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Can Fenbendazole Cure Cancer?
According to a case series published in an oncology journal, the answer could be a resounding yes.
The case report highlights three cancer patients who were in pretty bad shape. But after taking fenbendazole, they all experienced a complete remission.
What Is Fenbendazole, and How Does it Work?
Fenbendazole (FBZ) is a medicine originally designed to treat worms and parasites in animals. Its sister drugs, Mebendazole and Albendazole, have had remarkable success treating similar ailments in humans with few side effects.
Recently, anecdotal reports have praised fenbendazole as a potentially miraculous anti-cancer drug. It works by destabilizing microtubules, the structures that help cancer cells divide and grow. By disrupting this process, fenbendazole effectively halts cancer cell division and slows or stops tumor growth.
Miraculous Recoveries After Taking Fenbendazole
Case series #1 features a 63-year-old man with advanced kidney cancer (clear cell renal carcinoma) who experienced tumor recurrence and severe side effects from multiple cancer therapies, including surgery and two different medications.
With no effective options left, he turned to fenbendazole (FBZ), taking 1 gram three times a week at a friend’s suggestion. Over the next 10 months, his tumors—including those in his pancreas and spine—showed near-complete resolution on imaging. Remarkably, he experienced no side effects from FBZ, and follow-up scans have shown no signs of recurrence.
Case series #2 follows a 72-year-old man with metastatic urethral cancer that had spread to his lungs, lymph nodes, and brain. Despite undergoing multiple rounds of chemotherapy and radiation, one lymph node continued to grow, resisting all treatments.
Seeking alternatives, he decided to try fenbendazole (FBZ), taking 1 gram three times a week, along with vitamin E, curcumin, and CBD oil, while postponing further conventional therapies. Over the next nine months, imaging revealed a dramatic response, with the lymph node shrinking significantly until it completely resolved. Remarkably, he reported no side effects during this period.
Case series #3 focuses on a 63-year-old woman diagnosed with a large, invasive bladder tumor. Facing a challenging prognosis, she underwent chemotherapy while also taking fenbendazole (FBZ) at 1 gram three times a week.
After completing six cycles of treatment, follow-up scans showed a complete resolution of the tumor, with only minimal thickening remaining in the bladder wall. Confident in her recovery, she chose to decline further surgery and remains disease-free under regular surveillance.
The abstract concluded, “FBZ appears to be a potentially safe and effective antineoplastic agent that can be repurposed for human use in treating genitourinary malignancies.”
Reflecting on these remarkable case reports, Dr. John Campbell (@Johnincarlisle) urged drug regulators to “start looking at this as a matter of some urgency because people are dying from cancer now.”
“So if something is safe and effective, surely it can be accredited for human use by our national authorizing agencies pretty quickly if they want to,” Dr. Campbell added with a hint of sarcasm.
Of course, the key words here are “if they want to.”
“Three patients, basically… cured of their cancers. Read the paper for yourself. That’s what they seem to be saying to me.”
Doctors Source https://x.com/vigilantfox/status/1862727748189401143?s=61…
Mebendazole/ Fenbendazole/Albendazole Anticancer pathways and mechanisms A compound originally developed as a treatment for parasitic worms, mebendazole (MBZ) works by fatally disrupting the cellular microtubule formation in abnormal cancer cells that occurs as the cell is attempting to divide. Like the other benzimidazoles, Mebendazole binds to the tubulin colchicine-binding domain and appears to act by both p53-dependent and independent mechanisms. (728) MBZ inhibits many factors involved in tumor progressions such as tubulin polymerization, angiogenesis, pro-survival pathways, matrix metalloproteinases, and multi-drug resistance protein transporters. (729) MBZ inhibits cancer stem cells; this mechanism of action is critical in preventing metastasis. (223, 729) In addition, in a juvenile glioblastoma mouse model MBZ reduced tumor cell growth and invasion when evaluated under in-vitro and in-vivo conditions through inhibition of both the glutaminolysis and the glycolysis pathways. (304) In this study the effect of ketosis and MBZ were synergistic in inhibiting tumor growth. MBZ decreases the activity of the Hedgehog pathway, which is common in gliomas, melanomas, lung cancers, ovarian cancers, and colorectal cancer. (155) MBZ inactivates Bcl-2 and activates caspases to promote apoptosis in cancer cells and the release of cytochrome c which has also been shown to trigger apoptosis in malignant cells. Benzimidazole modulates the typically overactivated MAPK pathway, switching it to activate the apoptotic pathway, rather than the anti-apoptotic pathway; it also destabilizes microtubules, structural proteins required to maintain a cell’s integrity during the process of mitosis, among other functions; it also interferes with cancer cells’ glycolysis-dependent metabolism, upon which most cancers are heavily preferentially dependent, as well as functioning as an inhibitor of mitochondrial oxidative phosphorylation, or OXPHOS, which reduces