Presatovir is a novel inhibitor of respiratory syncytial virus (RSV) fusion F protein patented by Gilead Sciences, Inc. as an antiviral agent. Upon oral administration of GS-5806, this agent specifically binds to F protein on the viral surface, which inhibits RSV F protein-mediated fusion with the host cell membrane and prevents viral entry. This blocks RSV replication, reduces viral load, and decreases the severity of the disease. Presatovir exhibited potent antiviral activity against 75 RSV clinical isolates from both A and B subgroups in vitro. In vivo, presatovir demonstrated efficient penetration into the lung and epithelial lining fluid in Sprague‐Dawley rats and in dogs and cattle. Presatovir demonstrated dose‐dependent antiviral activity in both the upper respiratory tract and the lungs in a nonclinical study of RSV‐infected cotton rats as well as in a clinical study of healthy adults experimentally infected with RSV.

Dideoxyadenosine (2′,3′-dideoxyadenosine) is a prodrug form of didanosine (2',3'-dideoxyinosine), a nucleoside reverse transcriptase inhibitor analog of adenosine. 2',3'-Dideoxyadenosine and 2',3'-dideoxyinosine were shown to be equally effective in the inhibition of HIV proliferation in human T cells. Dideoxyadenosine competitively inhibits adenylyl cyclase, thereby reducing levels of cyclic adenosine monophosphate (cAMP). By inhibiting cAMP-mediated gene activation in tumor cells, this agent may retard tumor cell proliferation. 2',3'-dideoxyadenosine inhibits retroviral DNA synthesis and mRNA expression in T cells exposed to the virus that causes acquired immunodeficiency syndrome, and affords such cells long-term protection in vitro under conditions of substantial viral excess. 2',3'-dideoxyadenosine appears to completely block reverse transcription from viral RNA to viral DNA. 2',3'-dideoxyadenosine was also shown not only to possess antibacterial activity in vitro against a variety of Enterobacteriaceae, but also to be effective in vivo, dideoxyadenosine was active in experimental mouse infections by the oral route against 5 Salmonella strains, 2 of 3 Arizona strains, 5 of 7 Citrobacter strains, 3 of 8 Klebsiella strains, 3 of 5 Escherichia strains, 1 of 3 Shigella strains, and 3 of 15 Serratia strains at concentrations generally well below the toxic level.

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

Vedroprevir, or GS-9451, is a potent inhibitor of the HCV NS3 protease (Box 1). NS3 is a serine protease that cleaves the HCV polyprotein and helps generate the viral replication complex. Through binding NS3, vedroprevir halts the assembly of the viral replication complex, thus interfering with the assembly and release of viral particles. Vedroprevir is a potent inhibitor of NS3 protease with high selectivity against off-target proteases. It has rapid association kinetics and slow dissociation kinetics. Preclinical studies of vedroprevir showed high oral bioavailability in rats, dogs, and monkeys. Preclinical studies of vedroprevir demonstrated potent NS3 inhibition using laboratory strains as well as patient-derived NS3 protease gene isolates. In a phase I, randomized trial of vedroprevir monotherapy, doses of 200 and 400 mg/day yielded median maximal HCV RNA reductions of −3.2 log10 in genotype 1a patients and −3.5 log10 in genotype 1b patients. Significantly less activity was seen against genotype 2a HCV when compared to genotype 1. Vedroprevir was not listed on the Gilead Sciences pipeline in its 2014 annual report and appears to have been discontinued for the once-daily treatment of Hepatitis C.

Samatasvir (also known as IDX 719) was developed by Idenix Pharmaceuticals as a pan-genotypic inhibitor of the hepatitis C (HCV) non-structural protein 5A (NS5A). This drug was studied in phase II clinical trials for the treatment of Hepatitis C, and Chronic Hepatitis C Infection. However, the development of samatasvir was discontinued.

Pocapavir is a capsid-binding molecule. It is a capsid inhibitor that blocks virus uncoating and viral RNA release into cells, which in turn prevents virus replication. Pocapavir is a potent, selective, anti-enterovirus molecule with in vitro and in vivo activities. Antiviral testing against viruses of the 15 most commonly isolated enterovirus serotypes indicates that pocapavir inhibits 80% of the immunotypes (154 viruses) at a concentration that is within the levels of the molecule achievable in plasma after oral dosing in higher animals. Persistent low viral load after therapy completion may indicate lack of antiviral effect from pocapavir for neonatal enteroviral sepsis treatment. Pocapavir had been in phase II clinical trial for the treatment of poliomyelitis but no recent reports on development were identified.

Ravidasvir (RDV, ASC16) is a second‐generation, pan‐genotypic non‐structural (NS) 5A inhibitor, which inhibits viral replication and assembly. Ravidasvir exhibits high antiviral potency with EC50 0.04–1.14 nM for HCV GT1–GT6. The pharmacokinetics results indicated that steady status achieved quickly after the first dose. Metabolism studies utilizing human clinical samples showed that Ravidasvir was very stable, with only modest (~2%) metabolite formation. Biliary excretion of Ravidasvir appears to be the primary route of elimination of the absorbed dose, while renal excretion of the intact drug appears to be negligible. In clinical trans twelve-week Ravidasvir and ritonavir-boosted Danoprevir in combination with ribavirinfor 12 weeks achieve the sustained virologic response rate of 100% in treatment-naïve non-cirrhotic Asian patients with HCV GT1 infection. Ravidasvir for treatment‐naïve, non‐cirrhotic HCV GT1 patients was safe and well tolerated. There was no death, treatment‐related serious adverse events, and discontinued cases due to adverse events.

Pritelivir is a thiazolylamide derivative patented by German multinational pharmaceutical and life sciences company Bayer A.-G. as helicase-primase enzyme inhibitor that is active against herpes simplex virus types 1 and 2 (HSV-1 and HSV-2). In preclinical Pritelivir was shown to be active when treatment was delayed to 72 h post viral inoculation and appeared to synergistically inhibit mortality in this model in combination with acyclovir. Pritelivir could be an alternative therapeutic agent for patients infected with acyclovir-resistant strains. Phase II clinical trials currently are ongoing.

Setrobuvir (also known as ANA-598 and RG7790) is an orally administered, small-molecule non-nucleoside polymerase inhibitor, which was in development by Roche company. Setrobuvir has been used in trials studying the treatment of chronic hepatitis C. Setrobuvir is a non–nucleoside NS5B inhibitor (NNI). It has shown potency and a high degree of specificity against HCV genotype 1 NS5B polymerase, leading to 73% SVR when orally administrated to patients in combination with pegylated interferon and ribavirin. An interferon-free setrobuvir based regimes of three direct acting antivirals (DAAs) plus ribavirin has also been shown to be safe and effective in genotype 1 treatment naive patients.

GS-9190 (Tegobuvir) a novel nonnucleoside inhibitor of hepatitis C virus NS5B polymerase was investigated for treatment Hepatitis C, Chronic, but on the clinical trial II was discontinued.