You: This is complete bullshit. Tons of money are being poured into drug candidates that may or may not treat certain types of cancers. Alzheimer's too.

Ivermectin, a potential anticancer drug derived from an antiparasitic drug - PMC

Ivermectin has powerful antitumor effects, including the inhibition of proliferation, metastasis, and angiogenic activity, in a variety of cancer cells. This may be related to the regulation of multiple signaling pathways by ivermectin through PAK1 kinase. On the other hand, ivermectin promotes programmed cancer cell death, including apoptosis, autophagy and pyroptosis. Ivermectin induces apoptosis and autophagy is mutually regulated. Interestingly, ivermectin can also inhibit tumor stem cells and reverse multidrug resistance and exerts the optimal effect when used in combination with other chemotherapy drugs.

Anticancer activity

The versatility of ivermectin continues to unfold, with much research on its role as a potential anticancer drug. It is postulated that ivermectin can inhibit tumorigenic cell proliferation through various pathways. Researchers first noted the anticancer effects of ivermectin in 2015 through its ability to induce autophagy in cancer cells [ 66]. Although autophagy can be a survival mechanism for cancer cells through which damaged organelles are removed and nutrients are recycled, it has recently been shown that autophagy can also be induced by agents that suppress cancer cells [ 67]. Various modes of action that support the theory that ivermectin induces apoptosis in certain cancers have recently been proposed [ 67- 70]. The potential roles of ivermectin in the management of different cancers have been explored. This includes breast cancer, gastric cancer, hepatocellular carcinoma, renal cell carcinoma, prostate cancer, leukemia, cervical cancer, ovarian cancer, glioblastoma, lung cancer, nasopharyngeal carcinoma, and melanoma [ 26]. The anticancer mechanism of ivermectin varies among cancers. Here, the postulated mode of action in breast cancer and glioblastoma is described. Overall, the anticancer effects of ivermectin are limited to the effects observed in human cell lines. Since this is a new horizon for ivermectin treatment, the literature evaluating this drug in human clinical trials is scarce.

Breast Cancer

Breast cancer is the leading cause of cancer among women worldwide [ 26]. One study revealed that after ivermectin treatment, breast cancer cell proliferation is significantly reduced in vitro and in vivo [ 67]. Ivermectin has been shown to inhibit the Akt/mTOR pathway, which induces autophagy in human breast cancer cell lines [ 26, 67]. It promotes the blockage of the Akt/mTOR pathway through ubiquitination-mediated degradation of p-21-activated kinase (PAK1) [ 67]. Targeting PAK1 by ivermectin may open its use in other cancers, as PAK1 is needed for growth in more than 70% of human cancers, including pancreatic, colon, prostate, and neurofibromatosis tumors in addition to breast cancer [ 71].

Triple-negative breast cancer, estrogen, progesterone, and human epidermal growth factor receptor 2 (HER2) negative carry the worst prognosis of breast cancer, as these are the most aggressive forms of breast cancer [ 26]. There is currently no known effective therapy to treat this subtype of cancer. Ivermectin has been shown to mimic the SIN-3 interaction domain (SID) to block the interaction between SID and the paired a- helix-2 [ 72]. Ivermectin has also been demonstrated to restore the sensitivity of triple-negative breast cancers to tamoxifen, a commonly used anticancer drug, by regulating the expression of the epithelial-mesenchymal transition (EMT)-related gene E-cadherin [ 72]. Given these promising findings, further investigations of the novel mechanisms of action of ivermectin in breast cancer are crucial. This could pave the way for its application as a therapeutic agent in the management of breast cancer.

Glioblastoma

Glioblastoma is one of the most lethal types of cerebral tumors, with a median survival time of 14-17 months [ 73]. Ivermectin has been shown to inhibit human glioblastoma cell proliferation in a dose-dependent manner [ 26]. Ivermectin can induce apoptosis in a caspase-dependent manner in these cells, which is related to the induction of mitochondrial dysfunction and oxidative stress [ 69]. Ivermectin inhibits angiogenesis by inducing apoptosis in human brain microvascular endothelial cells [ 69]. This allows ivermectin to prevent tumor angiogenesis and metastasis, which could be valuable anticancer effects. Ivermectin has also been demonstrated to inhibit the proliferation of these cells by blocking the Akt/mTOR pathway [ 69, 74]. However, because ivermectin cannot cross the blood-brain barrier, its possible use is limited in the treatment of human glioblastoma.

Ivermectin: A Multifaceted Drug With a Potential Beyond Anti-parasitic Therapy - PMC