Ivermectin- the new “old parasite” drug stops Covid 19 in the lab
An Australian study has published very encouraging results about the old veterinary drug Ivermectin against Covid19 in laboratory cells. Used as an anti-parasite drug in both animals and humans, it has also been proven to treat various cancers in humans. It has a high safety rating and numerous studies to back its currently FDA approved use against a variety of human cancers. It would need to be given clinically (to live humans) to determine the change, if any, in disease course for Covid19, but it looks good.
Coronavirus hope as drug prescribed for head lice ‘completely stops the deadly infection replicating in cells within 48 hours’. DailyMail.co.uk 5April20
…That’s based on the fact that SARS, a coronavirus closely related to the new one, has a weak link in its DNA which the team said could be a potential target for ivermectin.
Cells were infected with SARS-CoV-2, the scientific name designated to the novel coronavirus, for two hours.
Then ivermectin was injected. After 24 hours, there was a 93 per cent reduction of virus DNA in the cells compared to cells which were not treated with ivermectin…
‘This brief report raises the possibility that ivermectin could be a useful antiviral to limit SARS-CoV-2.’
The team suggested that until a drug is proven to be beneficial against COVID-19 in a clinical setting – which has not happened yet – ‘all should be pursued as rapidly as possible’.
Long history of safety in humans. Nobel Prize winning drug.
The 2015 Nobel Prize in Medicine went for discovery of Ivermectin, an “astonishingly safe” FDA approved anti-helminthic drug… Dr Sharmeen at the University of Toronto screened a library of 100 drugs for activity against a leukemic cell line, and reported Ivermectin as most promising, inducing leukemic cell death at low micromolar concentrations, while sparing normal cells. Ivermectin was also effective against leukemia mouse xenografts. Ivermectin was patented in 2012 for treating hematological malignancy. Dr Hashimoto reported in 2009, Ivermectin effective against ovarian cancer cell lines (14.)
Discovery and Synthesis
In 1970, microbiologist Satoshi Ōmura collected a soil sample from woods close to a golf course in Kawana, on the south east coast of Honshu, Japan . Ōmura isolated and cultured a Gram-positive bacterium, sample NRRL 8165–a then unknown species of Streptomyces, which was sent to William Campbell at Merck (along with 50 other strains of Streptomyces which were considered unusual in appearance or culture characteristics) to test for antiparasitic effects. NRRL 8165 cultures showed potent activity against Nematospiroides dubius (now known as Heligomosoides polygyrus) infection in mice, and the active components were purified, revealing a family of macrocyclic lactones. These naturally occurring compounds were named the avermectins (and the bacterium, Streptomyces avermitilis) to reflect the worm-free ‘averminous’ conditions they produced 7, 8.Mode of Action
How does it work?
While the efficacy of IVM in treating a broad spectrum of parasitic infections is well established, its mode of action is less clear. At nanomolar concentrations, IVM affects nematode motility, feeding, and reproduction and acts via ligand-gated chloride channels, specifically those gated by glutamate 31, 32. Glutamate-gated chloride channels (GluCls) are not present in vertebrates, and as such are thought to confer the broad safety margin of IVM. However, at micromolar concentrations, IVM can interact with a wider range of ligand-gated channels found in both invertebrates and vertebrates, including GABA, glycine, histamine, and nicotinic acetylcholine receptors (reviewed in )…
Ivermectin Promising Against Viral Pathogens
IVM has also shown promise in the treatment of certain viral pathogens. Consistent with the inhibition of RNA helicase DDX23 referred to above, IVM inhibits viral replication of several flaviviruses by blocking a viral helicase . Susceptible flaviviruses include those causing yellow fever, dengue, West Nile virus and tick borne encephalitis, and a patent application has been submitted for off-label antiflavivirus therapy in humans (patent application EP2010/065880). Encouragingly, serial passage of yellow fever virus with increasing concentrations of IVM did not appear to select for viral resistance, even after more than 30 passages over 6 months, leading the authors to conclude that adaptive mutations in the helicase domain may not be viable. In that study, no antiviral effect was detected in other genera of viruses, but inhibition of HIV-1 (and dengue) replication was reported after in vitro exposure to high concentrations (25–50 μM) of IVM. In this case, suppression of viral replication was thought to reflect disruption of viral protein trafficking between the host cell cytoplasm and nucleus by IVM inhibition of importin α/β-mediated transport .
Although IVM has a similar chemical structure to the macrolide antibiotics, it lacks activity against most bacteria. However, a number of studies have investigated IVM as an antimycobacterial agent, with varying degrees of success. One report described promising in vitroactivity of IVM against various species of Mycobacterium, including Mycobacterium tuberculosis, the causative agent of tuberculosis … In all studies, the in vitroantimycobacterial effects of IVM required significantly higher concentrations of drug than for antiparasiticeffects, but the dosage for in vivo efficacy remains to be established. The mode of action is unknown.
The FDA, CDC, WHO, etc. CANNOT dispute the safety of this drug in humans or its “other uses.” It’s a cheap drug used in veterinary medicine even today. Let’s hope someone in charge gets off their a**** and gets this out to the people since they’ve delayed and hamstrung chloroquine.
This is a very new paper from early March;
We show here that ivermectin’s broad spectrum antiviral activity relates to its ability to target the host importin (IMP) α/β1 nuclear transport proteins responsible for nuclear entry of cargoes such as integrase and NS5. We establish for the first time that ivermectin can dissociate the preformed IMPα/β1 heterodimer, as well as prevent its formation, through binding to the IMPα armadillo (ARM) repeat domain to impact IMPα thermal stability and α-helicity. We show that ivermectin inhibits NS5-IMPα interaction in a cell context using quantitative bimolecular fluorescence complementation. Finally, we show for the first time that ivermectin can limit infection by the DENV-related West Nile virus at low (μM) concentrations. Since it is FDA approved for parasitic indications, ivermectin merits closer consideration as a broad spectrum antiviral of interest.
Study title is misleading.
Ivermectin will fail in trial.
It was a false hope statement.
The podcast link attached, explains why it does not work