TRUST THE SCIENCE: IVERMECTIN

Why it works for C-19 patients and beyond?

Ivermectin:

The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug - PMC (nih.gov) www.ncbi.nlm.nih.gov/pmc/articles/PMC5835698/

The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug - PMC (nih.gov) Am J Cancer Res. 2018; 8(2): 317–331. Published online 2018 Feb 1.

Ivermectin belongs to the group of avermectins (AVM), a series of 16-membered macrocyclic lactone compounds discovered in 1967, and FDA-approved for human use in 1987. It has been used by millions of people around the world exhibiting a wide margin of clinical safety. (...) ivermectin exerts antitumor effects in different types of cancer. In humans it is considered that ivermectin generates low levels of toxicity because its targets are confined within the CNS. Indeed, most patients treated with ivermectin have no side-effects other than those caused by the immune and inflammatory responses against the parasite, such as fever, pruritus, skin rashes and malaise, and when present, they appear within 24-48 h after treatment. Certainly, moderate symptoms such as arthralgia, dizziness, fever, skin edema, dyspnea and hypotension may be more related with the microfilarial load in the patient rather than with the intrinsic toxicity of ivermectin. Reports on cases of encephalopathy in patients co-infected with onchocerciasis and lymphatic filariasis after 48 h of treatment with ivermectin can be found in the literature, but it is believed that this adverse reaction is due to the obstruction of the microcirculation of the brain by the accumulation of dead or paralyzed parasites, which leads to brain embolism. In conclusion, the immense number of patients who have been treated with ivermectin shows that it is a safe and a well-tolerated drug.

Antitumor mechanisms of ivermectin. 1. Ivermectin inhibits the P-glycoprotein pump, that induces a multidrug phenotype in the cancer cell. 2. Ivermectin acts as an ionophore and up-regulates chloride channels to generate apoptosis and osmotic cell death. 3. By decreasing the function of the mitochondrial complex I, ivermectin limits the electronic movement in the oxidative phosphorylation pathway that stimulates oxygen consumption rate to generate ATP for the cell. Concomitantly there is a reduction in the phosphorylation levels of Akt, impacting in the mitochondrial biogenesis process. Furthermore, alterations in the mitochondrial machinery are related with increased levels of reactive oxygen species that damage DNA. 4. Ivermectin induces ICD through the stimulation of an ATP- and HMGB1-enriched microenvironment, which promotes inflammation. This drug also increases ATP sensitivity and calcium signals in P2X membranal receptors, particularly P2X4 and P2X7, to induce ATP-dependent immune responses. 5. Ivermectin promotes the poly-ubiquitination of the kinase PAK1, which directs it to degradation in the proteasome. Defective PAK1, in turn, inhibits the Akt/mTOR pathway. At the same time, ivermectin stimulates the expression of Beclin1 and Atg5, both related with induction of autophagy and reduces the function of the negative regulator of apoptosis Bcl-2. Together, this generates autophagy and apoptosis. 6. Ivermectin represses AXIN2, LGR5 and ASCL2, all of them positive regulators of WNT-TCF while promotes the repressor of the WNT signaling FILIP1L. Concomitantly, ivermectin promotes the expression of several IFN-related genes, such as IFIT1, IFIT2, IF144, ISG20, IRF9 and OASL. 7. Ivermectin modifies the epigenetic signature and the self-renewal activity in the malignant cell due to its ability to mimic the SIN3-interaction that binds to the PAH2 motif of the cancer-associated deregulators SIN3A and SIN3B. SIN3A naturally induces NANOG and SOX2, which are stimulants of stem cell pluripotency. 8. Ivermectin limits the function of the RNA helicases NS3 and DDX23, both of which are related with ribosome biogenesis and post-transcriptional modifications, as well as with mRNA degradation. DDX23 acts as a promoter of miR-21, which is a well-recognized stimulator of tumor progression. 9. Ivermectin inhibitis preferentially the CSC population and up-regulates pluripotency and self-renewal genes NANOG, SOX2 and OCT4. IVM: ivermectin; ATP: adenosine triphosphate; OCR: oxygen consumption rate; ROS: reactive oxygen species.

This is exactly WHY Ivermectin works for Covid patients and for vaccine injuries.

I will address it in a separate post, but both Covid and vaccine injuries are caused by OXIDATIVE STRESS and ACUTE OXIDATIVE STRESS.

IF THIS IS REALLY ABOUT THE VIRUS, REGULATORY AGENCIES PLEASE EXPLAIN WHAT’S WRONG WITH IVERMECTIN?

Studies Show Zinc Inhibits Viral Replication, but There's a Catch (prnewswire.com) www.prnewswire.com/news-releases/studies-show-zinc-inhibits-viral-replication-but-theres-a-catch-301079772.html

One major function of zinc to human is its ability to boost the body's immunity and fight viruses. Studies show that zinc can block the replication and growth of viruses in the body and in lab tests. In the body, zinc improves the actions of immune cells like Neutrophils, T cells, B cells and NK that act as the police of the body, which attack infections. Zinc has a vital role in human health. Several studies showed that Zinc and Hinokitiol can repress viruses in the body, and in the lab. Consequently, Zinc and Hinokitiol supplements are useful in treating viral infections.

ZINC IONOPHORES Zinc is found and operates in every cell of the body, but it's a non-fat-soluble mineral that can't move through the fat-based cell membrane. Therefore, it needs help to cross the cell membrane from special transport systems. These systems include zinc ionophore and zinc binding-proteins. The zinc binding proteins are located in all membranes of every cell of the body for efficient inflow and outflow of zinc in the cells. Ionophore is a fat-soluble substance that can transport non-fat soluble elements across the cell membrane. Zinc-ionophores are zinc transporters in and out of the cell and can increase the effects of zinc in the cell. For example, Hinokitiol, a natural substance found in the Cupressaceae trees is a potent zinc-ionophore. It's known for its antimicrobial, antiviral and anticancer properties and it's regarded as the safest zinc ionophores compared to other ionophores like hydroxychloroquine, quercetin, epigallocatechin, pyrithione, zincophorin, etc. Hinokitiol doesn't accumulate in the body and it has no recorded drug allergy or unfavorable effects, unlike hydroxychloroquine. Conclusion: Zinc has a vital role in human health. Several studies showed that Zinc and Hinokitiol can repress viruses in the body, and in the lab. Consequently, Zinc and Hinokitiol supplements are useful in treating viral infections.

Ivermectin as an ionophore drug

The term ‘ionophore’ was first used in 1967 in reference of the ability of organic molecules to bind metal cations and to form lipid soluble complexes that facilitate their transport across cellular membranes. Thus, ionophores can diffuse back and forth between the extracellular and intracellular spaces, or may remain in the plasma membrane as their transport metal ions between intracellular and extracellular spaces.

*Of note, ivermectin significantly increased intracellular ROS and 8-OHdG levels, suggesting that the antitumoral effects of ivermectin are related to oxidative stress and DNA damage. This was confirmed by the abolition of the inhibitory effect of ivermectin in these renal cancer cell lines when co-treated with acetyl-L-carnitine (ALCAR) or N-acetyl-L-cysteine (NAC), a stimulant of mitochondrial biogenesis and an antioxidant, respectively

Oxidative stress and antioxidants are keywords.