung cancer cells
with 1.0 micromolar FZ for 24 hours resulted in:
partial alteration of the microtubule network
… the microtubule cage around the
nucleus appeared to have lost its intactness
when compared with control cells
… relatively mild tubulin depolymerizing
activity of FZ as compared to other known
microtubule-disrupting agents like nocodazole
and colchicine… (48)

p 318
Fenbendazole GLYCOLYSIS Inhibitor
FZ mimics the structure of glucose and
decreases glucose consumption by binding to
the enzymatic pocket of HK2, thus impairing
the function of hexokinase 2 (HK2). FZ shows
augmented anti-cancer effects in combination
with GLYCOLYSIS inhibitors DCA (dichloroacetate),
and 2DG (2-deoxyglucose). There was
“strong synergism by FZ and DCA.” See the
chapter 5 on DCA for more on this. Dr. Dogra
et al. studied oral dosing of fenbendazole to
mice bearing lung cancer xenografts over 12
days finding “marked reduction in tumor size
and weight” as well as reduced tumor vascularity.

p 318
Increased P53 in Nucleus and
Mitochondrial Fraction
In addition to its microtubule binding and
disruption activities, FZ has a unique ability to
induce p53 to a considerably high level, with
increased nuclear accumulation and increased
P53 protein in the mitochondrial fraction, targeting
the VDAC, resulting in activation of
apoptosis, mitochondrial cell death pathways.



p 218
Screening for Compounds that
Promote P53 Activity
In cancer cell types with a functioning (wildtype)
P53 gene, promoting that function is a
worthy anti-cancer activity. In 2019, Dr. Zuzana
Mrkvová et al. performed a high-throughput
screen of 2448 compounds on melanoma cells
with functional (wild-type) P53 gene looking
for compounds that promote P53 activity.
Fenbendazole and albendazole were the best
candidates, not only increasing P53-P21 pathway,
but also decreasing the MDM2 and MDMx
suppressor pathway. (60)
Note: Mdm2 and MdmX are negative regulators
of P53, so suppressing them with Fenbendazole
restores P53 function.

p 319
Niclosamide Effective
Regardless of P53 Status
P53 protein translocation to the mitochondria
is part of the mechanism of cell death for
fenbendazole (FZ). One should ask the following
question: Does the cancer cell type in question
have a functioning P53 gene (wild-type) or
a mutant P53? If we are dealing with a mutant
P53, since FZ relies on P53 accumulation in the
mitochondria to induce apoptosis, this mode
of action may not be effective. If the cancer is
not responding to the fenbendazole, then one
might consider alternate drugs that maintain
effect regardless of P53 status. For example,
Niclosamide induces apoptosis via mitochondrial
ETC (electron transport chain) uncoupling
and is effective in P53 mutated cancer
cell types, regardless of P53 status.

p 320
Fenbendazole for Human
Lymphoma Xenografts
In 2008, Dr. Ping Gao et al. studied the effect
of fenbendazole in human lymphoma mouse
xenografts, finding an “unexpected anti-tumorigenic
effect.” (61)

p. 322
29) Lai, Serene Ruth, et al. “In vitro anti‐tubulin effects
of mebendazole and fenbendazole on canine glioma
cells.” Veterinary and comparative oncology 15.4
(2017): 1445-1454.


48) Dogra, Nilambra, Ashok Kumar, and Tapas
Mukhopadhyay. “Fenbendazole acts as a moderate
microtubule destabilizing agent and causes cancer
cell death by modulating multiple cellular pathways.”
Scientific reports 8.1 (2018): 11926

61) Gao, Ping, Chi V. Dang, and Julie Watson.
“Unexpected antitumorigenic effect of fenbendazole
when combined with supplementary vitamins.”
Journal of the American Association for Laboratory
Animal Science 47.6 (2008): 37-40.

63) Duan, Qiwen, Yanfeng Liu, and Sara Rockwell.
“Fenbendazole as a potential anticancer drug.”
Anticancer research 33.2 (2013): 355-362.

64) Aycock-Williams, Ari N., et al. “Effects of fenbendazole
and vitamin E succinate on the growth and survival
of prostate cancer cells.” J Cancer Res Exp Oncol
3.9 (2011): 115-121.

65) Lai, Serene Ruth, et al. “In vitro anti‐tubulin effects
of mebendazole and fenbendazole on canine glioma
cells.” Veterinary and comparative oncology 15.4
(2017): 1445-1454

p 336
Blocking PIBF with Microtubule
Inhibitor Mebendazole
As luck would have it, elimination of PIBF
may be accomplished with another drug that
is widely available, a microtubule-disrupting
agent such as nocodazole, an imidazole
similar to mebendazole and fenbendazole

p 478
Once might speculate on taxane synergy
with other FASN inhibitors, such as orlistat,
fenofibrate and quercetin. (99)
One might also speculate on synergy of fenofibrate
with microtubule-disrupting agents,
mebendazole, and fenbendazole
















Published on by Jeffrey Dach MD

About Jeffrey Dach MD

Medical Director of TrueMedMD, a Clinic in Davie Florida specializing in Bioidentical Hormones and Natural thyroid. Office address 7450 Griffin Road Suite 190, Davie, Florida 33314 telephone 954-792-4663