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Antiviral pill reduces the risk of hospitalization or death due to COVID-19 by 50%

At the time of the analysis, 7.3% of molnupiravir-treated patients were hospitalized or died by Day 29, compared to 14.1% of placebo-treated patients who were hospitalized or died in the same time frame.

Early data provided by drug manufacturer, Merck, shows that an at-home coronavirus tablet reduces the likelihood of those newly diagnosed with COVID-19 ending up in the hospital or dying.

In patients at high risk of developing serious illness, the tablet, an antiviral drug called molnupiravir, was compared to a placebo. Within 29 days of beginning the experiment, 14.1% of the 377 people who received the placebo, or 53 people, were hospitalized, with eight of them dying. In comparison, 7.3% of the 385 patients who received the medication, or 28, were admitted to the hospital over the same time period. Officials from the Merck declared in a news release on October 1st that no one had died. Side effects were reported by a similar number of people receiving the medication and those taking the placebo, although fewer people in the drug group discontinued taking it because of them. The adverse effects were not specified in the press release.

In the intermediate study, almost 40% of individuals were infected with the coronavirus gamma, delta, or mu strains. According to the firm, molnupiravir was just as efficient against those variants as it was against earlier forms of the virus. The study’s full results aren’t yet public, and the data hasn’t been evaluated by other scientists.

“Antiviral treatments that can be taken at home to keep people with COVID-19 out of the hospital are critically needed,” Wendy Holman, CEO of Ridgeback Biotherapeutics said in the news release. Ridgeback and Merck have teamed together to develop molnupiravir, and the two companies will split the profits.

The most intriguing element of the medication, according to Mark Denison, a virologist at Vanderbilt University Medical Center in Nashville, is that it may be administered as a tablet rather than an intravenous infusion like remdesivir. He was heavily involved in the early lab testing of molnupiravir.

The molnupiravir study’s interim results were so promising that an independent review panel opted to call the worldwide trial off early. Merck said it intends to file for emergency use authorization from the US Food and Drug Administration, as well as authorization from other nations.

“To stop a trial for futility is pretty common, when a drug isn’t working or when it’s showing a negative effect,” Denison says. “But to stop a trial because of efficacy, because the drug is working so well is really unusual. He adds, “I’m amazed but not surprised” that the antiviral performed well in humans. In his experiments with cells grown in lab dishes and in animal tests, “I was blown away by its effectiveness against multiple coronaviruses.”

Molnupiravir, like the FDA-approved antiviral remdesivir, mimics the genetic material of the coronavirus, RNA. The false building blocks obstruct the coronavirus’s ability to replicate its RNA via the polymerase enzyme. However, the two medicines act in distinct ways. Denison describes Remdesivir as a “delayed stop sign.” When it’s put into a developing strand of RNA, it slows the polymerase down until it grinds to a halt, much like a car entering a junction as the traffic light turns yellow could stop in the midst of the intersection, he adds.

Molnupiravir, on the other hand, pockmarks the RNA with many mutations, leading the polymerase and other viral components to break down, similar to how a pothole-strewn road may cause a car to break down. These mutant potholes not only prohibit the RNA-copying enzyme from working, but they also harm other proteins that the virus needs to invade and reproduce in cells.

The news release was published on October 1st, 2021.

The preliminary study was published in The Lancet, on March 31st, 2021.

Abstract. Antiviral therapy is urgently needed to combat the coronavirus disease 2019 (COVID-19) pandemic, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The protease inhibitor camostat mesylate inhibits SARS-CoV-2 infection of lung cells by blocking the virus-activating host cell protease TMPRSS2. Camostat mesylate has been approved for treatment of pancreatitis in Japan and is currently being repurposed for COVID-19 treatment. However, potential mechanisms of viral resistance as well as camostat mesylate metabolization and antiviral activity of metabolites are unclear. Here, we show that SARS-CoV-2 can employ TMPRSS2-related host cell proteases for activation and that several of them are expressed in viral target cells. However, entry mediated by these proteases was blocked by camostat mesylate. The camostat metabolite GBPA inhibited the activity of recombinant TMPRSS2 with reduced efficiency as compared to camostat mesylate and was rapidly generated in the presence of serum. Importantly, the infection experiments in which camostat mesylate was identified as a SARS-CoV-2 inhibitor involved preincubation of target cells with camostat mesylate in the presence of serum for 2 h and thus allowed conversion of camostat mesylate into GBPA. Indeed, when the antiviral activities of GBPA and camostat mesylate were compared in this setting, no major differences were identified. Our results indicate that use of TMPRSS2-related proteases for entry into target cells will not render SARS-CoV-2 camostat mesylate resistant. Moreover, the present and previous findings suggest that the peak concentrations of GBPA established after the clinically approved camostat mesylate dose (600 mg/day) will result in antiviral activity.

Camostat mesylate inhibits SARS-CoV-2 activation by TMPRSS2-related proteases and its metabolite GBPA exerts antiviral activity Markus Hoffmann, Heike Hofmann-Winkler, Joan C. Smith, Nadine Krüger, Lambert K. Sørensen, Ole S. Søgaard, Jørgen Bo Hasselstrøm, Michael Winkler, Tim Hempel, Lluís Raich, Simon Olsson, Takashi Yamazoe, Katsura Yamatsuta, Hirotaka Mizuno, Stephan Ludwig, Frank Noé, Jason M. Sheltzer, Mads Kjolby, Stefan Pöhlmann bioRxiv 2020.08.05.237651; doi:

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