Newest Conspiracy Theory: Could Ivermectin and Fenbendazole Be Cancer's New Foes?
From Actor Mel Gibson's Claims to Scientific Insights - Exploring the Anticancer Potential of Two Antiparasitic Drugs
So, the new conspiracy theory is that Ivermectin and Fenbendazole, primarily known as antiparasitic drugs, could potentially have anticancer properties. This theory caused me to roll my eyes a couple of times, especially when I learned it was recently put forth by actor Mel Gibson, who stated that he has friends who used the combination to cure stage 4 cancer using Ivermectin and Fenbendazole, which are primarily known as antiparasitic drugs.
We do not know what types of cancer they had, and regardless, that is a wild claim that no double-blind scientific studies prove is possible. However, it does open the door for more rigorous testing. I sympathize with the oncologists out there who have to answer patients' questions based on something Mel Gibson said.
Being the curious researcher I am, I went down the rabbit hole nonetheless and found some interesting facts about the two compounds with regard to cancer cells. Whether this works in serious clinical trials remains to be seen.
Here's how they might affect cancer cells:
Ivermectin:
Apoptosis Induction: Ivermectin does promote programmed cell death (apoptosis) in various cancer cell lines. This happens by activating caspase-3/7, upregulating pro-apoptotic proteins like Bax, and downregulating anti-apoptotic proteins like Bcl-2. It can also lead to the release of cytochrome c from mitochondria, which is a key step in the apoptotic pathway.
Cell Cycle Arrest: Ivermectin can induce cell cycle arrest, particularly at the G1 phase, by affecting cyclin D1 expression and the mTOR/STAT3 signaling pathway, thereby preventing cancer cell proliferation.
Mitochondrial Dysfunction: Ivermectin causes mitochondrial dysfunction by increasing the production of reactive oxygen species (ROS), which can lead to oxidative stress and further promote apoptosis. This also involves a decrease in mitochondrial membrane potential and ATP levels.
Inhibition of Tumor Growth and Metastasis: Ivermectin has been observed to inhibit tumor growth, angiogenesis, and metastasis through various mechanisms, including the degradation of PAK1 in esophageal squamous cell carcinoma.
Reversal of Drug Resistance: Ivermectin can reduce the expression of P-glycoprotein (P-gp), which is involved in multidrug resistance in cancer cells, thereby enhancing the effectiveness of other chemotherapeutic agents.
A City of Hope study by Peter Lee, M.D., combined ivermectin with a checkpoint inhibitor for triple-negative breast cancer, showing promise in preclinical research. However, this was still in the stage of preparing for a first-in-human clinical trial as of 2022.
Some studies and reviews suggest that ivermectin could be beneficial, but they primarily discuss preclinical data or in vitro studies. The need for more clinical trials to establish its effectiveness in humans is acknowledged.
The FDA has not approved ivermectin for cancer treatment, and while preclinical studies are promising, there's a caution about the translation of these results to human clinical settings due to the complexity of
Oxidative Stress: It induces oxidative stress by increasing ROS levels, which can activate pathways leading to cell deahuman biology compared to cell cultures or animal models.
Fenbendazole:
Microtubule Disruption: As a benzimidazole, fenbendazole binds to β-tubulin, preventing microtubule polymerization, which is crucial for cell division. This leads to cell cycle arrest and apoptosis.
Glucose Metabolism Inhibition: Fenbendazole can inhibit glucose uptake in cancer cells by affecting glucose transporters (GLUT) and hexokinase II (HKII), an enzyme critical for glycolysis. This reduces the energy supply to cancer cells, promoting cell death.th. This effect is combined with its impact on microtubule function and energy metabolism.
Apoptosis and Autophagy: Fenbendazole promotes both apoptosis and autophagy, potentially via the mitochondrial pathway, by stabilizing p53, a protein integral to cell death mechanisms.
Immune Response Modulation: Evidence suggests that Fenbendazole may enhance the immune response against tumors, particularly with other compounds or dietary elements such as vitamins. This synergistic approach has demonstrated the potential to reduce tumor growth.
The FDA or EMA has not approved Fenbendazole for human use, whereas Ivermectin has been approved for use in humans; thus, there are no widespread clinical trials for cancer treatment in humans.
There are mentions of Joe Tippens, who claimed success using fenbendazole for his lung cancer, but this is anecdotal and not from a controlled clinical trial.
A review from the Integrative Medicine Center of Western Colorado discusses fenbendazole's potential but notes the absence of clinical trials in humans for cancer treatment. It highlights the challenge of no financial incentive for large-scale clinical trials due to its off-patent status.
There is a call for more rigorous research, including clinical trials, to assess cancer treatments' safety, efficacy, and dosing. Still, these are largely absent or in very early stages.
Both Ivermectin and Fenbendazole exhibit promising preclinical results in addressing multiple pathways involved in cancer cell survival, particularly those that traditional chemotherapy may not target. While this is all very interesting, I must reiterate that the FDA approves neither drug for cancer treatment, and the availability of human clinical trials remains limited or in preliminary stages. Their mechanisms of action are intricate and often involve synergistic effects when used alongside other therapeutic modalities or nutritional strategies.
https://www.onedaymd.com/2024/10/ivermectin-fenbendazole-and-mebendazole.html
https://imcwc.com/repurposed-drugs-for-cancer/
