Fenbendazole Cancer Treatment

The anthelmintic drug fenbendazole has been shown to inhibit the growth of colorectal cancer cells. It also increases the cytotoxic effects of radiation and other antineoplastic agents. However, it is not widely used in combination regimens. Intensive doses of fenbendazole were toxic to EMT6 cells in vitro, and long incubations reduced their survival.

It is a broad spectrum anti-parasitic drug

Fenben, or benzimidazole carbamate, is a broad spectrum anti-parasitic drug that was first used to deworm animals. It has been shown to inhibit the growth of cancer cells in culture and animal models. It also prevents the formation of microtubules, which help cancer cells to survive. It also interferes with the uptake of glucose in cancer cells and can promote apoptosis.

Researchers have discovered that fenben may also slow the progression of pancreatic cancer in mice. The drug works by targeting tubulin, which is a protein that acts as a highway for transport and a micro-skeleton. It then collapses tubulin, starving the parasite to death.

While fenben has shown promise as a treatment for human cancer, there isn’t enough evidence from peer-reviewed studies that it can cure the disease. Furthermore, it is not approved by Health Canada to be sold as a cancer treatment. However, research into anthelmintic drugs is continuing. In 2022, a study published in Scientific Reports observed that mebendazole, another antiparasitic drug, could reduce breast cancer cell proliferation.

It is a microtubule interfering agent

Fenbendazole is a dog wormer that appears to have a powerful effect on cancer cells. This molecule blocks the growth of microtubules, which provide structure to all cells. It also interferes with glucose metabolism, which leads to cell death. The benzimidazole compound binds to the colchicine binding site of tubulin and blocks its polymerization. This action is similar to those of the vinca alkaloids and taxanes, but has lower toxicity. It can also overcome multidrug resistance caused by the overexpression of b-tubulin isoforms and mutations21.

The moderate microtubule destabilizing activity of MBZ can be exploited in combination with other anti-cancer agents. Its effect in combination with paclitaxel is synergistic, and it has been shown to prevent the formation of unattached kinetochores in mitosis. It also inhibits glycolysis and enhances oxidative phosphorylation by blocking the hexokinase II enzyme. Glucose uptake is elevated in many cancer cells, and inhibition of this pathway can be an effective strategy to curb tumor growth.

It is a p53 activator

Fenbendazole is a commonly used antiparasitic drug that has been shown to have an anticancer effect in vitro. However, the biological mechanisms behind this phenomenon are not fully understood. This is mainly because of the complexity of cell growth and different nutritional compositions and densities within the culture medium.

In addition to the moderate microtubule disruption, fenbendazole has been shown to stabilize WT p53 and interfere with cancer cells’ glucose metabolism. The resulting preferential elimination of cancer cells in vivo and in vitro has been linked to several factors, including the inhibition of autophagy and ferroptosis.

To test the effectiveness of fenbendazole, researchers treated human non-small cell lung cancer cells with it and analysed the cells with immunofluorescence technique. They found that fenbendazole causes partial alteration of the microtubule network around the cell nucleus, which is correlated with enhanced cell death-inducing activity. It also decreases the expression of Glut-4 transporters and hexokinase II, which are key glycolytic enzymes. This leads to an increase in DAMP, which is a crucial trigger for ferroptosis-augmented apoptosis.

It inhibits glucose uptake

Researchers studied the effect of fenbendazole on the growth of non-small cell lung cancer (NSCLC) cells and found that it inhibited the proliferation of these cells by altering microtubule dynamics. It also induced the apoptosis of these cells. These effects were attributed to the disruption of microtubules, activation of p53 and interference with glucose uptake and glycolysis.

Benzimidazole compounds interfere with energy metabolism by blocking the uptake of glucose and decreasing intracellular ATP levels. This enables them to depress drug efflux systems and sensitize cancer cells to apoptosis.

To test the antitumor activity of fenbendazole, H4IIE cells were treated with varying concentrations of fenbendazole under different growth conditions. Increasing doses of fenbendazole inhibited the active growth of these cells and induced apoptosis-associated changes. In addition, fenbendazole decreased glucose uptake and glucose oxidation in the culture supernatants of these cells. This was caused by the inhibition of hexokinase II, a key glycolytic enzyme. fenben cancer treatment

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