Molnupiavir was introduced in the early 2000s as preventative medicine and treatment against SARS-CoV, MERS, or other respiratory viruses. It is effective against many viruses that employ an RNA-dependent RNA polymerase, SARS-CoV-2 virus is also from the same class. The polymerase is an enzyme that copies the genetic material of the virus into new genetic material and produces the messenger RNAs that direct the production of all the viral proteins. Molnupiravir is a shape-shifter that is why it is called a tautomer. It has two forms, one which closely resembles uracil and the other cytosine. And, because of these two different forms, the replicating polymerase develops transition mutations, when it is recopied and causes the conversion of U nucleotide to C nucleotide and C nucleotide to U nucleotide. This newly copied RNA contains Molnupiravir that causes fatal flaws in the sequence and replication stops. This results in the shortening of infection and limiting the transmission.
In vitro studies revealed that Molnupiravir showed a dose-dependent drop in the production of viruses such as SARS-CoV-2. This is because the RdRp of SARS-CoV-2 and SARS-CoV, which the drug was initially intended to treat, have 99.1% nucleotide similarity. Whole-genome deep-sequencing showed dose-dependent accumulation of random low-frequency mutations. The effectiveness of the drug was rapid and intact upon repeat exposure of virus populations to the drug, which confirms that none of the random mutations’ mediate resistance to the drug.