ICD-10 Specific code U04: Severe acute respiratory syndrome [SARS]

Bamlanivimab is a recombinant, neutralizing human IgG1 monoclonal antibody (mAb) directed against the spike protein of SARS-CoV-2. It is designed to block viral attachment and entry into human cells, thus neutralizing the virus, potentially treating COVID-19.

Bamlanivimab is a recombinant neutralizing human IgG1_K monoclonal antibody (mAb) to the spike protein of SARS-CoV-2 and is unmodified in the Fc region. Etesevimab is a recombinant neutralizing human IgG1_K mAb to the spike protein of SARS-CoV-2, with amino acid substitutions in the Fc region (L234A, L235A) to reduce effector function. Bamlanivimab and etesevimab bind to different but overlapping epitopes in the receptor binding domain (RBD) of the S-protein. Using both antibodies together is expected to reduce the risk of viral resistance.

Casirivimab (IgG1κ) and imdevimab (IgG1λ) are two recombinant human monoclonal antibodies which are unmodified in the Fc regions. Casirivimab and imdevimab bind to non-overlapping epitopes of the spike protein receptor binding domain (RBD) of SARS-CoV-2. This prevents RBD binding to the human ACE2 receptor, so preventing virus entry into cells.

Minocycline is a semi-synthetic derivative of tetracycline. Minocycline inhibits protein synthesis in susceptible bacteria. In common with other tetracyclines it is primarily bacteriostatic and has a similar spectrum of activity to other tetracyclines.

Molnupiravir is indicated for treatment of mild to moderate coronavirus disease 2019 (COVID-19) in adults with a positive SARS-COV-2 diagnostic test and who have at least one risk factor for developing severe illness. Molnupiravir is a prodrug that is metabolised to the ribonucleoside analogue N-hydroxycytidine (NHC) which distributes into cells where it is phosphorylated to form the pharmacologically active ribonucleoside triphosphate (NHC-TP).

Nirmatrelvir in combination with ritonavir is indicated for the treatment of coronavirus disease 2019 (COVID-19) in adults who do not require supplemental oxygen and who are at increased risk for progressing to severe COVID-19.

Nirmatrelvir is a peptidomimetic inhibitor of the SARS-CoV-2 main protease (Mpro), also referred to as 3C-like protease (3CLpro) or nsp5 protease. Inhibition of the SARS-CoV-2 Mpro leads to the prevention of viral replication. Ritonavir inhibits the CYP3A-mediated metabolism of nirmatrelvir, thereby providing increased plasma concentrations of nirmatrelvir.

Remdesivir is an adenosine nucleotide prodrug that is metabolized within host cells to form the pharmacologically active nucleoside triphosphate metabolite. Remdesivir triphosphate acts as an analog of adenosine triphosphate (ATP) and competes with the natural ATP substrate for incorporation into nascent RNA chains by the SARS-CoV-2 RNA-dependent RNA polymerase, which results in delayed chain termination during replication of the viral RNA. As an additional mechanism, remdesivir triphosphate can also inhibit viral RNA synthesis following its incorporation into the template viral RNA as a result of read-through by the viral polymerase that may occur in the presence of higher nucleotide concentrations.

Sotrovimab is a dual action, engineered human IgG1 mAb that binds to a conserved epitope on the spike protein receptor binding domain of SARS-CoV-2. It is used for the treatment of symptomatic adults and adolescents with acute covid-19 infection who do not require oxygen supplementation and who are at increased risk of progressing to severe covid infection.

Tixagevimab and cilgavimab are two recombinant human IgG1 monoclonal antibodies, with amino acid substitutions in the Fc regions, to extend antibody half-life and to reduce antibody effector function and potential risk of antibody-dependent enhancement of disease. Tixagevimab and cilgavimab can simultaneously bind to non-overlapping regions of the spike protein receptor binding domain (RBD) of SARS-CoV-2. Tixagevimab, cilgavimab and their combination bind to spike blocking its interaction with the human ACE2 receptor, resulting in a blockade of virus entry.