Science
Following the Medical and Scientific Facts: A Look at Fenbendazole
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Nov 22, 2021 - 7:56:07 AM

(HealthNewsDigest.com) - By promoting the polymerization of tubulin, Fenbendazole can destabilize the microtubules of cancer cells. Research shows that Fenbendazole may bind to the tubulin just like colchicine does on the same part of the molecule. Fenbendazole affects microtubules in a much milder way than niclosamide the anti-cancer agent although Fenbendazole has a more severe effect than Taxol.

By inhibiting the cell cycle, Fenbendazole can inhibit the growth of cancer cells. The other mechanism through which Fenbendazole arrests cell cycle in mitotic phase of non-small cell lung cancer cells of A549 is yet unknown. This type of cell cycle diversity led to cancer cells dying by apoptosis molecular machinery.

Fenbendazole led to the expression of the most important tumor suppressor gene p53 while also activating the cyclin-dependent kinase protein p21 charged with regulating the cell cycle. These efefeoare are responsible for the apoptosis of cancer cells. This cell-killing mechanism (which is cancer-characteristic – which means it stops the cell cycle of precancerous cells, making them apoptotic) is believed to effects and kill more brutally than normal cells (see fig. 2)

Nearly all the official microtubules inhibiting chemotherapy including docetaxel, vincristine, paclitaxel, and vinblastine are known to make cancer resistant to chemo. This phenomenon is a resultant effect of treating cancer with chemotherapy drugs leading to cancer’s ability to develop multiple resistance via alternate gene expression then synthesis machinery which fights chemotherapies and limits its effectiveness. The major chemoresistance mechanism is found at the point where cancer cells adapt to excrete drugs from themselves through a special drug efflux pump known as P-glycoproteins. Since Fenbendazole is not a substrate for P-glycoproteins, it cannot be excreted out of cancer cells once it is ingested. This is why the tumors and cancer cells are often unable to develop resistance against fenbendazole which is still able to kill cancer cells, unlike vincristine, docetaxel, and paclitaxel. Other Benzimidazole-related drugs may act the same way but that hasn’t been proven scientifically yet.

When it comes to parasites, Fenbendazole does not only function through the inhibition of cell cytoskeleton (active microtubules) instead it also works by inhibiting glucose uptake (a lot like Metformin in some instances)

Fenbendazole’s effect on lactate and glucose levels was tested due to the presumption. This led to the discovery of Fenbendazole’s ability to inhibit the uptake or consumption of glucose over 20 times what the normal treatment offers. (10µM concentration of  Fenbendazole)

The mechanics of this event is in the inhibition of glycolytic pathway enzymes GLUat-4 and Hexokinase II by Fenbendazole. The protein p53 discussed earlier also checks the growth of cancer by inhibiting the expression and activity of GLUT1 and GLUT4 „glucose gates“ of the cell. Naturally, the lactate levels were noticeably reduced. Experiments also showed that Febendazole powder works together with other notable anti-glycolytic molecules DCA (sodium dichloroacetate) and 2-DDG (2-deoxyglucose)

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