Is Fenbendazole For Cancer Safe

Fenbendazole, a dog wormer ingredient, has been shown to inhibit cancer cells in the lab and in mice. However, there isn’t enough evidence that it can actually cure cancer in humans or be safe to use.

There are plenty of drugs out there that work by killing cancer cells, but it can take years to develop a new drug. This can make it difficult to find one that is safe and effective.

Anticancer Activity

Fenbendazole is an effective anthelmintic that works by blocking the ability of worms to produce energy. It is effective against a variety of helminth parasites, including roundworms, hookworms and whipworms.

In animal models, fenbendazole inhibited growth of EMT6 tumors in BALB/c mice. Fenbendazole was given either in the diet or as three daily i.p. injections at a dose of 50 mg/kg/day.

Benzimidazole antihelminthics have also been shown to block the growth of human breast cancer cells and other tumors by targeting microtubules, which are organelles that regulate cell cycle progression and the movement of nutrients throughout the body.

This activity appears to be mediated through a cellular response to hypoxia, which may account for the ability of this anthelmintic to kill cancer cells by reducing their survival rate in vivo and inhibiting tumor growth in laboratory cultures. Despite the potential anticancer properties of this drug, further testing is needed to evaluate its use as an anticancer agent in humans.

Moderate Microtubule Disruption

The microtubules (MTs) are one of the important targets of many widely used anticancer drugs. They are involved in cell proliferation, cell division, the intercellular transport of organelles, and the maintenance of cells’ shape and structure. These molecules are a major target for benzimidazole carbamates, which inhibit tubulin polymerization and disrupt MTs primarily.

Fenbendazole is an anthelmintic drug which is effective against parasitic worms due to its ability to inhibit tubulin polymerization and promote MT disruption in parasite cells. It also blocks glucose uptake and negatively affects energy management in worms.

In order to further assess the fenbendazole for cancer activity of fenbendazole, researchers treated cancer cells with the drug and analysed them using immunofluorescence techniques. They found that the drug caused partial alteration of the microtubule network around the nucleus and promoted cell death in tumor cells.

In addition, fenbendazole inhibited the growth of a colorectal cancer cell line in a mouse model by causing apoptosis and cell cycle arrest at G2/M phase. Moreover, it was observed that fenbendazole increased the levels of necroptosis-related proteins, including phospho-receptor-interacting protein kinase (pRIP), RIP3, and phosphor-mixed lineage kinase domain-like protein (MLKL).

Stabilization of WT p53

p53 is responsible for three functions in cancer cells: growth arrest, DNA repair and apoptosis (cell death). The growth arrest function prevents the proliferation of cancer cells in response to environmental stress signals. The DNA repair function helps rewrite damaged DNA and protect against replication defects. The apoptosis function kills cancer cells and also prevents their formation of new tumors.

Fenbendazole induced p53 activation in SNU-C5 cells and apoptosis in SNU-C5/5-FUR cells without changing the expression of LC3, Atg7, and active caspase-8. In addition, fenbendazole induced ferroptosis by suppressing the expression of GPX4, SLC7A11 and Atg11.

Recently, Tal’s group selected short peptide aptamers that can bind to mutant p53, but not wt p53. These peptides were found to inhibit p53 transcriptional activity and promote selective apoptotic death of cancer cells carrying mutant p53, and decreased the growth of human cell line-derived mouse xenograft tumors representing several highly aggressive cancer types [112].

Interference with Cancer Cells’ Glucose Metabolism

Fenbendazole is a drug used in dog wormers, but there aren’t any clinical trials that show it’s safe or effective for treating human cancer. It does, however, appear to interfere with cancer cells’ glucose metabolism – a process that helps cells obtain ATP.

The interference with glucose metabolism has been seen in many cancers, such as non-small cell lung cancer (NSCLC), melanoma, breast cancer and leukemia. This is because cancer cells re-program many of their glucose metabolism reactions into glycolysis – a process that provides fewer ATP molecules than oxidative phosphorylation.

Therefore, a cancer cell needs more glucose than normal cells to make up for this ineffective glucose conversion process. This can be seen on a positron emission tomography (PET) machine, which detects the presence of fluorodeoxyglucose in the tumor.

The anticancer effects of fenbendazole have been found to be moderate, with minimal toxicity in animal studies. It acts through moderate microtubule disruption, p53 stabilization and interference with glucose metabolism to preferentially kill cancer cells in both cell culture and in vivo.

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