Retrocyclin-101

Retrocyclin-101 (50 μM; 1 h) inhibits the infection of H1299 cells by SARS-CoV-2 spike protein-pseudotyped lentivirus, but this effect is only observed when it is pre-incubated with viral particles (no such effect occurs when pre-incubated with cells), and serum abrogates this effect^[1].
Retrocyclin-101 (0.5-5 μM; 1 h) inhibits the binding of recombinant prefusion-stabilized SARS-CoV-2 spike protein to ACE2 in a concentration-dependent manner, and reduces the binding rate to approximately 25% of that in the control group at 5 μM after pre-incubation at 37°C^[1].
Retrocyclin-101 (3-50 μM; 1-24 h) inhibits natural SARS-CoV-2 infection in Vero E6 cells; its IC₅₀ is 29 μM without pre-incubation with the virus; when pre-incubated with the virus for 1 h under serum-free conditions, it exerts strong inhibitory activity at a concentration of 50 μM^[1].
Retrocyclin-101 (0-50 μM; 47 h) potently inhibits ZIKV PRVABC59 infection in Vero cells, with an IC₅₀ of 7.033 μM^[2].
Retrocyclin-101 (0-50 μM; 71 h) inhibits ZIKV MR766 infection in Vero cells, with an IC₅₀ of 15.58 μM^[2].
Retrocyclin-101 (0-100 μM) significantly reduces the viral titers of ZIKV PRVABC59 and MR766 in Vero cells and U251 glioma cells in a dose-dependent manner^[2].
Retrocyclin-101 (40 μM; 48-72 h) inhibits infections by ZIKV PRVABC59 and MR766 in Vero cells during the viral entry and replication stages, but does not act through direct virucidal activity or blocking cellular receptors^[2].
Retrocyclin-101 (25-50 μM; 50 h) inhibits ZIKV replication in BHK-21 cells but has no effect on the translation of initial replicon RNA^[2].
Retrocyclin-101 (0-50 μM; 24 h) inhibits the activity of JEV NS2B-NS3 serine protease in BHK-21 cells, reduces the expression level of NS3 and increases the content of unprocessed polyprotein precursors at lower concentrations^[2].
Retrocyclin-101 (0-50 μM; 24 h) inhibits JEV AT31 infection in BHK-21 and U251 cells, with an IC₅₀ of 10.67 μM^[2].
Retrocyclin-101 (50 μM; 24 h) inhibits wild-type (WT), N154A, H144A, and Q258A strains of JEV in BHK-21 cells, whereas the DE mutant and T410A JEV strains are resistant to RC-101^[2].
Retrocyclin-101 can be cleaved from its GFP fusion partner in vitro by Factor Xa protease; partial cleavage occurs naturally in chloroplast extracts of plastid-transformed tobacco due to endogenous Factor Xa-like activity^[3].
Retrocyclin-101 (2.5-20 μM; 16 h) potently inhibits the growth of Staphylococcus aureus nasal colonizing strains D20-7, D535-6, D30 and clinical strain USA300 in a concentration-dependent manner; specifically, at a concentration of 20 μM, the growth inhibition duration of nasal colonizing strains exceeds 10 h, and that of USA300 reaches 5 h^[4].
Retrocyclin-101 (2.5-10 μM; 0.25-9 h) is a rapidly acting, concentration-dependent bactericide active against Staphylococcus aureus nasal carriage strains D20-7, D535-6, D30 and clinical strain USA300; it achieves complete growth inhibition within 30 min at 10 μM and retains activity even against high bacterial inocula^[4].
Retrocyclin-101 (1-10 μg/tissue; 9 h) inhibits the adhesion and survival of Staphylococcus aureus nasal colonization strains D20-7, D535-6, D30 and clinical strain USA300 on human nasal epithelial cells (RPMI 2650), with 10 μg/tissue completely blocking bacterial adhesion^[4].
Retrocyclin-101 (4-20 μg/tissue; 9 h) completely inhibits the adhesion of S. aureus nasal colonization strain D20-7 to organotypic human airway epithelium at a concentration of 20 μg/tissue^[4].
Retrocyclin-101 (30 μg/mL; 30-60 min) inhibits TRIF- and MyD88-dependent TLR4-mediated proinflammatory cytokine gene expression in human monocyte-derived macrophages^[5].

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