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Source: Medical News - COVID-19 Drugs -Remdesivir  Aug 13, 2022  1 year, 6 months, 1 week, 5 days, 15 hours, 2 minutes ago

BREAKING! Japanese Study Finds U.S. FDA Approved And Promoted COVID-19 Drug Remdesivir Induces Cardiomyocyte Dysfunction And Is Cardiotoxic!

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BREAKING! Japanese Study Finds U.S. FDA Approved And Promoted COVID-19 Drug Remdesivir Induces Cardiomyocyte Dysfunction And Is Cardiotoxic!
Source: Medical News - COVID-19 Drugs -Remdesivir  Aug 13, 2022  1 year, 6 months, 1 week, 5 days, 15 hours, 2 minutes ago
COVID-19 Drugs: A new study by Japanese researchers from Tohoku University, Kyushu University, Okayama University and the National Institutes of Natural Sciences, Okazaki-Japan has alarmingly found that the U.S. FDA approved and heavily promoted drug for COVID-19 ie Remdesivir activates the urotensin II receptor and induces cardiomyocyte dysfunction that can lead to heart issues that can also end up with fatal outcomes! In simple terms, the American promoted COVID-19 drug is basically cardiotoxic!

Thailand Medical News had been sounding alerts about the dangers of this bogus drug that had many greedy American billionaires and politicians behind its fast approval despite lack of any substantial efficacy. Many unethical researchers and institutions were discreetly paid to come up with bogus studies to demonstrate its efficacy and when the actual clinical observations in hospitals were showing that it was not working, the people behind it started coming up with more bogus studies showing that it worked alongside with other drugs or treatments protocols. Dr Anthony Fauci and the U.S. NIH was basically behind the drug development and bogus studies and it is believed that Dr Fauci indirectly made undisclosed millions from the drug. All development cost, research cost and drug-purchase for use to treat COVID-19 was made possible by tax payers monies!,-lopinavir-and-interferon-have-no-effect-on-covid-19-mortality
& amp;nbsp;$3120-for-gilead%E2%80%99s-remdesivir,-price-war-in-india-has-led-prices-dropping-to-below-us$50,-now-dr-fauci-peddling-remdesivir-with-more-lies--1-06-million-americans-tested-pos
Many other stupid countries also followed suit and adopted Remdesivir into their COVID-19 treatment protocols despite any real substantial evidence of its efficacy.
Numerous cardiovascular (CV) side effects have been associated with remdesivir; however, the underlying molecular mechanism remains unknown.
The Japanese study team performed a large-scale G-protein-coupled receptor (GPCR) screening in combination with structural modeling and found that remdesivir is a selective agonist for urotensin-II receptor (UTS2R). Functionally, remdesivir treatment induced prolonged field potential in human induced pluripotent stem cell (iPS)-derived cardiomyocytes and reduced contractility in neonatal rat cardiomyocytes, both of which mirror the clinical pathology. Importantly, remdesivir-mediated cardiac malfunctions were effectively attenuated by antagonizing UTS2R signaling.
The COVID-19 Drugs study team also characterized the effect of 110 single-nucleotide variants (SNVs) in UTS2R gene reported in genome database and found four missense variants that show gain-of-function effects in the receptor sensitivity to remdesivir.
The study findings show a previously unknown mechanism underlying remdesivir-related CV events and that genetic variations of UTS2R gene can be a potential risk factor for CV events during remdesivir treatment, which collectively paves the way for a therapeutic opportunity to prevent such events in the future. Remdesivir‘s activity as a selective agonist of urotensin-II receptor underlies its known cardiotoxicity in anti-viral therapy.
The study findings were published on a preprint server and are currently being peer reviewed.
Many nucleoside analogs have been long used for designing antiviral drugs. Nucleoside analogs inhibit viral RNA-dependent RNA polymerase (RdRp). Several such analogs, such as remdesivir, favipiravir, and molnupiravir, have been approved to treat COVID-19 despite lack of real substantial proof of their efficacy and in fact most are extremely toxic.
The drug Remdesivir, is a modified adenosine analog, is rapidly converted to a mono-nucleoside form upon intravenous administration. Subsequently, it is metabolized by host enzymes to the active triphosphate state. The active drug is a selective and potent inhibitor of RdRp of many viruses. Initially used for treating the Ebola virus, remdesivir was fast-tracked and approved for COVID-19 amid the pandemic by the US.FDA with Dr Fauci’s influence.
Commonly reported adverse events with remdesivir usage initially include a rash, nausea, headache, and elevated transaminases.
