Fenbendazol - Educational materials

Effects of fenbendazol

Fenbendazol, chemically recognized as [5-(phenylthio)-1H-benzimidazol-2-yl] methyl carbamate, belongs to the benzimidazole class of drugs [1]. It is commonly used to treat a wide range of parasitic infections in animals, from pets to livestock. Originally developed in the 1970s by Janssen Pharmaceutica, it was designed to eliminate internal parasites in animals, such as roundworms and tapeworms. However, studies, from the 1970s onward, have shown its efficacy against other gastrointestinal parasites, including giardia and other helminths, including pinworms, strongyles, Strongyloides, aelurostrongylus and paragonimosis.

Although it was originally intended to protect animals from parasites, recent studies have shown its potential benefits for humans, especially in the fight against serious conditions such as cancer [1, 1A]. The fenbendazol story changed significantly in 2011, when a person, struggling with serious health problems, took fenbendazol, hoping for relief. The improvement in his condition aroused curiosity and led to a deeper investigation into the potential of fenbendazol for human health. This incident, followed by the establishment of an online community and the sharing of success stories, promoted fenbendazol as a potential unconventional treatment for a wide range of diseases beyond its original purpose.

Commonly referred to as "Fenben" in these communities, fenbendazol has gained tremendous attention for its possible uses in treating conditions such as cancer, autoimmune diseases and neurological disorders. Despite the lack of formal human clinical trials, anecdotal evidence suggests that fenbendazol may offer hope to those seeking alternative treatments. Fenbendazol's potential mechanisms of action involve attacking the cellular structure of parasites and interfering with their ability to survive and reproduce. These mechanisms, while originally effective against parasites in animals, are now being investigated for their implications in treating human diseases, particularly against cancer cells [1-4].

Although fenbendazol is currently approved only for veterinary use, the significant diverse effects observed in both laboratory and animal studies indicate the need for additional research. Studies suggest that in addition to its antiparasitic effects, fenbendazol may affect microtubule dynamics, indicating a new strategy for treating cancer and other diseases [1-4]. Its minimal systemic absorption and selective action on parasite tubulin, compared to mammalian cells, underscore its therapeutic potential and likely safe profile. Therefore, ongoing research has the potential to transform fenbendazol from a veterinary deworming agent to a valuable agent in human health care.

Fenbendazol against cancer

Fenbendazol is mainly used to treat worm infections in animals, but recent research suggests it can also help fight cancer. Traditionally targeted at eliminating worm infections, surprising research shows that fenbendazol can also stop the growth of cancer cells. Fenbendazol attacks cancer through a variety of pathways, disrupting key processes that cancer cells need to grow and survive.

Human studies on the use of fenbendazol against cancer

A study in South Korea examined the anti-cancer potential of fenbendazol among cancer patients [2]. Many cancer patients, especially those in advanced stages of the disease, have begun to turn to fenbendazol and other antiparasitic agents as an alternative treatment. Remarkably, a significant majority, some 79.1%, reported experiencing physical improvement after using antiparasitic agents, including fenbendazol, against various types of cancer. Although the study focused mainly on patients' experiences, it additionally reported that antiparasitic agents work against cancer by disrupting the life cycle of cancer cells by interfering with microtubule formation, similar to the action against parasites, but with a caveat - targeting key cancer pathways, such as the p53 pathway, to induce cancer cell death. The study included a variety of self-administered dosing regimens, with many following a schedule of taking the drug for consecutive days and then taking a break. The study reported minimal side effects associated with antiparasitic agents, including fenbendazol. However, some patients experienced gastrointestinal problems, liver abnormalities and blood-related side effects, highlighting the importance of medical supervision when using fenbendazol as a treatment for cancer [2]. This study not only reveals the potential of antiparasitic agents, including fenbendazol, as a new cancer treatment, but also highlights the broader possibility of drug repurposing in oncology. The encouraging results reported by patients in South Korea provide a basis for further scientific research into the role of fenbendazol in oncology care.

Animal and laboratory studies on the use of fenbendazol against cancer

In 2018, researchers Dogra, Kumar and Mukhopadhyay found that fenbendazol disrupts the structural integrity of cancer cells and the waste processing system [1]. It also affects the way these cells consume glucose for energy by transferring a protein called p53, which is important because p53 plays a key role in controlling cell death. Fenbendazol translocates p53 into the cell's mitochondria and reduces cancer cells' glucose uptake, suppressing their survival and growth. A significant advantage of fenbendazol is its unique mode of action. It targets a specific site (the colchicine binding site) on cancer cells, helping to avoid the common problem of drug resistance seen with many cancer therapies [1]. In addition, fenbendazol does not interact with P-glycoprotein (P-gp), a molecule often responsible for cancer cell resistance to therapy. This feature potentially makes fenbendazol a safer and more effective option in the fight against cancer.

