Let's read what the FDA has to say... Why You Should Not Use Ivermectin to Treat or Prevent COVID-19 https://www.fda.gov/consumers/consu...-not-use-ivermectin-treat-or-prevent-covid-19 "Ivermectin is not an anti-viral (a drug for treating viruses)." This statement mirrors what the manufacturer, Merck, has stated.
sigh.... https://en.wikipedia.org/wiki/Ivermectin#Research https://en.wikipedia.org/wiki/Ivermectin#Tropical_diseases Although several clinical trials are now underway to test possible therapies, the worldwide response to the COVID-19 outbreak has been largely limited to monitoring/containment. We report here that Ivermectin, an FDA-approved anti-parasitic previously shown to have broad-spectrum anti-viral activity in vitro, is an inhibitor of the causative virus (SARS-CoV-2), with a single addition to Vero-hSLAM cells 2 h post infection with SARS-CoV-2 able to effect ~5000-fold reduction in viral RNA at 48 h. Ivermectin therefore warrants further investigation for possible benefits in humans. Targeting host responses to invading viruses has been the focus of recent antiviral research. Venezuelan Equine Encephalitis Virus (VEEV) is able to modulate host transcription and block nuclear trafficking at least partially due to its capsid protein forming a complex with the host proteins importin α/β1 and CRM1. We hypothesized that disrupting the interaction of capsid with importin α/β1 or the interaction of capsid with CRM1 would alter capsid localization, thereby lowering viral titers in vitro. siRNA mediated knockdown of importin α, importin β1, and CRM1 altered capsid localization, confirming their role in modulating capsid trafficking. Mifepristone and ivermectin, inhibitors of importin α/β-mediated import, were able to reduce nuclear-associated capsid, while leptomycin B, a potent CRM1 inhibitor, confined capsid to the nucleus. In addition to altering the level and distribution of capsid, the three inhibitors were able to reduce viral titers in a relevant mammalian cell line with varying degrees of efficacy. The inhibitors were also able to reduce the cytopathic effects associated with VEEV infection, hinting that nuclear import inhibitors may be protecting cells from apoptosis in addition to disrupting the function of an essential viral protein. Our results confirm that VEEV uses host importins and exportins during part of its life cycle. Further, it suggests that temporarily targeting host proteins that are hijacked for use by viruses is a viable antiviral therapy. © 2013 Elsevier B.V. All rights reserved. Infection by one of the 4 distinct serotypes of dengue virus (DENV) threatens >40% of the world's population, with no efficacious vaccine or antiviral agent currently available. DENV replication through the virus-encoded nonstructural protein (NS) 5 protein occurs in the infected cell cytoplasm, but NS5 from DENV2 has thus far been shown to localize strongly in the nucleus throughout infection. Here we use specific antibodies cross-reactive with NS5 from DENV1-4 to demonstrate nuclear localization of NS5 from all DENV serotypes for the first time in both infected as well as transfected cells, although to differing extents. The small-molecule inhibitor Ivermectin was inhibitory towards both DENV 1 and 2 NS5 interaction with its nuclear transporter importin α/β in vitro, and protected against infection from DENV1-4. Ivermectin thus has potential in the clinical setting as a dengue antiviral. © 2013 Elsevier B.V. The movement of proteins between the cytoplasm and nucleus mediated by the importin superfamily of proteins is essential to many cellular processes, including differentiation and development, and is critical to disease states such as viral disease and oncogenesis.We recently developed a high-throughput screen to identify specific and general inhibitors of protein nuclear import, from which ivermectin was identified as a potential inhibitor of importin α/β-mediated transport. In the present study, we characterized in detail the nuclear transport inhibitory properties of ivermectin, demonstrating that it is a broad-spectrum inhibitor of importin α/β nuclear import, with no effect on a range of other nuclear import pathways, including that mediated by importin β1 alone. Importantly, we establish for the first time that ivermectin has potent antiviral activity towards both HIV-1 and dengue virus, both of which are strongly reliant on importin α/βnuclear import, with respect to the HIV-1 integrase and NS5 (non-structural protein 5) polymerase proteins respectively. Ivermectin would appear to be an invaluable tool for the study of protein nuclear import, as well as the basis for future development of antiviral agents. © The Authors Journal compilation © 2012 Biochemical Society.
You do realize the material that you are quoting and placed in Wikipedia is taken from low quality non-peer reviewed studies put forward by anti-vaccine Ivermectin advocates. This is exactly the stuff mainstream scientists, regulatory agencies and the manufacturer have debunked.
sure, sure, russian trolls went years back in time and published those studies & quack doctors were doing research to push misinformation a month into the pandemic. https://www.abc.net.au/radionational/programs/healthreport/coronavirus-ivermectin-drug/12125192 https://research.monash.edu/en/projects/ivermectin-as-an-anti-viral-against-sars-cov-2 https://research.monash.edu/en/persons/kylie-wagstaff
Yeah, it's "invitro" all right. According to Trump, you just have to "in anal" it. Inject the bleach, and shove the UV light bulb up the ass.
I don’t need to call Merck, Big Pharma Bro. I can ask your wife, an executive at J&J …she will lie to me. Out of patent Antiparasitic agent with anti viral properties.
So why are all these magatards who are taking IVM dying then? Why the spike of deaths in magatard states?
Not to mention all the Trump supporters showing up at ERs with Ivermectin side-effects which are clogging up beds needed for Covid patients (who are over 99% unvaccinated).