ASF-006 sodium is a tetrapodal tryptophan derivative and an effective viral invasion inhibitor. It demonstrates potent antiviral activity against multiple SARS-CoV-2 Omicron variants but is ineffective against the SARS-CoV-2 ancestral strain [Wuhan-Hu-1]. ASF-006 sodium competitively inhibits the binding of the receptor-binding domain [RBD] to ACE2 through an allosteric mechanism. The IC50 values for inhibiting infections of Omicron BA.1, Omicron XBB.1.5, respiratory syncytial virus [RSV], and Ebola virus are 0.02 μM, 0.3 μM, 1.52 μM, and 0.2 μM, respectively. ASF-006 sodium also inhibits cell invasion by HIV and enterovirus A71.

ASF-006 sodium (20 μM) exhibits significant inhibitory effects on VSV pseudotyped infections with Omicron BA.2 or BA.4/5 variants, while showing no apparent cytotoxicity. It displays antiviral activity against various SARS-CoV-2 Omicron variants, but its effectiveness is limited against older strains (Wuhan-Hu-1) or distantly related coronaviruses (SARS-CoV). ASF-006 sodium also possesses strong antiviral activity against RSV-A, with IC50 values ranging from 0.05 to 0.2 μM in A549, HEp-2, or Vero cells. The compound shows no antiviral activity against VSV (Rhabdoviridae), Nipah virus, or Sindbis virus. ASF-006 sodium interacts with the S protein, disrupting its binding with the cell receptor ACE2. The binding affinity constants (K d) for ASF-006 sodium with RBDBA.1 and SBA.1 proteins are approximately 60 μM and 5 μM, respectively.

ASF-006 sodium (100 mg/kg, administered intranasally once daily for 3 consecutive days) reduced viral load in a mouse model infected with SARS-CoV-2 Omicron BA.1.