AusperBio Therapeutics, Inc. and Ausper Biopharma Co., Ltd. have reported sustained functional cure responses lasting up to 15 months after discontinuation of all hepatitis B treatment in selected participants receiving their investigational antisense oligonucleotide AHB-137. Announced on 5 November 2026 for presentation at the American Association for the Study of Liver Diseases’ The Liver Meeting, the findings include maintained responses in both previously treated patients and individuals who received AHB-137 without conventional nucleoside analogue therapy.
In the nucleoside analogue-treated population, 16 of 17 evaluable participants maintained functional cure at 12 months after discontinuing antiviral treatment, while all nine evaluable participants at the 15-month assessment remained responders. Among seven treatment-naïve participants who had achieved a complete response after 16 weeks of AHB-137 monotherapy, six maintained functional cure through 15 months after treatment cessation.
The results strengthen the evidence supporting AHB-137 as a potential finite-duration therapy for chronic hepatitis B, a disease commonly managed through prolonged antiviral suppression. However, the reported durability percentages concern selected responders and evaluable participants, rather than the complete populations originally enrolled in the parent trials.
That distinction is central to the commercial and clinical interpretation. A hepatitis B treatment capable of sustaining viral control after discontinuation could address a substantial unmet need, but developers must establish both how frequently functional cure occurs and how reliably it persists in a broader patient population.
AusperBio is already evaluating AHB-137 in a Phase 3 programme in China, while extending clinical development internationally. The new follow-up results provide information about durability, but do not themselves establish the efficacy or safety required for regulatory approval.
What do AusperBio’s 12-month and 15-month functional cure findings actually establish?
The data come from study AB-10-8004, a long-term follow-up investigation involving participants from earlier Phase 2 AHB-137 studies. The follow-up programme was designed to assess whether virological and serological responses could be maintained after treatment discontinuation.
The nucleoside analogue-treated cohort enrolled 34 participants, including 21 who had achieved complete response and 13 classified as partial responders at the end of their parent studies. These participants came from studies AB-10-8002 and AB-10-8003.
Among participants evaluable at 12 months following nucleoside analogue discontinuation, 16 of 17 maintained functional cure. At the 15-month assessment, nine of nine evaluable participants remained in functional cure.
These results describe strong response persistence within the available follow-up populations. However, the denominator becomes progressively smaller at later assessments, and the 15-month figure should not be interpreted as evidence that every participant in the original cohort maintained functional cure.
The distinction between 16 of 17 and nine of nine is particularly important. The smaller 15-month group reflects the number of participants evaluable at that time point, rather than a new efficacy population directly comparable with all patients initially enrolled.
The company also reported that no participant in the nucleoside analogue-treated follow-up cohort required antiviral treatment to be restarted during the observation period. This provides additional information about clinical management after treatment discontinuation, although longer monitoring remains necessary.
A meaningful assessment of the therapy’s potential will ultimately need to account for all treated participants, including those who do not achieve an initial complete response. Durability among responders is valuable, but it answers a different question from the probability that an unselected patient starting treatment will achieve sustained functional cure.
Why is treatment-free functional cure different from conventional hepatitis B suppression?
Current chronic hepatitis B treatment commonly involves nucleoside or nucleotide analogues that suppress viral replication. Medicines such as tenofovir and entecavir can substantially reduce circulating hepatitis B virus DNA and lower the risk of disease progression in appropriately treated patients.
However, viral suppression is not equivalent to elimination of hepatitis B surface antigen, and many patients require prolonged treatment to maintain control of infection. Conventional therapy rarely produces functional cure, particularly among patients with established chronic infection.
Functional cure is generally defined through sustained loss of hepatitis B surface antigen, together with continued viral suppression after treatment withdrawal. It is a clinically important development objective because it suggests that treatment may no longer be required to maintain the specified virological response.
AusperBio used a study-specific definition requiring hepatitis B surface antigen below 0.05 IU/mL and hepatitis B virus DNA below the lower limit of quantification of 10 IU/mL. The company defined functional cure as maintenance of this complete response for at least 24 weeks without any hepatitis B treatment.
The definition is clinically meaningful but should not be confused with sterilising cure. Hepatitis B viral genetic material may persist within liver cells even after circulating viral markers become undetectable.
Consequently, patients achieving functional cure may still require appropriate long-term clinical assessment, particularly where pre-existing liver disease or other risk factors remain relevant. Surface antigen loss does not automatically mean that all consequences of chronic infection have been eliminated.
The commercial importance of functional cure lies in potentially reducing the duration of treatment while sustaining control of the disease. However, a medicine producing functional cure in a selected proportion of patients would need to demonstrate that the benefits justify its costs, safety risks and monitoring requirements.
How did 16 weeks of AHB-137 monotherapy perform in treatment-naïve patients?
AusperBio’s treatment-naïve findings provide a separate line of evidence because participants had not previously received nucleoside analogue treatment for chronic hepatitis B. They received AHB-137 monotherapy for 16 weeks, followed by observation without ongoing hepatitis B treatment.