Furthermore, in a study evaluating the role of fenbendazol in cancer research, this antiparasitic agent was found to potentially suppress tumor growth when used together with vitamins. In an experiment involving SCID mice with human lymphoma grafts, those fed a diet containing fenbendazol and additional vitamins showed significant suppression of tumor growth compared to control groups [3]. This result suggests a possible synergistic effect, highlighting the need for further research into the mechanisms behind this interaction. In addition, another study by Park in 2022 focused on liver cancer cells in rats showed that fenbendazol specifically attacks cells that are dividing and growing [4]. It causes these cells to undergo programmed cell death, leaving non-dividing, normal cells intact. This selective action makes fenbendazol a potential cancer-targeted therapy, reducing damage to healthy cells. Based on these findings, such as its ability to interfere with the growth, energy consumption and survival mechanisms of cancer cells, combined with minimal side effects and avoidance of typical drug resistance pathways, fenbendazol is a promising candidate for future cancer research and therapy.

A further study by Peng et al. in 2022 investigated the therapeutic potential of fenbendazol and its derivative, analog 6, against cancer cells [5]. They found that analog 6 showed increased sensitivity in targeting human cervical cancer HeLa cells compared to its parent compound, fenbendazol. Through a detailed study of the mechanism of action, it was reported that both compounds induced oxidative stress by increasing the accumulation of reactive oxygen species (ROS) [5]. They activated the p38-MAPK signaling pathway and played a key role in interfering with HeLa cell proliferation (growth). In addition, both drugs promoted apoptosis (programmed cell death) and significantly disrupted energy metabolism and suppressed cells' ability to migrate and invade. In addition, analog 6 was less toxic to normal cells while retaining potent anti-tumor activity [5]. These findings underscore the repurposing potential of fenbendazol and its derivatives as effective anticancer agents with limited side effects. In another study, mebendazol and fenbendazol showed significant results against gliomas in dogs. A study by Lai et al. (2017) demonstrates their significant anti-tumor effects, with mebendazol showing particularly low mean inhibitory concentrations (IC50) in three canine glioma cell lines [6]. Although it was slightly less effective, fenbendazol also effectively inhibited cancer cell growth without harming healthy canine fibroblasts, suggesting good therapeutic potential. Both substances disrupted the microtubules of cancer cells, which likely contributes to their ability to target and destroy glioma cells [6].

In addition, a study by Park et al. (2019) investigated the effects of fenbendazol beyond its known antiparasitic uses, particularly its anticancer and anti-inflammatory properties [7]. Studies on porcine cells revealed that fenbendazol significantly reduces cell growth, even at low doses. It induces apoptosis by affecting mitochondria, disrupting calcium balance and altering genes associated with cell death. Analyzing key signaling proteins, the study also reported how fenbendazol interfered with cell growth and death processes, especially during the early stages of pregnancy [7]. Innе study by Han and Joo (2020) examines the potential of fenbendazol against leukemia, focusing on its effects on HL-60 leukemia cells and the role of reactive oxygen species (ROS) [8]. Fenbendazol showed significant anti-tumor activity, reducing cell viability and inducing apoptosis in these cells. It is noteworthy that this effect intensified at higher doses, particularly disrupting mitochondrial function and increasing markers of cell death. The study also showed that blocking ROS production reduced the effect of fenbendazol, highlighting the key role of ROS in its anticancer mechanism [8]. These findings reveal the promising potential of fenbendazol as a treatment for leukemia and pave the way for further research into its applications in cancer therapy.

In addition, a recent study by Park et al. explored the potential of fenbendazol in treating colorectal cancer that no longer responds to standard chemotherapy [9]. The researchers found that fenbendazol was particularly effective against colon cancer cells resistant to the drug 5-fluorouracil. It acted by promoting cell death and stopping cell division in both normal and resistant cancer cells [9]. Interestingly, it seemed to affect resistant cells through different pathways than non-resistant ones, including reducing cell self-purification and increasing a type of cell death called ferroptosis. The study indicates that fenbendazol may offer a new approach to treating hard-to-treat colorectal cancer by targeting specific mechanisms of cancer cell growth and survival. A study by Chang et al. (2023) explored the potential of fenbendazol in the treatment of ovarian cancer, a multi-drug resistant disease [10]. Despite fenbendazol's significant anticancer properties, its poor water solubility limited its use. The team solved this problem by packaging fenbendazol into small, innovative nanoparticles, allowing for better delivery to the body and more effective targeting of ovarian cancer. The nanoparticles were found to significantly slow the growth of cancer cells and reduce tumor size in animal models [10], suggesting a promising new therapeutic agent for ovarian cancer and potentially other difficult-to-treat cancers. 

