N-0385

N-0385 potently inhibits SARS-CoV-2 infection in human lung epithelial cells (IC₅₀ = 12.3 nM) and Calu-3 cells by targeting TMPRSS2^[1].
N-0385 (1 μM; 3 h pretreatment, 72 h VLP incubation) potently inhibits TMPRSS2-dependent entry of Omicron subvariant (BA.1, BA.2, BA.5) and pre-Omicron SARS-CoV-2 VLPs into human Calu-3 lung cells^[2].
N-0385 (3 h pretreatment, 48 h viral infection) exhibits broad-spectrum, low nanomolar antiviral activity against SARS-CoV-2 Omicron subvariants (BA.1, BA.2, BA.5, BQ.1.1, XBB.1.5, EG.5.1, BA.2.86) in human Calu-3 lung cells, with EC₅₀ values ranging from 2.0 nM to 29.1 nM^[2].
N-0385 (20 nM; 3 h pretreatment) robustly inhibits SARS-CoV-2 Omicron BA.5 infection in normal human bronchial epithelial cells, achieving 85.7% inhibition at a concentration of 20 nM^[2].
N-0385 (3 h pretreatment, 48 h viral infection) acts synergistically with Nirmatrelvir (HY-138687) and Remdesivir (HY-104077) to inhibit SARS-CoV-2 Omicron subvariants (BA.1, BA.2, BA.5) in human Calu-3 lung cells, with Loewe synergy scores ranging from 19.94 to 49.23^[2].
N-0385 forms tight, specific binding interactions with human ACE2, DPP4, IL-10, NLRP3, TLR7, and TMPRSS2 proteins via hydrogen bonding, hydrophobic interactions, ionic bonding, and pi-based interactions^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.