KHashmi316 Posted October 25, 2023 Report Share Posted October 25, 2023 (edited) Just heard about this .... seems to be the "Ivermectin" of cancer [Fenbendazole is a de-wormer, like Ivm]. Cheap, potentially highly effective, and generic anti-cancer treatment, with little side effects and quick action: https://aacrjournals.org/cancerres/article/82/12_Supplement/2313/701049/Abstract-2313-Fenbendazole-induces-cell-cycle Quote 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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3580766/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9437363/ https://aacrjournals.org/cancerres/article/82/12_Supplement/2313/701049/Abstract-2313-Fenbendazole-induces-cell-cycle https://en.wikipedia.org/wiki/Fenbendazole https://ar.iiarjournals.org/content/43/3/1207 Quote Background/Aim: An increasing number of studies are reporting anticancer activity of widely used antiparasitic drugs and particularly benzimidazoles. Fenbendazole is considered safe and tolerable in most animal species at the effective doses as an anthelmintic. Little is known about the redox-modulating properties of fenbendazole and the molecular mechanisms of its antiproliferative effects. Our study aimed to investigate the possibility of selective redox-mediated treatment of triple-negative breast cancer cells by fenbendazole without affecting the viability and redox status of normal breast epithelial cells. Materials and Methods: The experiments were performed on three cell lines: normal breast epithelial cells (MCF-10A) and cancer breast epithelial cells (MCF7 – luminal adenocarcinoma, low metastatic; MDA-MB-231 – triple-negative adenocarcinoma, highly metastatic). Cells were treated with fenbendazole for 48-h and three parameters were analyzed using conventional assays: cell viability and proliferation, level of intracellular superoxide, and level of hydroperoxides. Results: The data demonstrated that MDA-MB-231 cells were more vulnerable to fenbendazole-induced oxidative stress than MCF-7 cells. In normal breast epithelial cells MCF-10A, fenbendazole significantly suppressed oxidative stress compared to untreated controls. These data correlate with the effect of fenbendazole on cell viability and the IC50 values, which is indirect evidence of the potential targeting anticancer effect of the drug, especially in MDA-MB-231 cells. Conclusion: The difference in the levels of oxidative stress induced by fenbendazole in MDA-MB-231 and MCF-7 indicates that the two types of breast cancer respond to the drug through different redox-related mechanisms. https://www.nature.com/articles/s41598-018-30158-6 Quote Abstract Drugs that are already clinically approved or experimentally tested for conditions other than cancer, but are found to possess previously unrecognized cytotoxicity towards malignant cells, may serve as fitting anti-cancer candidates. Methyl N-(6-phenylsulfanyl-1H benzimidazol-2-yl) carbamate [Fenbendazole, FZ], a benzimidazole compound, is a safe and inexpensive anthelmintic drug possessing an efficient anti-proliferative activity. In our earlier work, we reported a potent growth-inhibitory activity of FZ caused partially by impairment of proteasomal function. Here, we show that FZ demonstrates 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, expression of GLUT transporters as well as hexokinase (HK II) - 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. The results, in conjunction with our earlier data, suggest that FZ is a new microtubule interfering agent that displays anti-neoplastic activity and may be evaluated as a potential therapeutic agent because of its effect on multiple cellular pathways leading to effective elimination of cancer cells. Edited October 25, 2023 by KHashmi316 Quote Link to comment Share on other sites More sharing options...
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