In addition, another study by He et al. (2017) investigated the effect of fenbendazol on chronic myeloid leukemia (CML) using K562 cells to understand its potential as a treatment for CML [11]. Various tests were performed, including the CCK-8 assay for cell viability, Trypan blue exclusion for cell growth, flow cytometry for cell cycle analysis and Western blot for protein changes. The study showed that fenbendazol specifically stopped the growth of certain leukemic cells without harming healthy cells [11]. It also caused these leukemia cells to stop dividing and led to a breakdown of their normal cell division process, as shown by unusual cell nuclei and changes in markers indicating cell division. These findings suggest that fenbendazol may be a safer, concentrated treatment for chronic myelogenous leukemia (CML), deserving further research into its effects and potential use in cancer treatment. A study by Sung et al. examined the combined use of fenbendazol and paclitaxel (PA), a commonly used anticancer drug, against leukemia cells [12]. They found that this combination significantly reduced the growth of leukemia cells more than either drug alone. It appears that this enhanced effect may be due to an increase in reactive oxygen species (ROS), a type of molecule that can damage cells [12], suggesting a new way in which these drugs may work together to fight cancer. These findings suggest that the use of fenbendazol with established anti-cancer therapies, such as PA, could improve outcomes for leukemia patients, offering a new approach to cancer treatment at cancer centers. 

In addition, a study by Kim et al. examined the anti-tumor effects of fenbendazol on oral melanoma cancer cells in dogs [13]. The researchers treated five melanoma cell lines with different concentrations of fenbendazol and evaluated the effects on cell viability, cell cycle progression and microtubule disruption using several assays. The results showed that fenbendazol treatment led to a dose-dependent decrease in cell viability, with cell viability decreasing significantly at 100 μM fenbendazol [13]. In addition, cells experienced a marked arrest in the G2/M phase, particularly evident in the UCDK9M5 cell line at higher doses of fenbendazol. In addition, Western blot analysis showed increased markers of apoptosis, and immunofluorescence microscopy indicated significant microtubule disruption and signs of mitotic escape [13]. The study concluded that fenbendazol is effective against canine melanoma cancer by reducing cell viability, causing cell cycle arrest, inducing cell death and damaging cellular structures. However, more detailed research and animal studies are needed to confirm its full potential in treating canine melanoma cancer and other cancers. A study by Noha et al. investigated the use of fenbendazol as a potential treatment for ovarian cancer [14]. The researchers tested its effects on ovarian cancer cells and normal cells in the laboratory, and then studied how it worked in animal models of ovarian cancer. The results showed that fenbendazol was able to stop the growth of both cancer and normal cells in the lab, suggesting that it does not specifically target cancer cells. In animal tests, administration of the drug orally or directly into the abdomen, even at high doses, produced no significant difference in tumor size [14]. However, when administered through a poly(lactic-glycolic acid) (PLGA) vein, it noticeably reduced tumor size without harming the animals. These findings suggest that although fenbendazol may be promising in the treatment of ovarian cancer, its success depends largely on how it is delivered or absorbed into the bloodstream. 

In addition, a study by Jung et al. examined the effects of fenbendazol on EL-4 mouse lymphoma cells compared to normal spleen cells [15]. They found that fenbendazol significantly damaged the lymphoma cells, especially at higher concentrations, with an observed decrease of 52%. In contrast, normal spleen cells showed only a slight decrease in health. Lymphoma cells treated with fenbendazol also experienced greater oxidative stress and mitochondrial damage, leading to cell death. In addition, fenbendazol caused lymphoma cells to get stuck in a part of the cell cycle where they could not divide, leading to cell death. These effects were not observed in normal spleen cells [15]. These findings suggest that fenbendazol may be a valuable cancer treatment option that minimizes damage to the immune system, but further research is needed to fully understand its capabilities and potential use in treating patients. A study by Semkova et al. aimed to test whether fenbendazol could harm cancer cells without affecting normal breast cells [16]. The study included three different cell lines: MCF-10A (normal breast cells), MCF7 (a less aggressive form of breast cancer cells) and MDA-MB-231 (aggressive, triple-negative breast cancer cells). The study showed that MDA-MB-231 cells were particularly susceptible to fenbendazol-induced damage through oxidative stress, more so than MCF-7 cells. On the other hand, fenbendazol seemed to protect normal breast cells (MCF-10A) by reducing oxidative stress [16]. The different effects of fenbendazol on these cell lines suggest that it offers targeted action against aggressive breast cancer cells while protecting normal cells. The different responses of cancer and normal cells to fenbendazol warrant additional studies to optimize its use in cancer therapy. 

In addition, a study by Florio et al. reported significant anti-cancer potential of a formulation of fenbendazol nanoparticles [17]. They tested fenbendazol nanoparticles on prostate cancer cells in the laboratory, checking their effects on cancer cell survival, oxidative stress and ability to prevent the spread of cancer. The results showed that the new formulation of fenbendazol was more toxic to prostate cancer cells, increased oxidative stress more effectively and inhibited cancer cell movement more than fenbendazol alone or fenbendazol with unmodified nanoparticles [17]. The results suggest that nanotechnology can overcome the solubility and accessibility challenges of fenbendazol, enhancing anti-cancer effects. Similarly, Esfahani et al. developed a special type of PEG-coated nanoparticles (PEG-MCM) for direct delivery of fenbendazol to cancer cells, making it more soluble and accessible to fight cancer [18]. They studied how effectively these nanoparticles could kill prostate cancer cells in laboratory dishes, observing their effects on cell survival, proliferation and their ability to produce reactive oxygen species (ROS) and prevent cell proliferation. They found that the new formulation of nanoparticles with fenbendazol significantly reduced cell movement and was more effective in killing cancer cells than fenbendazol alone or fenbendazol loaded into non-PEGylated nanoparticles [18]. In addition, it increased ROS production, which helps kill cancer cells. They concluded that this innovative method of using fenbendazol-loaded nanoparticles shows promise in treating prostate cancer by more effectively delivering fenbendazol to cancer cells, increasing its ability to kill them and prevent their spread.

