Fenbendazole (commonly known as Fenben or Panacur) is an anthelmintic drug in the benzimidazole class. It was discovered in 1974 and has been widely used across the world since then. (Ref.)
Over the last few decades, fenbendazole and other related medications have been noted to possess decent anti-cancer qualities. (Ref.1, Ref.2)
As a result, it is being speculated that it can be used as complementary anticancer medicine in addition to being a registered dog dewormer. In reality, benzimidazole class drugs may have similar applications as many of the modern chemotherapeutic drugs including vinca alkaloids and taxols. (Ref). According to available toxicological information, humans seem to have a high tolerance to fenbendazole after ingesting orally, however, there is limited research on humans. (Ref).
In average conditions, pure fenbendazole takes a powdery form, is white in color, and is poorly soluble in water.
Reabsorption of the medication in the intestinal tract is low. Bioavailability improves when food is present in the gut.
How Does Fenbendazole Work?
The original purpose of Fenbendazole was to cure parasites through selective blocking of microtubules synthesis by forming bonds with β-tubulin. This causes the polymerization of tubulin dimers in the cells to stop, leading to the death of parasites.
Surprisingly, it may appear that fenbendazole and other benzimidazole affect tumor cells in a similar way. It is currently believed that fenbendazole kills cancer through 3 major techniques.
Apoptosis Induction: It is believed that the anti-tumor effect is a result of the interaction between the drug and the β-tubulin, which leads to the interruption of the cell cycle and cytotoxic.
There is sufficient documentation on how benzimidazole carbamates inhibit the polymerization of tubulin into microtubules. (Ref.1, Ref.2)
Inhibition of the Glucose Uptake by Cancer Cells: Malignant cells are notorious for their massive glucose uptake. Because of aerobic glycolysis (Walburg effect), the rate of glucose consumption by cancer cells is 200 times faster than average cells. This shows up in PET scans – the sites that are metabolically active and consume more radioactive glucose are seen clearly and are generally believed to be sites of inflammation and cancerous tumors.
Fenbendazole prevents the fueling of cancer cells by inhibiting the glucose intake, reducing the number of GLUT carriers (canals that transport glucose from the blood to the cancer cells), and the Hexokinase II enzyme. The latter is essential to the survival of cancer cells, helping the tumors thrive through the generation of sugar and acceleration of lactic acidosis in the extracellular matrix. (Ref.1, Ref.2)
In addition, reactivation of the protein p53 also prevents the production of fuel for cancer. As soon as p53 is reactivated, it limits the activity and expression of GLUT 1 and GLUT 4 carriers, also known as glucose gates, of the cell. (Ref.)
Reactivation of the p53 Gene: There is still some controversy concerning this work mechanism and more research is required to verify the effect of fenben as regards this.
However, more and more studies are emerging to confirm that fenbendazole may indeed increase the body’s most powerful tumor suppressors – p53. (Ref).
While humans only have 1 copy of the p53 gene, elephants are known to have 20 copies in their genome. Interestingly, this is why the occurrence of cancer in elephants is less than in humans, irrespective of the huge body size of these creatures, their higher number of cells, and a larger number of possible genetic mutations.
Cancer Cells are not Chemo-resistant to Fenbendazole: The interesting thing is that cancer cells cannot adapt to or evade the presence of this dewormer drug. Unfortunately, this is the case with many other biological therapies and chemotherapy medications.
The major mechanism of chemoresistance is the adaptation of cancer cells to expel the drugs out of themselves through specialized drug efflux pumps known as P-glycoproteins. P-glycoproteins do not target fenbendazole, hence, fenbendazole does not get expelled from cancer cells once it gets in.
Therefore, the tumors will not become resistant to fenbendazole. Fenbendazole maintains its effectiveness and has the ability to destroy cancer cells, unlike docetaxel, paclitaxel, vincristine, vinblastine, and other chemotherapies. (Ref.)
Fenbendazole May Sensitize Tumors to Radiotherapy: Fenbendazole may act in a similar way to chemotherapy agents belonging to the taxane group by sensitizing tumors to radiotherapy.
***Fenbendasole leads to the death of cancer cells by acting as a mild microtubule destabilizing agent. ***
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Read more:
Introduction to Fenbendazole
