After seeing millions of people die from COVID-19, a new discovery has been found that could be the first long term treatment option to give patients suffering from COVID-19 a chance to fight it off, but how sure can we be that the treatment pill will work?
New data about an antiviral pill made by Merck with its partner Ridgeback Pharmaceuticals show that the treatment pill is not as stellar as first believed. The drug has drawbacks that could outweigh its potential to fight the coronavirus and keep people out of the hospital.
The U.S. Food and Drug Administration is now deciding whether to grant emergency use authorization for the drug called molnupiravir, after the agency’s advisory panel narrowly voted to recommend it on November 30. The drug was authorized to be of use in the United Kingdom on November 4, and if the FDA follows suit, it could wind up being just a temporary treatment. Some advisers have already urged the agency to be ready to withdraw the authorization as soon as something better comes along.
Finding an early treatment for COVID-19 hasn’t been easy due to the constant trial and error that scientists keep facing, so when the development of molnupiravir came out a lot of experts hailed it as they thought it could be a potential game changer for the pandemic. It would be utilized as a pill that could be given to people early in the infection, keep health care systems from being overwhelmed, and spare people at high risk from the most severe complications.
In a clinical trial, the drug showed early signs of preventing hospitalization and death from COVID-19 in people who are at high risk. In fact, the results were so promising — a 48 percent reduction in the relative risk of hospitalization or death — that the trial was stopped so that the drug might potentially reach the public earlier.
But on November 26, Merck announced in a news release that when all the available data from the trial was in, the reduction in relative risk fell to 30 percent against hospitalization and death compared with a placebo. The shift stemmed from an unexplained decrease in severe disease among people in the placebo group in the last part of the trial.
Overall, among the 709 people in the molnupiravir group, there were 48 hospitalizations and one death compared with 68 hospitalizations and nine deaths among the 699 people who got a placebo, dropping the effectiveness from the initial 48 percent to 30 percent.
Taking that lower-than-expected efficacy into account, the FDA’s antimicrobial drugs advisory committee came to a split 13–10 decision about whether the antiviral drug should be granted emergency use authorization, with experts on each side of the vote often agreeing with points made by the opposing side. The debate and vote reflected a storm of uncertainty about the drug’s efficacy and who should use it — the list of people who would not be eligible is far longer than those most experts would give the drug to. The panel also looked into whether the drug could lead to even more dangerous versions of the coronavirus, whether it can cause growth delays in children or mutations in human DNA, and other unanswered questions.
The antiviral pill works by making mutations in viral RNA so that viruses are rendered noninfectious and eventually stop replicating. Such mutations happen throughout the virus’s genetic instruction book, or genome.
Some of those mutations could land in the spike protein, which helps the coronavirus break into cells, or other proteins and make the virus more transmissible or more evasive to vaccines. As learned in AP Biology, the spike proteins enable the host cell to be taken over by the virus and multiply and infect the surrounding cells. The vaccine that is being administered to people all around the world contains the antibodies that you would get if you were to be infected with the COVID-19 virus, so that if you were to get the virus, your body would go into its secondary immune response. This is when the memory cells facilitate a faster, stronger and longer response to the same COVID-19 antigen. Getting the vaccine would protect your body from having a life threatening reaction to the virus. If there is a mutation that lands on the spike protein, then the vaccine will be of no use to people since that is a completely different makeup of the virus. That’s especially a fear if people don’t finish the full five-day course of the drug needed to render the virus inoperable, leading potentially to highly mutated new forms of the virus that could infect others.
Merck representatives said that possibility is unlikely, because after five days of taking even a half dose of the drug, infectious viruses were no longer detectable among study participants tested. In one study, the company found seven patients who had changes in the coronavirus’s spike protein after taking molnupiravir, but there was no evidence that the viruses spread to other people or affected the patient’s health.
Molnupiravir might also create mutations in human DNA, researchers say. The drug is a nucleoside analog — an artificial RNA building block that can mimic the bases cytosine and uracil. Some enzymes in human cells might convert those RNA subunits to a DNA building block, which may lead to mutations in human DNA, especially in rapidly reproducing cells, such as blood cells. How likely that is is an open question.
Still, there are no good remedies for people with mild to moderate COVID-19. As of November 30, more than 82,000 people in the United States are being diagnosed with COVID-19 each day and more than 800 die. Those numbers are expected to increase as case counts surge in some parts of the country. The new omicron variant might add fuel to that fire if it proves more contagious than the currently dominant delta variant.
So even with all of molnupiravir’s drawbacks, federal regulators might decide a 30 percent reduction in hospitalizations and deaths is worth giving the drug temporary authorization.
The drug might be helpful for “the right patient population, the right virus at the right time,” said Lindsey Baden, an infectious diseases doctor at Brigham and Women’s Hospital in Boston who chaired the FDA’s advisory committee. “To me that at least suggests there are populations where there may be benefit.”
But more studies need to be done to address concerns about the drug, he said. “It’s the absence of data that makes many of us uncomfortable.”
President Joe Biden said December 2 during remarks laying out a plan to combat the omicron variant that the government has secured a supply of the drugs and, if authorized, will distribute them similarly to vaccines.