In addition, a study by Mukhopadhyay et al. reported that fenbendazol interferes with the structure and growth of cancer cells in several ways [19]. It interferes with cellular building blocks, activates cell death processes and cuts off cancer cells' access to an energy source. Unlike drugs that target a single pathway and can become less effective over time, fenbendazol works on multiple fronts, offering hope for better outcomes and less drug resistance. Studies show that fenbendazol can attack lung cancer cells, stress them, stop their growth and kill them without harming healthy cells [19], making it a promising broad-spectrum cancer therapy that deserves further study. In another study conducted by Aycock-Williams et al, the anticancer effects of fenbendazol and vitamin E succinate (VES) against prostate cancer cells were investigated [20]. The study showed that fenbendazol alone inhibited cancer cell growth faster than VES in both human and mouse prostate cancer cells. However, when used together at lower doses, fenbendazol and VES significantly blocked cell growth in addition to their separate effects beginning on the third day of treatment [20]. This potent combined effect, leading to cell death by apoptosis, suggests a new treatment option for prostate cancer. Importantly, the best results were obtained with 25 µg/ml VES and 14 ng/ml fenbendazol together. The combination was safe in normal mice, causing no abnormalities or changes in the prostate, suggesting that this may be a safe and effective approach to prostate cancer therapy.

In addition, Mrkvová et al. revealed that commonly used anthelmintics, particularly albendazol and fenbendazol, may have potential in cancer treatment [21]. They reported that both albendazol and fenbendazol increased the activity of p53, a key player in cancer prevention, and its critical pathway that repairs DNA damage and disrupts the cell cycle during stress, potentially reversing the tumor's ability to suppress this protein. Importantly, these drugs led to a significant reduction in cancer cell viability and induced a state of mitotic catastrophe, disrupting the ability of cancer cells to divide properly and leading to cell death [21]. These findings underscore the potential of repurposing antitumor drugs as anticancer therapies, particularly for tumors resistant to current therapies, taking advantage of the drugs' ability to reactivate the p53 pathway. In addition, a study by Rena et al. investigated benzimidazoles as a treatment for glioblastoma [22]. They identified flubendazole, mebendazol and fenbendazol as having potent activity against GBM cells, both in laboratory dishes and animal models. These drugs were effective in stopping the growth, migration and invasion of GBM cells and altering important markers associated with disease spread and drug resistance [22]. These drugs can disrupt the cell cycle in GBM cells, forcing them into a state where they cannot divide and inducing cell death through mechanisms involving inflammatory and mitochondrial pathways. Importantly, flubendazole has been tested in mice and shown to safely reduce tumor growth.

Surprising benefit of fenbendazol in spinal cord regeneration

The researchers also found that fenbendazol showed unexpected benefits in recovery from spinal cord injury (SCI). In a study by Yu et al, female C57BL/6 mice treated with fenbendazol for four weeks before experiencing moderate spinal cord injury showed significant improvements in movement and nerve protection [23]. Fenbendazol was administered at a dose of approximately 8 mg/kg body weight/day. The mice showed enhanced locomotor abilities and better preservation of spinal cord tissue compared to those that were not treated with fenbendazol. The positive effects are attributed to fenbendazol's ability to modulate the immune response, particularly by reducing B-lymphocyte proliferation, which in turn reduces harmful autoantibodies that can worsen SCI outcomes [23]. This study not only underscores the drug's role in reducing immune-mediated damage after SCI, but also points to the importance of exploring unconventional therapies in medical research.

Fenbendazol shows promise against bovine herpes virus

The study revealed that fenbendazol showed powerful antiviral properties, particularly against bovine herpes virus 1 (BoHV-1) [24]. Cell culture treatment and advanced gene and protein analysis were used to evaluate the effect of fenbendazol on BoHV-1 infection. Fenbendazol effectively prevented BoHV-1 infection in MDBK cells in a dose-dependent manner and blocked various stages of the virus life cycle. Specifically, it interfered with the early and late processes of viral replication and interfered with key viral genes and the production of proteins essential for BoHV-1 development [24]. Importantly, these antiviral activities did not affect the PLC-γ1/Akt cell signaling pathway, indicating that fenbendazol selectively targets the virus. This study underscores the potential of fenbendazol beyond antiparasitic treatment, suggesting that it could be transformed for broader therapeutic applications, including combating viral infections.

