Pevifoscorvir sodium (previously known as ALG-000184) was derived from initial IP licensed from the laboratory of Dr. Raymond Schinazi at Emory University, which was further optimized by Aligos. Our potent best/first-in-class oral small molecule capsid assembly modulator (CAM-E) is being developed for chronic hepatitis B virus (HBV) infection.

Chronic HBV infection is the most common chronic viral infection in the world. There are more than 240 million chronic carriers worldwide and approximately 1.1 million individuals become newly infected every year. Chronic HBV infection is the primary cause of liver cancer worldwide, and the mortality associated with HBV-related liver cancer continues to increase.¹

Pevifoscorvir sodium is designed to exploit the dual role of CAMs by preventing the establishment and replenishment of cccDNA levels and its derived transcripts by reducing expression of viral markers such as DNA, RNA, and the relevant antigens (HBsAg, HBeAg, HBcrAg). Phase 1 studies have demonstrated after single and multiple daily doses that ALG-000184 was well-tolerated, with no safety signals observed, and demonstrated linear PK and excellent antiviral activity. In longer term Phase 1 studies of pevifoscorvir sodium 300mg QD x ≤96 weeks ± entecavir (ETV), pevifoscorvir sodium monotherapy demonstrated best-in-class reductions in HBV DNA, RNA, HBsAg, HBeAg, and HBcrAg.

The Phase 2 B-SUPREME study (NCT06963710) is a randomized, double-blind, active-controlled multicenter study evaluating the safety and efficacy of pevifoscorvir sodium monotherapy compared with tenofovir disoproxil fumarate in approximately 200 untreated HBeAg+ and HBeAg- adult subjects with chronic HBV infection for 48 weeks. The primary endpoint in the HBeAg+ part will be HBV DNA < LLOQ (10 IU/mL, target detected [TD] or target not detected [TND]) and the primary endpoint in the HBeAg- part will be HBV DNA < LLOQ (10 IU/mL, target not detected [TND]). The study will also evaluate the safety, pharmacokinetics, and other secondary and exploratory biomarkers, including reductions in HBV antigens and other markers of HBV infection. Enrollment has been completed and topline data are expected to be available in late Q3 2027.

ALG-170675 was discovered by Aligos as part of a research collaboration with Xiamen Amoytop Biotech (Amoytop), who maintain rights in Greater China. Novel intellectual property has been filed for this candidate, which has showed improved RNase H mediated in vivo activity over GSK-836 (bepirovirsen) with similar hTLR8 agonist activity observed in vitro and in vivo. In addition, ALG-170675 has demonstrated advantages compared with GSK-836 with better in vitro safety, enhanced liver exposure, liver to kidney ration, and improved in vivo efficacy in mice.

Additionally, nonclinical studies have showed additive to synergistic effects when combined with CAM-E.

Amoytop plans to initiate a Phase 1 study in China in 3Q2026.

ALG-055009 was designed by Aligos to be a potent best-in-class oral, small molecule thyroid receptor beta agonist (THR-β) for the treatment of metabolic dysfunction-associated steatohepatitis (MASH) and obesity. ALG-055009 was designed to improve upon the potency and selectivity of competitor THR-β agonists and was further optimized for pharmacokinetics (PK).

Phase 1 studies have demonstrated after single and multiple daily doses that ALG-055009 was well tolerated, had dose proportional PK and low variability, and demonstrated expected thyromimetic effects.

The Phase 2a HERALD study was designed to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of oral daily doses of ALG-055009 for 12 weeks. Topline data demonstrated that ALG-055009 dose groups met the primary endpoint with statistically significant reductions in liver fat at Week 12 as measured by MRI-PDFF and was well-tolerated, with rates of GI-related AEs similar to placebo. 11/14 subjects on stable GLP-1 treated with ALG-055009 had liver fat decreases, whereas 4/4 subjects on stable GLP-1 treated with placebo had liver fat increases.