| Stereochemistry | ACHIRAL |
| Molecular Formula | C22H30N6O2 |
| Molecular Weight | 410.5126 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCCOC1=NC2=C(NC(=O)CN2CC3=CC=CC(CN4CCCC4)=C3)C(N)=N1
InChI
InChIKey=VFOKSTCIRGDTBR-UHFFFAOYSA-N
InChI=1S/C22H30N6O2/c1-2-3-11-30-22-25-20(23)19-21(26-22)28(15-18(29)24-19)14-17-8-6-7-16(12-17)13-27-9-4-5-10-27/h6-8,12H,2-5,9-11,13-15H2,1H3,(H,24,29)(H2,23,25,26)
| Molecular Formula | C22H30N6O2 |
| Molecular Weight | 410.5126 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Vesatolimod, also known as GS-9620, is being developed in clinical studies for the treatment of chronic hepatitis B viral (HBV) infection, with the goal of inducing a liver-targeted antiviral effect without inducing the adverse effects associated with current systemic interferon-α (IFN-α) therapies. It is demonstrate interferon-stimulated gene induction without detectable serum interferon at low oral doses. GS-9620 is a potent and oral agonist of Toll-like receptor-7, a pattern-recognition receptor whose activation results in innate and adaptive immune stimulation
Originator
Approval Year
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
Drug as perpetrator
Drug as victim
Sourcing
PubMed
Patents
Sample Use Guides
1, 2, or 4 mg tablets administered orally every 7 days
Route of Administration:
Oral
The antiviral activity of GS-9620 was assessed in isolated macrophages, CD4+T cells and in total peripheral blood mononuclear cells (PBMCs) following infections with a replication component HIV-1BaL. In uninfected cultures, the viability of each cell type remained unchanged up to 10 μM GS-9620, the maximum concentration tested. GS-9620 was inactive against HIV in isolated CD4+ T cells and macrophages up to the highest concentration tested (10 µM), but did show dose-dependent inhibition of HIV-1 replication in complete PBMCs following infection with either HIV-1BaL (EC50 = 536 nM) or HIV-1VSVg (EC50 = 953 nM). Although GS-9620-mediated antiretroviral activity varied significantly between individual donors, its antiretroviral potency in PBMCs was enhanced by approximately 35-fold when GS-9620 was added 48 hours prior to infection with HIV-1VSVg (EC50 = 27 nM).