Potential of fenbendazol in the treatment of asthma

The researchers also found that fenbendazol affects asthmatic responses in mice. In a study by Cai et al, they examined the effects of fenbendazol on key asthma markers, including lung eosinophilia, antigen-specific IgG1, and Th2 cytokines such as IL-5 and IL-13 [25]. Fenbendazol significantly reduced lung eosinophilia, levels of antigen-specific IgG1 and production of Th2 cytokines, indicating a potential therapeutic effect on asthma. In addition, fenbendazol-treated cells showed reduced proliferation and reduced production of IL-5, IL-13 along with reduced activation markers on immune cells, suggesting a direct effect of fenbendazol on Th2-mediated responses [25]. Reductions in eosinophilia and Th2 responses were seen even four weeks after fenbendazol treatment, indicating long-term benefits. These results underscore fenbendazol's ability to modulate asthma-related immune responses, potentially offering a new perspective on the treatment of Th2-mediated diseases such as asthma.

The role of fenbendazol in osteomyelitis

A recent study by Park, S.R., and Joo, H.G., focused on the ability of fenbendazol to alleviate inflammation in bone marrow cells (BMs) induced by lipopolysaccharide (LPS), a compound that simulates osteomyelitis-like inflammation under laboratory conditions [26]. They found that fenbendazol significantly reduced metabolic activity and mitochondrial membrane potential (MMP) in LPS-treated BMs, indicating its efficacy against inflammation. In addition, treatment led to a reduction in the number of viable cells, suggesting fenbendazol's ability to induce apoptosis and cell necrosis in inflamed BMs [26]. Interestingly, fenbendazol specifically targeted granulocytes more than B lymphocytes in inflammatory BMs. These results propose that fenbendazol may be a potent anti-inflammatory agent, offering a new therapeutic avenue to treat bone marrow-associated inflammation.

Fenbendazol against vesicular echinococcosis

Researchers have reported that fenbendazol may be an effective new treatment option for alveolar echinococcosis (AE), a serious parasitic infection in humans [27]. Current treatments, such as albendazol and mebendazol, come with some drawbacks, such as high costs, the need for a lifetime of medication, and the risk of recurrence. Küster, T., Stadelmann, B., Aeschbacher, D., and Hemphill, A. conducted an experimental study of treating AE-infected mice with fenbendazol and obtained results comparable to albendazol [27]. They found that mice treated with fenbendazol showed a significant reduction in parasite weight, similar to those treated with albendazol, without adverse effects. Importantly, fenbendazol caused structural changes in the parasite, affecting microtrichia, the tiny structures necessary for parasite attachment and nutrient uptake. These results underscore the potential of fenbendazol as a cost-effective and efficient alternative to AE chemotherapy.

Fenbendazol vs Mebendazol in pinworm infection

Researchers compared the efficacy of Fenbendazol and Mebendazol with placebo in the treatment of pinworm (Enterobius vermicularis) infection in a study involving 72 participants over the age of five [28]. The purpose of this study was to evaluate the safety and efficacy of these drugs, excluding those with serious health problems or recent antiparasitic treatment. Fenbendazol, known for its safety and broad effects on nematodes in animals, was tested on humans after promising results against various parasites at different doses in previous studies. Participants received one 100 mg tablet of fenbendazol, mebendazol or placebo every 12 hours after meals for one day. The presence of pinworm eggs was confirmed using Graham's swab method before treatment, and stool tests checked for the presence of other parasites. Results showed that both fenbendazol and mebendazol were significantly superior to placebo in treating pinworm infections, with 20 patients treated with fenbendazol and 17 with mebendazol achieving full recovery. Both drugs also effectively relieved symptoms such as anal itching and abdominal pain, with fenbendazol slightly superior to mebendazol in some cases [28]. Side effects were minor, including a burning sensation during urination and anal redness in a few fenbendazol recipients, but did not require treatment discontinuation. The study concludes that both fenbendazol and mebendazol are safe and effective in the treatment of pinworm infections, supporting the potential use of fenbendazol in humans.

Fenbendazol dosage for cancer and other ailments

The use of fenbendazol in humans, inspired by Joe Tippens' claim (the Joe Tippens protocol) to have cured his lung cancer, involves a dosing regimen of 222 mg per day for three consecutive days, followed by a four-day break. This regimen was part of a combination therapy that also included curcumin (600 mg daily) and cannabidiol oil (25 mg daily) [2]. It is important to always consult a doctor or pharmacist before taking any medication.

Other clinical studies testing the efficacy of fenbendazol in humans have shown that a single dose of 200 mg was effective against Ascaris, while higher doses (up to 1000 mg) were required for roundworm and trichomoniasis infections. In particular, doses of 1.0 g and 1.5 g per person were effective against Ascaris and provided significant reductions in roundworm eggs and good results against trichomoniasis [28, 30].

In animals, fenbendazol at a dose of 50 mg/kg once daily for 3 days effectively eradicated some parasites, including Giardia duodenalis, Cystoisospora spp., Toxocara canis, Toxascaris leonina, Ancylostomidae, Trichuris vulpis, Taenidae and Dipylidium caninum. Among other antiparasitic agents, fenbendazol showed the highest efficacy against Taenidae infections, achieving a 90-100% success rate [31].