The long-term follow-up cohort included 11 participants from Part A of study AB-10-8008, consisting of seven complete responders and four partial responders. Among the seven participants who had achieved complete response, six maintained functional cure at nine months after treatment discontinuation and continued to maintain it through 15 months.
The seventh participant experienced viral rebound and withdrew from the study. This observation is important because it demonstrates that even a patient initially achieving complete response may subsequently lose virological control.
The broader parent study provides additional context for the selected follow-up population. Results presented earlier in 2026 showed that 17 of 25 evaluable participants receiving AHB-137 achieved complete response at the end of the 16-week treatment period.
At 24 weeks after treatment discontinuation, eight of those 25 participants met the study’s functional cure criteria. This represented 32% of the AHB-137-treated per-protocol population at that assessment.
The longer-term follow-up results therefore should not be described as showing a functional cure rate of six out of seven across all treatment-naïve patients. The seven individuals represented a selected group of complete responders entering the subsequent assessment.
Baseline hepatitis B surface antigen concentration also appeared relevant in the earlier study. Among participants with initial surface antigen levels of 1,000 IU/mL or less, seven of ten achieved functional cure at the 24-week off-treatment assessment.
These findings suggest that baseline viral antigen burden may influence treatment response. However, the subgroup was small, and its predictive significance requires confirmation in larger, appropriately designed studies.
For AusperBio, the treatment-naïve results are commercially interesting because they indicate that a finite course of AHB-137 may produce sustained responses without requiring conventional antiviral pretreatment in some patients. Establishing whether this approach can work reliably across a broader range of baseline viral characteristics remains essential.
How does AHB-137’s antisense mechanism attempt to achieve sustained hepatitis B control?
AHB-137 is an unconjugated antisense oligonucleotide designed to bind hepatitis B viral RNA. It was developed using AusperBio’s proprietary Med-Oligo platform and is intended to suppress the production of hepatitis B surface antigen while reducing viral replication.
Antisense oligonucleotides use short sequences of synthetic nucleic acid to interact with specific RNA targets. By promoting the degradation or functional inhibition of selected RNA molecules, they can reduce the production of proteins associated with disease.
In chronic hepatitis B, reducing surface antigen expression is considered particularly important because persistent exposure to viral antigens may contribute to impaired virus-specific immune responses. Lowering this antigen burden could potentially create conditions that support improved immune control.
However, the relationship between antigen suppression and durable immune recovery is complex. A reduction in circulating surface antigen does not independently establish that normal immune function has been restored.
AusperBio’s approach seeks to combine direct antiviral activity with the possibility of sustained control after treatment cessation. The longer-term findings are consistent with that development rationale, but they do not identify the precise mechanism responsible for response persistence in individual patients.
Some participants may maintain antigen suppression because of changes in virus-specific immunity, while other biological factors may contribute. Establishing causal mechanisms would require appropriately designed immunological analyses and further clinical evidence.
The therapy’s unconjugated design also distinguishes it from certain targeted oligonucleotide delivery approaches. Its pharmacokinetics, tissue distribution and cellular uptake will influence how reliably it suppresses viral RNA.
Manufacturing consistency will become increasingly important during late-stage development. Oligonucleotide medicines require control of sequence identity, impurities, formulation characteristics and exposure-related variables to support reproducible clinical performance.
What does the peer-reviewed Phase 1 evidence reveal about AHB-137 safety?
The expanding Phase 2 and Phase 3 programmes build on earlier clinical evidence, including a first-in-human study published in the journal Hepatology in August 2026. That investigation enrolled 40 healthy participants and 24 patients with chronic hepatitis B receiving stable nucleoside analogue treatment.
The study evaluated single and multiple doses of AHB-137, including subcutaneous administration at 300 mg. Investigators assessed safety, pharmacokinetics and initial antiviral activity under defined experimental conditions.
Treatment-related adverse events occurred in 73% of healthy participants and 71% of patients with chronic hepatitis B. Most were mild or moderate, with injection-site reactions and headaches among the commonly reported events.
No treatment-related serious adverse events, treatment discontinuations or deaths were reported in that Phase 1 study. Mean hepatitis B surface antigen reductions of approximately 0.7 to 1.0 log10 IU/mL were observed in treated patients.
Those findings supported additional development, although the study’s short treatment period and small population limited conclusions about functional cure. It also found that initial surface antigen loss occurred among patients with particularly low baseline antigen levels.
The later Phase 2 programme has generated stronger evidence of antiviral activity following longer treatment exposure. However, safety must continue to be evaluated separately from antiviral response because a treatment capable of altering viral dynamics may also produce clinically significant biochemical changes.
Earlier treatment-naïve Phase 2 results included reversible liver enzyme elevations and a treatment-related serious adverse event involving elevated liver enzymes, bilirubin and hepatitis B virus DNA. The event was reported to have resolved without clinical sequelae.
The new long-term follow-up announcement stated that no clinical relapse, severe hepatic flares, hepatic decompensation or new safety signals were observed during the disclosed observation period. This is encouraging, but it does not erase events recorded in earlier treatment studies or establish that the therapy is free from important hepatic risks.
