| MDL | MFCD03142961 |
|---|---|
| Molecular Weight | 380.42 |
| Molecular Formula | C20H16N2O4S |
| SMILES | O=C(NC1=CC=CC=C1OC)C2=CC=CC=C2SC3=CC=C([N+]([O-])=O)C=C3 |
IC50: 6 μM (nonpermissive H9 cell) [1]
RN-18 and RN-19 exhibits potent antiviral activity in the nonpermissive H9 and CEM cells but not in MT4 or CEM-SS cells, confirming that the antiviral activity was Vif specific. RN-18 shows the greater potency (IC 50 =4.5 μM in CEM cells) and specificity (IC 50 >100 μM in MT4 cells) among the two compounds [1] . In the presence of the inhibitor, RN-18, reverse transcriptase activity in the nonpermissive H9 and CEM cells decreases substantially and in a dose-dependent manner. RN-18 also exhibits antiviral activity in CEM-SS modified to stably express A3G but does not exhibit antiviral activity in the parental CEM-SS cell line. RN-18 antagonizes Vif function and inhibits HIV-1 replication only in the presence of A3G. RN-18 increases cellular A3G levels in a Vif-dependent manner and increases A3G incorporation into virions without inhibiting general proteasome-mediated protein degradation. RN-18 enhances Vif degradation only in the presence of A3G, reduces viral infectivity by increasing A3G incorporation into virions and enhances cytidine deamination of the viral genome [2] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Solid
Room temperature in continental US; may vary elsewhere.
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
DMSO : 100 mg/mL ( 262.87 mM ; Need ultrasonic)
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 2.6287 mL | 13.1434 mL | 26.2867 mL |
| 5 mM | 0.5257 mL | 2.6287 mL | 5.2573 mL |
| 10 mM | 0.2629 mL | 1.3143 mL | 2.6287 mL |