As for the safety and side effects of fenbendazol in humans, the drug is generally well tolerated in several clinical trials. Moreover, based on animal studies, veterinary use and actual human use, it rarely causes any adverse effects. The most commonly reported side effects are mild and include gastrointestinal disturbances such as nausea, diarrhea and abdominal discomfort. These side effects usually resolve on their own without the need for medical intervention, making fenbendazol a potentially safe option for treating certain parasitic infections in humans, although its use and dosage in cancer treatment, popularized by anecdotal claims, remain controversial and not medically approved.

Metabolism of fenbenzadol

In recent studies, researchers have learned more about how the body processes fenbendazol [29]. For the first time, they discovered which specific enzymes, named CYP2J2 and CYP2C19, are key in transforming fenbendazol into its active form, making it work better. In their experiments, they found that CYP2C19 and CYP2J2 performed this transformation much better than other enzymes. They verified this further by analyzing liver samples from humans and confirmed that these two enzymes are indeed the main helpers in the metabolism of fenbendazol [29]. This discovery is quite important because it helps us understand exactly how fenbendazol works inside the body. This knowledge can help doctors predict how the drug may interact with other drugs and how it may act differently in different people. This can lead to better, more personalized ways of using the drug to fight parasitic infections and other conditions.

Summary

In summary, these findings underscore the unconventional but promising potential of fenbendazol, a drug initially used to fight parasitic infections, for a variety of therapeutic applications beyond its traditional use. Researchers have explored applications of fenbendazol ranging from cancer treatment and antiviral capabilities to its effects on inflammatory responses and metabolic pathways, revealing an impressively wide range of uses. In South Korea, cancer patients have reported positive experiences with fenbendazol, observing improvements in their physical condition and suggesting its potential as an alternative cancer treatment. Numerous animal and laboratory studies have demonstrated its selective anticancer activity, particularly its ability to disrupt microtubule dynamics and induce cell cycle arrest and apoptosis in cancer cells without significantly affecting normal cells. This selective cytotoxicity, along with fenbendazol's ability to modulate immune responses and potentially reduce inflammation, underscore its therapeutic versatility. In addition, the reapplication of fenbendazol to cancer therapy is further supported by its combination with vitamin E succinate (VES) to enhance anti-tumor efficacy, particularly in prostate cancer models, where synergistic effects significantly inhibited cancer cell proliferation. This combined approach, along with fenbendazol's antiviral potential against bovine herpes virus and potential reduction of inflammation in the bone marrow, suggests a broad spectrum of therapeutic benefits. In addition, fenbendazol's success in overcoming chemo-resistance in colorectal cancer and aiding recovery from spinal cord injury demonstrates its versatility in many areas of medicine. These achievements further support its reputation as a widely used therapeutic agent.

In addition, its efficacy in the treatment of vesicular echinococcosis, pinworm infections and its role in metabolism involving CYP2J2 and CYP2C19 enzymes reveal its extensive pharmacological profile. Taken together, these studies reveal fenbendazol's potential to address a variety of health problems and underscore the need for further research and clinical trials to fully explore its therapeutic potential. As the medical community continues to explore drugs with new applications, fenbendazol stands out as a promising compound for future therapies against cancer, parasitic infections and more. It represents significant potential in developing therapeutic strategies. For patients seeking alternative or complementary options, fenbendazol offers a ray of hope.

Disclaimer

This article was written for educational purposes and is intended to raise awareness of the substance being discussed. It is important to note that the substance discussed is a substance, not a specific product. The information contained in the text is based on available scientific research and is not intended to serve as medical advice or promote self-medication. The reader should consult any health and treatment decisions with a qualified health professional.

Sources

1. Dogra, N., Kumar, A., & Mukhopadhyay, T. (2018). Fenbendazol acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways. Scientific reports, 8(1), 11926. https://doi.org/10.1038/s41598-018-30158-6 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6085345/

1A. Sultana, T., Jan, U., Lee, H., Lee, H. and Lee, J.I., 2022 Exceptional repositioning of dog dewormer:

Fenbendazol fever. Current Issues in Molecular Biology, 44(10), pp.4977-4986. https://www.mdpi.com/1467-3045/44/10/338