the residual energy available via the ordinary metabolic ATP production pathway. MBZ can cross the blood-brain barrier and has been demonstrated to slow the growth of gliomas by targeting signaling pathways involved in cell proliferation, apoptosis, invasion, and migration, as well as by making glioma cells more susceptible to conventional chemotherapy and radiotherapy. (730) MBZ can also sensitize cancer cells to conventional therapy, such as chemotherapeutics and radiation, enhancing their combined antitumor potential, confirming that MBZ may be useful as an adjuvant therapeutic combined with traditional chemotherapy. (730) When combined with low-dose chemotherapy there is also evidence these drugs help to destroy the tumor-associated macrophage cells that may help maintain a favorable environment for the cancer to flourish. Clinical studies The use of benzimidazoles in cancer is limited to a few case reports (731, 732) and a small case series. (733) Mebendazole is a component of the multidrug cocktail used in the METRICS study.(257) The use of benzimidazoles, and in particular fenbendazole, has achieved much attention as a repurposed drug for cancer due to the reported experience of Joe Tippens. (146) In 2016, Tippens was diagnosed with non-small-cell lung cancer with extensive metastatic disease. At the advice of a veterinarian friend, he took Fenbendazole together with nanocurcumin, and three months after starting these drugs his PET scan was completely clear. He remains alive and disease-free up until the present; however, some questions surround his apparent cure. Types of cancers that mebendazole may be beneficial for A wide variety of cancers, including non-small cell lung cancer, adrenocortical, colorectal, chemo-resistant melanoma, glioblastoma multiforme, colon, leukemia, osteosarcoma/soft tissue sarcoma, acute myeloid sarcoma, breast (ER+ invasive ductal), kidney, and ovarian carcinoma, have been shown to be responsive to benzimidazoles, including MBZ. (252, 728-730, 734-743) Dosing and cautions We suggest Mebendazole 100-200 mg/day. The cost of mebendazole in the U.S. skyrocketed once this drug was discovered to have activity against cancer ($555 for a single 100 mg tablet?). However, mebendazole is available from international (India) and local compounding pharmacies for between 25c to $2 for a 100 mg tablet. Ivermectin can be considered an alternative if mebendazole is unavailable. However, it I likely that both drugs combined may have additive or synergistic anticancer activity. 8. Green Tea Anticancer pathways and mechanisms Green tea is a significant source of a type of flavonoid called catechin, which includes epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC). The most abundant individual catechin in fresh tea leaves is EGCG, which is more than 40% of the total content of catechins. (234) Green tea catechins (GTCs) have been proven to be effective in inhibiting cancer growth in several experimental models. (744-746) In addition, GTCs may have synergistic anticancer activity when combined with other phytochemicals, particularly resveratrol. (747, 748) GTCs, particularly EGCG, may have a role in both the prevention and treatment of cancers, (749) specifically those dependent on the glutamate pathway as a source of energy. Mitochondrial glutamate dehydrogenase (GDH) catalyzes the oxidative deamination of L-glutamate. Activation of GDH is tightly correlated with increased glutaminolysis. Furthermore, glutamate serves as a mitochondrial intracellular messenger when glucose is being oxidized and the GDH participates in this process by synthesizing glutamate. (750) Li and colleagues demonstrated in vitro that EGCG allosterically inhibits GDH in nanomolar concentrations. (301, 302) GTCs have an important anticarcinogenic role by promoting and/or inhibiting signal transmission through the targeted regulation of multiple links in the signal pathways that are activated or inhibited in cancer cells. (234) EGCG regulates signaling pathways by interacting with membrane receptors. EGCG significantly inhibited the expression of VEGF and reduced VEGF receptors. Inactivation of the VEGF signaling pathway suppresses angiogenesis, a common strategy for inhibiting carcinogenesis. EGCG activates PKA, which dephosphorylates related proteins such as the tumor suppressor Merlin and inhibits the proliferation of cancer cells. (751) EGCG inhibits STAT3 phosphorylation by blocking JAK2 phosphorylation. STAT3 suppresses anti-tumor immune responses and promotes the proliferation and migration of cancer cells. EGCG inhibits the MAPK signaling by competing for the phosphorylation sites of downstream proteins. EGCG inhibits the Wnt pathway by phosphorylating β-catenin and promoting its degradation. EGCG inhibits transcription factors involved in activating the Sonic hedgehog pathway. EGCG inhibited the activities of MMP2 and MMP9 and promoted the expression of tissue inhibitor of MMPs (TIMp1/2) to suppress the invasion and metastasis of tumor cells. (751) Green tea extract has been demonstrated to suppress cancer stem cells. (752, 753) GTCs have anticancer effects via additional pathways. (234) GTCs exert potent and selective in vitro and in vivo pro-apoptotic activity in cancer cells via several pathways. (744, 745, 754) GTC inhibits A549 cells by regulating its cell cycle arrest, increasing the expressions of p21 and p27, and inhibiting the expressions of p-AKT and cyclin E1 in