GS 9620 - CAS 1228585-88-3
Catalog number: B0084-473893
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Toll-like Receptor (TLR)
A potent and oral agonist of TLR7
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-473893 300 mg $499 In stock
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Brife Description:
A potent and oral agonist of TLR7
Solid powder
4-amino-2-butoxy-8-[[3-(pyrrolidin-1-ylmethyl)phenyl]methyl]-5,7-dihydropteridin-6-one; GS-9620; GS9620; Vesatolimod
Soluble in DMSO, not in water
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Quality Standard:
Shelf Life:
>2 years if stored properly
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)
Canonical SMILES:
1.Effects of Treatment of Chronic Hepatitis B Virus Infection on Patient-Reported Outcomes.
Younossi ZM;Stepanova M;Janssen HLA;Agarwal K;Nguyen MH;Gane E;Tsai N;Younossi I;Racila A Clin Gastroenterol Hepatol. 2018 Mar 2. pii: S1542-3565(18)30225-8. doi: 10.1016/j.cgh.2018.02.037. [Epub ahead of print]
BACKGROUND & AIMS: ;Chronic infection with hepatitis B virus (HBV) causes liver disease and cirrhosis. It is not clear how treatment of chronic HBV infection affects patient-reported outcomes (PROs). We aimed to assess changes in PROs in patients treated for chronic HBV infection.;METHODS: ;We collected and analyzed PRO data from 242 patients with chronic HBV infection (without advanced fibrosis or cirrhosis) enrolled in 2 international phase 2 blinded controlled clinical trials from 2015 through 2017. In these trials, patients were treated with an approved oral antiviral regimen (tenofovir, entecavir, adefovir, lamivudine, or telbivudine) and then randomly assigned to groups given vesatolimod (an oral agonist of Toll-like receptor 7) or placebo. PROs were collected using the Short Form-36, the Chronic Liver Disease Questionnaire, and the Work Productivity and Activity Impairment: Specific Health Problem questionnaires before treatment and during treatment weeks 12, 24, and 48.;RESULTS: ;We did not observe significant differences in PROs between patients receiving vesatolimod vs placebo. At baseline, patients with viral suppression (HBV DNA level, <20 IU/mL) had higher PRO scores (by up to +10.
2.Safety and efficacy of vesatolimod (GS-9620) in patients with chronic hepatitis B who are not currently on antiviral treatment.
Agarwal K;Ahn SH;Elkhashab M;Lau AH;Gaggar A;Bulusu A;Tian X;Cathcart AL;Woo J;Subramanian GM;Andreone P;Kim HJ;Chuang WL;Nguyen MH J Viral Hepat. 2018 May 31. doi: 10.1111/jvh.12942. [Epub ahead of print]
Vesatolimod is an oral agonist of toll-like receptor 7 designed to minimize systemic exposure and side effects. We assessed the safety and efficacy of vesatolimod in viremic chronic hepatitis B (CHB) patients not currently on oral antiviral treatment (OAV) in a phase 2, multicentre, double-blind, randomized, placebo-controlled study. A total of 192 patients stratified by HBeAg status and alanine aminotransferase level were randomized 2:2:2:1 to receive oral vesatolimod (1-, 2- or 4-mg) or placebo once weekly for 12 weeks; tenofovir disoproxil fumarate (300-mg daily) was administered daily for 48 weeks. Efficacy was assessed by quantitative serum HBsAg decline at Week 24 from baseline. In addition to safety assessments, changes in whole-blood interferon-stimulated gene (ISG) transcripts and serum cytokines were explored. Most patients were male (64.1%) and HBeAg-negative (60.9%) at baseline. Among vesatolimod-treated patients, most (60.4%-69.1%) experienced ≥1 treatment-emergent adverse event; the majority were mild or moderate in severity. No clinically meaningful differences in HBsAg changes from baseline were observed between treatment groups. No patients experienced HBsAg loss, while 3 patients experienced HBeAg loss and hepatitis B e-antibody seroconversion at week 48.
3.Hot News: Hepatitis B Gene Therapy Coming to Age.
Soriano V AIDS Rev. 2018 Apr-Jun;20(2):125-127.
The major pandemics caused by chronic viral infections is produced by HIV, hepatitis C virus (HCV), and hepatitis B virus (HBV), with estimates of 38, 70, and 250 million people worldwide, respectively (Fig. 1). During the last couple of years, the advent of direct oral antivirals has allowed pursuing global HCV eradication. In an unprecedented manner, these drugs cure more than 95% of hepatitis C patients when given for only 2-3 months. The enthusiasm on HCV has renewed the interest for curative strategies for both HIV and HBV. However, important biological differences between all three viruses may preclude envisioning a similar rapid success for either HIV or HBV than for HCV infection. As shown in figure 1, once infection of targeted cells has occurred, the viral genetic material only replicates in the cytosol for HCV whereas it enters the nucleus and integrates into the chromosomes as provirus for HIV or is converted in a circular covalently closed form (cccDNA) for HBV (Fig. 1). Blocking viral nucleic acid replication for a minimum lag of time allows definitive clearance of HCV infection, with degradation of residual cytoplasmic HCV-RNA strands. In contrast, blocking viral replication has only a transient effect on HIV or HBV, as mRNA expression resumes following treatment discontinuation, given the stability of the HIV provirus or the HBV cccDNA, respectively.
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