Fenbendazole For Cancer

Posts on social media, such as Twitter and TikTok, have recently spread a false claim that the anthelmintic drug fenbendazole cures cancer in humans. These posts are based on the anecdotal experience of a patient with advanced nonsmall cell lung cancer who self-administered fenbendazole. These results provided no evidence that fenbendazole warrants further testing as a potential agent for use in anticancer therapy, but suggested that related compounds could be valuable. Biodistribution studies demonstrated that both free fenbendazole and the fenbendazole/rapamycin mixture were present in tissues at 8 h after injection. Fenbendazole is a cytotoxic agent Cancer is a major cause of morbidity and mortality in humans. Its incidence and death rates have been steadily increasing over the past century. New cytotoxic agents are urgently needed to combat the disease, but developing new compounds requires significant time and cost. Moreover, the toxicity of some agents may also limit their use in clinical practice. Repurposing veterinary drugs with microtubule depolymerizing activity can provide rapid and inexpensive alternatives. Fenbendazole (FZ) is a broad-spectrum benzimidazole anthelmintic that has been used in numerous animal species. A previous study showed that FZ interfered with cell cycle progression and induced mitotic catastrophe in A549 cells. This effect was mediated by inhibiting the formation of a complex between cyclin B1 and cyclin-dependent kinase 1 (CDK1), leading to degradation of cyclin B1. In the present experiments, we examined the effects of three fenbendazole treatments given one day before or 2 h before irradiation on radiation response using a rigorous colony formation assay. We found that treatment with fenbendazole did not alter the radiation dose-response curves of aerobic or hypoxic EMT6 tumor cells. It is a cytostatic agent Fenbendazole is an effective cytostatic agent that can be used to treat malignant tumours. It inhibits cell growth and prevents the formation of cellular microtubules, leading to a loss of cell structure and subsequent cell death. It can also be used as an alternative to chemotherapeutic agents. This compound has several different mechanisms of action and targets different metabolic pathways in cancer cells. It interferes with glycolysis by blocking glucose uptake and inhibits expression of the GLUT transporters. It also decreases the activity of hexokinase II, a key enzyme in glycolysis. It also induces p53 translocation and alters microtubule dynamics. The FEN/RAPA-loaded mPEG-b-PCL micelles displayed higher encapsulation efficiency and drug loading capacity than the solution formulation. The encapsulated compounds were subsequently analysed by phase-contrast and fluorescent microscopy to identify morphological changes associated with apoptosis and autophagy. The mPEG-b-PCL nanoparticles were also evaluated for their biodistribution in vivo using an in vivo mouse model. The mice received either the FEN solution or the FEN/RAPA-loaded micelles intravenously, and their lungs were analysed for RAPA accumulation. It is a chemotherapeutic agent Cancer is a leading cause of death worldwide and is responsible for considerable economic losses. Benzimidazole compounds, which are commonly used as antihelmintic agents, have been repurposed to target cancer and have promising results in various human cancer models. However, overcoming the resistance to conventional therapy is still a challenge. To overcome this, fenbendazole was tested as a potent chemotherapeutic agent in 5-fluorouracil resistant colorectal cancer cells. It was found to inhibit cell viability by disrupting microtubule dynamics and activating p53. It also down regulates GLUT transporters and hexokinase, which are key glycolytic enzymes in cancer cells. Oral administration of fenbendazole resulted in a significant reduction in tumor size and weight in A549 xenograft mice. This effect was mediated by a decrease in tumor vascularity, as assessed by spectrophotometrically measuring hemoglobin content in tumours (Fig. 9). Moreover, fenbendazole was shown to have synergistic effects in combination with the microtubule targeting drug taxol and the glycolytic inhibitor dichloroacetate (DCA) that shifts glucose metabolism towards oxidation over glycolysis. It is a hepatotoxic agent Fenbendazole is a benzimidazole-based anthelmintic that displays antiparasitic activity in mammals. It binds to the -tubulin complex and inhibits microtubule polymerization. It also interferes with the energy metabolism of cancer cells by blocking glucose uptake. It is known that many malignant cells use glucose more than normal cells, so limiting their access to energy could lead to tumor cell death. The hepatotoxicity of fenbendazole is related to its effect on the mitochondrial enzyme fumarate reductase. This enzyme converts succinate to fumarate in lower organisms and to pyruvate in mammalian mitochondria. Succinate dehydrogenase is a known tumour suppressor gene that is downregulated in human cancer cells. It is also possible that hepatotoxicity of fenbendazole may be mediated by an imbalance in the redox status of the liver. A recent study demonstrated that fenbendazole suppresses the growth of human lung cancer xenografts in athymic mice. The drug inhibits hepatic phase I biotransformation reactions and reduces the expression of genes involved in RAS-related pathways.fenben for cancer

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