2. Song, B., Kim, K.J. and Ki, S.H., 2022. Experience with and perceptions of non-prescription anthelmintics for cancer treatments among cancer patients in South Korea: A cross-sectional survey. Plos one, 17(10), p.e0275620. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0275620
3. Gao, P., Dang, C.V. and Watson, J., 2008. Unexpected antitumorigenic effect of fenbendazol when combined with supplementary vitamins. Journal of the American Association for Laboratory Animal Science, 47(6), pp.37-40. https://www.ingentaconnect.com/content/aalas/jaalas/2008/00000047/00000006/art00006
4. Park, D., 2022. Fenbendazol suppresses growth and induces apoptosis of actively growing H4IIE hepatocellular carcinoma cells via p21-mediated cell-cycle arrest. Biological and Pharmaceutical Bulletin, 45(2), pp.184-193. https://www.jstage.jst.go.jp/article/bpb/45/2/45_b21-00697/_article/-char/ja/
5. Peng, Y., Pan, J., Ou, F., Wang, W., Hu, H., Chen, L., Zeng, S., Zeng, K. and Yu, L., 2022. Fenbendazol and its synthetic analog interfere with HeLa cells' proliferation and energy metabolism via inducing oxidative stress and modulating MEK3/6-p38-MAPK pathway. Chemico-Biological Interactions, 361, p.109983. https://www.sciencedirect.com/science/article/abs/pii/S0009279722001880
6. Lai, S.R., Castello, S.A., Robinson, A.C. and Koehler, J.W., 2017 In vitro anti-tubulin effects of mebendazol and fenbendazol on canine glioma cells. Veterinary and comparative oncology, 15(4), pp.1445-1454. https://onlinelibrary.wiley.com/doi/abs/10.1111/vco.12288
7. Park, H., Lim, W., You, S. and Song, G., 2019. Fenbendazol induces apoptosis of porcine uterine luminal epithelial and trophoblast cells during early pregnancy. Science of the total environment, 681, pp.28-38. https://www.sciencedirect.com/science/article/abs/pii/S0048969719321400
8. Han, Y. and Joo, H.G., 2020. Involvement of reactive oxygen species in the anti-cancer activity of fenbendazol, a benzimidazole anthelmintic. Korean Journal of Veterinary Research, 60(2), pp.79-83. https://www.kjvr.org/journal/view.php?doi=10.14405/kjvr.2020.60.2.79
9. Park, D., Lee, J.H. and Yoon, S.P., 2022. Anti-cancer effects of fenbendazol on 5-fluorouracil-resistant colorectal cancer cells. The Korean Journal of Physiology & Pharmacology: Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology, 26(5), p.377. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9437363/
10. Chang, C. S., Ryu, J. Y., Choi, J. K., Cho, Y. J., Choi, J. J., Hwang, J. R., Choi, J. Y., Noh, J. J., Lee, C. M., Won, J. E., Han, H. D., & Lee, J. W. (2023). Anti-cancer effect of fenbendazol-incorporated PLGA nanoparticles in ovarian cancer. Journal of gynecologic oncology, 34(5), e58. https://doi.org/10.3802/jgo.2023.34.e58 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10482585/
11. HE, L., Shi, L., Gong, R., DU, Z., GU, H. and Lü, J., 2017. Inhibitory effect of fenbendazol on proliferation of human chronic myelogenous leukemia K562 cells. Chinese Journal of Pathophysiology, pp.1012-1016. https://pesquisa.bvsalud.org/portal/resource/pt/wpr-612833
12. Sung, J.Y. and Joo, H.G., 2021. Anti-cancer effects of Fenbendazol and Paclitaxel combination on HL-60 cells.  Vet. Med, 45, pp.13-17. https://www.e-sciencecentral.org/upload/jpvm/pdf/jpvm-2021-45-1-13.pdf
13. Kim, S., Perera, S.K., Choi, S.I., Rebhun, R.B. and Seo, K.W., 2022. G2/M arrest and mitotic slippage induced by fenbendazol in canine melanoma cells. Veterinary medicine and science, 8(3), pp.966-981. https://onlinelibrary.wiley.com/doi/full/10.1002/vms3.733
14. Noh, J.J., Cho, Y.J., Choi, J.J., Shim, J.I. and Lee, Y.Y., 2021. Differential effects of fenbendazol by administration route as an anti-cancer drug in human epithelial ovarian cancer. 대한부인종양학회 학술대회지, 36, pp.244-245. https://kiss.kstudy.com/Detail/Ar?key=3889843
15. Jung, H., Lee, Y.J. and Joo, H.G., 2023. Differential cytotoxic effects of fenbendazol on mouse lymphoma EL-4 cells and spleen cells. Korean Journal of Veterinary Research, 63(1). https://www.kjvr.org/journal/view.php?number=3907
16. Semkova, S., Nikolova, B., Tsoneva, I., Antov, G., Ivanova, D., Angelov, A., Zhelev, Z. and Bakalova, R., 2023. Redox-mediated Anticancer Activity of Anti-parasitic Drug Fenbendazol in Triple-negative Breast Cancer Cells. Anticancer Research, 43(3), pp.1207-1212. https://ar.iiarjournals.org/content/43/3/1207.abstract