a dose-dependent manner in the cancer cells. (755) EGCG inhibited the proliferation of human lung cancer cells by targeting the epidermal growth factor receptor (EGFR) signaling pathway. GTCs have been demonstrated to alter the tumor microenvironment (TME) thereby attenuating immunosuppression and the risk of metastases. (748) Flavonoids including GTCs (and resveratrol) are potent modulators of pro-inflammatory gene expression being, therefore, of great interest as agents selectively suppressing molecular targets within pro-inflammatory TME. GTCs have been demonstrated to increase the ratio of active cytotoxic T lymphocytes to Tregs in tumors, indicating a switch of “cold” tumors to “hot” with significantly improved anti-tumor immune therapeutics. (756) GTCs have anticancer effects by enhancing anticancer immunity via PD-1 axis and TLR4 pathways. (757, 758) In addition, GTCs repolarize tumor-associated macrophages (M2 to M1 macrophages), triggering an immune response and limiting metastases. (759) GTCs have been demonstrated to attenuate MDSC-mediated immunosuppression and increased the proportions of CD4+ and CD8+ T cells. (760) Studies have shown that 20% of cancer-related deaths were directly due to TLR-induced cancer cachexia, in which cancer cells released heat shock proteins that acted as TLR-4 agonists in macrophages, skeletal muscle, and fat cells, causing downstream signal transduction. EGCG effectively downregulates the TLR-4 signal pathway. (758) GTCs inhibit the accumulation of MDSCs, leading to restoration of the IFN-γ, enhancing the activity of CD8+ T-cells, and improvement of the ratio of CD4(+) to CD8(+) T-cells, which is beneficial to the improvement of the immune system’s attack on tumor cells. (234) In addition, a phytochemical mixture including GTCs exerted anti-tumor activity by repolarization of M2-polarized macrophages and induced the production of IL-12, which recruit cytotoxic T lymphocytes and natural killer cells (NK) with the tumor microenvironment. (759) In addition to all these beneficial effects, GTCs potentiate the effects of conventional chemotherapeutic agents. Due to their effects on the important signaling pathways in vivo, catechins are often used as sensitizing agents in combination with chemotherapeutic drugs. The combination of anticancer drugs with catechins, whether before or after drug administration, reduced the toxicity of these drugs and enhanced the clinical efficacy by accelerating apoptosis of cancer cells. (234) Importantly, the combination of a number of chemotherapeutic drugs with GTCs will improve the chemotherapeutic sensitivity of cells to the drug, allowing a reduction in the dose of the chemotherapeutic drug. (234) Clinical studies Numerous experimental models have explored the mechanistic anticancer effects of GTCs; this data is supported by epidemiologic data, a case series of patients with B cell malignancies,(761) several case reports,(762, 763) and a RCT. A meta-analysis including 18 prospective cohorts and 25 case-control studies showed a significant inverse association between intake of tea catechins and risk of various cancers, with a relative risk (RR) being 0.935 (95% CI = 0.8910.981). (234) Similarly an umbrella review and meta-analysis by Kim et al, which included 64 observational studies (case-control or cohort) demonstrated that GTC significantly reduced the risk of gastrointestinal cancer (oral, gastric, colorectal, biliary tract, and liver), breast cancer, and gynecological cancer (endometrial and ovarian cancer) as well as leukemia, lung cancer, and thyroid cancer. (243) In a phase I dose finding study in patients with Chronic Lymphocytic Leukemia EGCG was well tolerated and a decline in the absolute lymphocyte count and/or lymphadenopathy was observed in the majority of patients. (764) Lemanne et al reported on a patient who demonstrated a complete and durable remission of chronic lymphocytic leukemia (CLL) following high dose EGCG. (763) In a randomized, double-blind, placebo-controlled study, treatment with 600 mg/day of green tea catechins reduced the risk of prostate cancer from 30% to 3% in men with high-grade prostate intraepithelial neoplasia. (303) Types of cancers that green tea may be beneficial for Green tea catechins may be effective against a range of tumors including cancers of the prostate, breast, uterus, ovary, colorectal, glioma, liver and gallbladder, melanoma, and lung cancers. (234) GTCs appear to be particularly beneficial for prostate cancer as well as breast cancer. (299, 303, 744-747, 760, 765) Dosing and cautions Green tea catechins should be taken in a dose of 500-1000 mg/day. Green tea extract should be taken during/after a meal rather than on an empty stomach. (244) Green tea extract has rarely been associated with liver toxicity. (766) The safety of green tea extract was evaluated by the US Pharmacopeia (USP) Dietary Supplement Information Expert Committee (DSIEC). (244) The DSIEC concluded that “when dietary supplement products containing green tea extracts are used and formulated appropriately the Committee is unaware of significant safety issues that would prohibit monograph development.” (244) Based on this data we suggest that green tea exacts be taken in the dosages recommended by the manufacturer. Regular liver function tests are suggested in patients taking green tea extract and green tea exact should be avoided/used cautiously in those with underlying liver disease.