Long-term monitoring will need to assess viral rebound, changes in liver function and the consequences of stopping conventional antiviral treatment. These considerations are particularly important when developing a medicine intended to allow patients to remain off therapy.
Why is AusperBio’s Phase 3 programme a more important regulatory test than the follow-up percentages?
AusperBio received clearance from China’s Center for Drug Evaluation in July 2025 to initiate Phase 3 testing of AHB-137. The programme is designed as a randomised, double-blind, multicentre study evaluating a 24-week course of AHB-137 at 300 mg in patients with hepatitis B e antigen-negative chronic infection who are receiving stable nucleoside analogue therapy.
The study represents a more advanced level of clinical development than the responder-enriched long-term follow-up investigation. Its purpose is to generate a stronger evidence package concerning efficacy and safety in a defined population under controlled conditions.
A successful pivotal programme must establish not only the proportion achieving the prespecified virological endpoint but also the reliability of the response and the acceptability of the treatment’s safety profile.
The current durability findings may be useful when selecting follow-up periods and defining clinically relevant outcomes. However, they cannot substitute for evidence generated through the Phase 3 protocol.
The distinction also affects regulatory expectations. A treatment may demonstrate substantial antigen reductions without meeting the full criteria required for functional cure. Conversely, a subset of patients may achieve durable responses even when the overall trial population has a more modest response rate.
For commercial planning, the difference between the overall response probability and the durability of response will influence the potential value proposition. Healthcare providers and payers would need to understand how many patients are likely to benefit from a finite treatment course and how frequently retreatment or renewed viral suppression may become necessary.
A product offering short treatment duration but requiring extensive monitoring could still face adoption barriers if the likelihood of sustained response is uncertain. Comparative evidence will therefore be important when assessing its potential role alongside established long-term antiviral therapy.
How could AHB-137 fit into emerging hepatitis B combination treatment strategies?
AusperBio is also investigating approaches intended to build on AHB-137’s antiviral activity through additional immune-directed treatment. This reflects a wider industry hypothesis that reducing viral antigen burden and supporting immune recovery may together improve the likelihood of sustained functional cure.
The company’s research includes the evaluation of sequential treatment strategies involving AHB-137 and investigational immune therapies. A registered Phase 1/2 study is examining AHB-137 followed by TVAX-008 in patients receiving nucleoside analogue therapy.
That programme remained listed as not yet recruiting in its October 2026 registry update. It should therefore be considered an investigational development plan rather than evidence that combination treatment has produced clinical benefit.
The underlying scientific rationale is that initial viral antigen suppression might improve the environment in which an immune-directed treatment acts. Whether that strategy is more effective than AHB-137 alone remains unestablished.
Combination regimens also introduce new safety and manufacturing considerations. Developers must evaluate the effects of each component, potential interactions, treatment sequencing and the additional burden associated with administration.
The wider hepatitis B development field includes approaches based on antisense oligonucleotides, small interfering RNA, therapeutic vaccines and other immune-modulating technologies. These programmes target different components of viral persistence and immune dysfunction.
However, response rates from separate studies cannot be ranked reliably without accounting for baseline antigen levels, antiviral treatment history, endpoint definitions and follow-up. A smaller responder-enriched population may appear to have substantially higher durability than a broader, more difficult-to-treat cohort.
The commercial opportunity associated with successful finite-duration treatment remains substantial because chronic hepatitis B continues to affect approximately 240 million people worldwide, according to the World Health Organization’s 2026 global hepatitis reporting. Yet only a fraction of that population represents patients who are diagnosed, eligible for a particular treatment and able to access it.
What must happen before AHB-137 can change the chronic hepatitis B treatment market?
The immediate next milestone is the detailed scientific presentation of the long-term follow-up results at The Liver Meeting on 8 November 2026. Investigators Jinlin Hou and Junqi Niu are scheduled to present the nucleoside analogue-treated and treatment-naïve datasets, respectively.
The presentations may provide additional methodological detail concerning follow-up completeness, patient characteristics and the circumstances associated with maintained or lost responses. Such information will be important for assessing how broadly the findings can be generalised.
AusperBio is privately held, and the announcement does not disclose new financing terms, revenue projections or a commercial launch timeline. The significance of the development is therefore primarily clinical rather than an immediate public-market valuation event.
The company must still demonstrate that the response rates and safety profile can be reproduced in larger patient populations. It will also need to establish how best to identify candidates for treatment and whether baseline viral antigen levels can reliably guide selection.
Regulatory assessment will depend on an appropriate clinical and manufacturing evidence package, while commercial adoption would require pricing, reimbursement and treatment monitoring arrangements capable of supporting access.
The most consequential finding from the November update is that selected patients maintained complete virological and serological responses long after AHB-137 and conventional antiviral therapy had been discontinued. The smaller denominators at later assessments mean the results must not be mistaken for population-wide cure rates, but the durability observations provide a meaningful rationale for continued development. AusperBio’s Phase 3 programme will determine whether that promise can translate into a reproducible finite-duration treatment option for a substantially larger proportion of people living with chronic hepatitis B.