17. Florio, R., Carradori, S., Veschi, S., Brocco, D., Di Genni, T., Cirilli, R., Casulli, A., Cama, A. and De Lellis, L., 2021. Screening of benzimidazole-based anthelmintics and their enantiomers as repurposed drug candidates in cancer therapy. Pharmaceuticals, 14(4), p.372. https://www.mdpi.com/1999-4923/14/4/884
18. Esfahani, M.K.M., Alavi, S.E., Cabot, P.J., Islam, N. and Izake, E.L., 2021. PEGylated Mesoporous Silica Nanoparticles (MCM-41): A promising carrier for the targeted delivery of fenbendazol into prostate cancer cells. Pharmaceutics, 13(10), p.1605. https://www.mdpi.com/1999-4923/13/10/1605
19. Mukhopadhyay, T., Fenbendazol acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways. https://drjohnson.com/wp-content/uploads/2023/10/Fenbendazol-acts-as-a-moderate-microtubule-destabilizing-agent-and-causes-cancer-cell-death-by-modulating-multiple-cellular-pathways.pdf
20. Aycock-Williams, A., Pham, L., Liang, M., Adisetiyo, H.A., Geary, L.A., Cohen, M.B., Casebolt, D.B. and Roy-Burman, P., 2011. Effects of fenbendazol and vitamin E succinate on the growth and survival of prostate cancer cells. J Cancer Res Exp Oncol, 3(9), pp.115-121. https://prairiedoghall.com/wp-content/uploads/2020/05/Effects_of_fenbendazol_and_vitamin_E_succinate_on.pdf
21. Mrkvová, Z., Uldrijan, S., Pombinho, A., Bartůněk, P. and Slaninová, I., 2019. benzimidazoles downregulate Mdm2 and MdmX and activate p53 in MdmX overexpressing tumor cells. Molecules, 24(11), p.2152. https://www.mdpi.com/1420-3049/24/11/2152
22. Ren, L.W., Li, W., Zheng, X.J., Liu, J.Y., Yang, Y.H., Li, S., Zhang, S., Fu, W.Q., Xiao, B., Wang, J.H. and Du, G.H., 2022. Benzimidazoles induce concurrent apoptosis and pyroptosis of human glioblastoma cells via arresting cell cycle. Acta Pharmacologica Sinica, 43(1), pp.194-208. https://www.nature.com/articles/s41401-021-00752-y
23. Yu, C.G., Singh, R., Crowdus, C., Raza, K., Kincer, J., and Geddes, J.W., 2014. Fenbendazol improves pathological and functional recovery following traumatic spinal cord injury. Neuroscience, 256, pp.163-169. https://www.sciencedirect.com/science/article/abs/pii/S0306452213008920
24. Chang, L., & Zhu, L. (2020). Dewormer drug fenbendazol has antiviral effects on BoHV-1 productive infection in cell cultures. Journal of veterinary science, 21(5), e72. https://doi.org/10.4142/jvs.2020.21.e72 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7533386/
25. Cai, Y., Zhou, J., and Webb, D.C., 2009. Treatment of mice with fenbendazol attenuates allergic airways inflammation and Th2 cytokine production in a model of asthma. Immunology and cell biology, 87(8), pp.623-629. https://onlinelibrary.wiley.com/doi/abs/10.1038/icb.2009.47
26. Park, S.R. and Joo, H.G., 2021. Inhibitory effects of fenbendazol, an anthelmintic, on lipopolysaccharide-activated mouse bone marrow cells. Korean Journal of Veterinary Research, 61(3), pp.22-1. https://web.archive.org/web/20210922161506id_/https://kjvr.org/upload/pdf/kjvr-2021-61-e22.pdf
27. Küster, T., Stadelmann, B., Aeschbacher, D. and Hemphill, A., 2014. Activities of fenbendazol in comparison with albendazol against Echinococcus multilocularis metacestodes in vitro and in a murine infection model. International journal of antimicrobial agents, 43(4), pp.335-342. https://www.sciencedirect.com/science/article/abs/pii/S0924857914000272
28. Bhandari; A. Singhi. (1980). Fenbendazol (Hoe 881) in enterobiasis. , 74(5), 691-0. doi:10.1016/0035-9203(80)90175-3  https://www.bothonce.com/10.1016/0035-9203(80)90175-3
29. Wu, Z., Lee, D., Joo, J., Shin, J.H., Kang, W., Oh, S., Lee, D.Y., Lee, S.J., Yea, S.S., Lee, H.S. and Lee, T., 2013. CYP2J2 and CYP2C19 are the major enzymes responsible for metabolism of albendazol and fenbendazol in human liver microsomes and recombinant P450 assay systems. Antimicrobial agents and chemotherapy, 57(11), pp.5448-5456. https://journals.asm.org/doi/full/10.1128/aac.00843-13
30. Bruch K, Haas J. Effectiveness of single doses of Fenbendazol Hoe 88I against Ascaris, hookworm and Trichuris in man. Ann Trop Med Parasitol. 1976 Jun;70(2):205-11. doi: 10.1080/00034983.1976.11687113. PMID: 779682. https://pubmed.ncbi.nlm.nih.gov/779682/
31. Miró G, Mateo M, Montoya A, Vela E, Calonge R. Survey of intestinal parasites in stray dogs in the Madrid area and comparison of the efficacy of three anthelmintics in naturally infected dogs. Parasitol Res. 2007 Jan;100(2):317-20. doi: 10.1007/s00436-006-0258-0. Epub 2006 Aug 17. PMID: 16915389. https://pubmed.ncbi.nlm.nih.gov/16915389/