However cardiovascular events such as bradycardia, hypertension, T-wave abnormality, and QT prolongation have been reported.
The drug is known to distribute to multiple tissues, including the heart; however, the mechanisms underlying the cardiovascular complications remain unknown.
The study team carried out a large-scale GPCR screening using the three anti-COVID-19 drugs. The nucleoside analogs were screened against 348 GPCRs in a transforming growth factor (TGF)-α shedding assay. Initially, screening was performed using Gα subunits for efficient detection of receptor activation.
The study team shockingly found that remdesivir selectively activated the urotensin II receptor (UTS2R).
Subsequent concentration-response analysis showed a half-maximal effective concentration (pEC50) of 4.89 for remdesivir, albeit lower than that of urotensin II, the endogenous ligand of UTS2R. Intriguingly, remdesivir did not induce a β-arrestin recruitment response, unlike urotensin II, and thus was a G-protein-biased ligand. The major and minor metabolites of remdesivir, GS-441524, and GS-704277, did not affect the activation of UTS2R.
Detailed further investigation revealed that receptor activation required both the nucleoside base and the McGuigan prodrug moiety of remdesivir.
In silico structural docking of UTS2R and remdesivir identified multiple residues in the orthosteric pocket, potentially stabilizing binding to remdesivir. Three residues of UTS2R (T304, N297, and M134) were found to interact with remdesivir. Substituting these residues with others abolished the activation potency of remdesivir.
Subsequently in the study, HEK293 cells expressing UTS2R were stimulated with remdesivir, and the phosphorylation of extracellular signal regulation kinase (ERK) 1/2 was examined.
Remdesivir treatment induced long-lasting phosphorylation of ERK1/2 in a dose-dependent manner. Remdesivir-mediated phosphorylation was abolished in the presence of a UTS2R antagonist.
Next, the impact of remdesivir on cardiomyocytes was assessed given the high expression of UTS2R and urotensin II in cardiovascular systems. The drug’s effect was analyzed on the field potential (FP) using human-induced pluripotent stem (iPS) cell-derived cardiomyocytes, in which UTS2R levels are comparable to that of the heart.
A thorough multielectrode assay showed that remdesivir-treated cells showed prolonged FP duration that was significantly suppressed in the presence of a UTS2R antagonist. The effects of the drug on cardiac contractility were assessed on neonatal rat cardiomyocytes (NRCMs). Chronic remdesivir application on NRCMs resulted in reduced contractility attenuated by UTS2R antagonist.
The study team then constructed 110 missense mutants corresponding to human single nucleotide variants (SNVs) in the UTS2R gene. Of these, 44 SNVs exhibited lower sensitivity to remdesivir relative to the wildtype receptor. In contrast, 47 SNVs had reduced sensitivity to urotensin II.
Importantly, four missense SNVs increased sensitivity to remdesivir relative to wildtype. Of these, two SNVs had lower sensitivity to urotensin II, while the other two had a moderate/insignificant increase in sensitivity to urotensin II. Individuals with these mutations might be more susceptible to remdesivir/UTS2R-mediated cardiotoxicity.
The research findings discovered that remdesivir selectively activated UTS2R. UTS2R activation by urotensin II has been implicated in cardiac dysfunction. As such, UTS2R activation by remdesivir in cultured cardiomyocytes induced electrical abnormalities and impaired contractility, resembling the reported cardiac events in humans. Notably, the adverse effects were negated by antagonizing UTS2R or blocking the downstream signaling.
The study findings suggested that the current recommended clinical dose of remdesivir was adequate to trigger UTS2R activation leading to cardiotoxicity.
The research findings provided mechanistic insights into remdesivir-mediated cardiac effects and discovered that it acts as a selective UTS2R agonist.
The drug is still being used in the United States, Europe, Australia and Japan!
Thailand Medical News strongly recommends that people who suspect that their loved ones had died due to remdesivir to start taking legal actions against stupid doctors and hospitals that used it and also against the drug regulatory agencies that approved it and also against the US. FDA and U.S. NIH.
People should stay away from whatever medical advice with regards to COVID-19 or Monkeypox that originates from the United States and in coming months, lots of stupid Americans will pay a price with their lives for listening to stupid directives coming from the U.S. CDC, U.S. FDA, U.S. NIH and various so called experts including the charlatans that can be found on twitter.
For the latest on COVID-19 Drugs, keep on logging to Thailand Medical News.


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