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A Short Introduction To Fenbendazole

Fenbendazole, which goes by the names of Fenben or Panacur, is an anthelmintic (anti-parasite) drug based on benzimidazole that was discovered in 1974. It has since been widely employed around the world.

In the last few decades, there has been a remarkable impression made by Fenbendazole and other anti-tumor medications.

Rumors have it that this approved canine dewormer may be taken as an extra anti-cancer therapy due to the discoveries. Drugs such as taxols and vinca alkaloids belonging to the benzimidazole class are similar to many currently used chemotherapy treatments. However, currently existing toxicology information shows that humans could take fenbendazole orally without issue.

Fenbendazole powder usually comes in a powered form with a pale color and is not soluble in water.

This medication is not effectively absorbed by the digestive tract. Eating with it can improve absorption.

What is the mechanism of action for fenbendazole?

The main purpose of the anti-parasite drug fenbendazole is to stop parasites from forming microtubules by connecting them to the tubulin molecule. This blocks the combination of tubulin dimers to form bigger molecules in parasite cells, leading to the death of the parasites.

Despite appearing to be equally effective against tumor cells, it is unexpected that fenbendazole and other benzimidazoles can produce the same results. Fenbendazole is predicted to act in three distinct ways to combat cancer: by modifying immunity, antioxidative effects, and changing the metabolism.

The drug’s capacity to lead to apoptosis is regarded as the possible anti-cancer activity. Its response with -tubulin, which prevents the progression of cell cycle and causes cell death, is likely to be the main factor.

Research has demonstrated that benzimidazole carbamates impede the process in which tubulin forms microtubules in both parasitic worms and cancerous human cells.

Cancer cells consume glucose at an incredibly high rate, due to the Warburg effect, which means they absorb sugar two hundred times faster than normal cells. By utilizing positron emission tomography scans, the metabolically active regions, which take up more radioactive sugar, are easily known and are usually assumed to denote malignant tumors or areas of inflammation; this can be seen.

Fenbendazole diminishes the occurrence of GLUT conduits (channels which transport glucose from the bloodstream to the cancer cells) and the enzyme Hexokinase II, thus weakening the capacity of cancer cells to utilize sugar as fuel. Additionally, Hexokinase II is essential for the survival of cancer cells, since it accelerates tumor development by producing additional sugar and augmenting lactic acidosis in the outer cellular matrix.

The reactivation of the protein p53 curbs cancer’s capacity to generate energy. After p53 correctly guides GLUT1 and GLUT4 transporters inside the cell, it controls their production and functioning (“glucose gates”).

The function of the p53 gene is reopened for debate, and further studies should be conducted to prove that fenben is responsible for this action.

Studies are increasingly finding that fenbendazole could potentially increase the activity of the greatest cancer-combating agent inside our bodies.

Elephants possess twenty copies of the p53 gene in their genetic structure, in contrast to humans who possess just one. This may be why elephants are less susceptible to cancer when compared to people. Despite having a larger body size, greater quantities of cells, and additional possibilities of genetic mutations, elephants still have a low level of genetic mutation.

Fenbendazole does not allow cancer cells to develop a resistance to chemotherapy treatments, nor can cancer cells adapt to this de-wormer medication. Regrettably, this is also true of many other chemotherapy and biological therapy medicines used to treat cancer.

Cancer cells have the ability to defend against certain drugs by using P-glycoproteins to expel them from the cells. However, fenbendazole is not affected by this mechanism, as it can’t be pushed out by P-glycoproteins, meaning that it remains inside the cells.

Consequently, tumors are unable to become resistant to fenbendazole like with paclitaxel, docetaxel, vinblastine, vincristine, and other chemotherapies. This in turn makes the drug remain effective and has the potential to obliterate cancer cells.

It has been demonstrated that fenbendazole increases susceptibility to radiation, meaning that radiation may be more effective in targeting tumour cells.

Fenbendazole has been found to be somewhat successful in disrupting microtubules, which then leads to the death of cancer cells.

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Jeff Campbell