Management's Discussion and Analysis of Financial Condition and Results of Operations

The condensed consolidated financial statements and this Management's Discussion and Analysis of Financial Condition and Results of Operations should be read in conjunction with the consolidated financial statements and notes thereto for the year ended December 31, 2025 and the related Management's Discussion and Analysis of Financial Condition and Results of Operations, both of which are contained in our Annual Report on Form 10-K for the fiscal year ended December 31, 2025 filed with the U.S. Securities and Exchange Commission on March 19, 2026 (2025 Annual Report). In addition to historical information, this discussion and analysis contains forward-looking statements that involve risks and uncertainties. Our actual results could differ materially from those expressed or implied in any forward-looking statements as a result of various factors, including those set forth under "Part I. Item 1A. Risk Factors" in our 2025 Annual Report and "Part II. Item 1A. Risk Factors" in this report.

Overview

We are a biotechnology company developing innovative therapeutics targeting serious viral and liver diseases with the potential to improve the lives of patients worldwide. Our pipeline includes multiple clinical-stage investigational therapies, including: (1) two long-acting helicase-primase inhibitors (HPI) for the treatment of recurrent genital herpes, GS-5366 (5366) and GS-1179 (1179), which have been exclusively licensed to Gilead Sciences, Inc. (Gilead); (2) an orally bioavailable sodium taurocholate co-transporting peptide (NTCP) inhibitor, ABI-6250 (6250), for the treatment of (a) chronic hepatitis delta virus (HDV) infection and (b) primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC), both cholestatic liver diseases (CLD); and (3) a highly potent next-generation capsid assembly modulator (CAM) designed to disrupt the replication cycle of hepatitis B virus (HBV) at several key points, ABI-4334 (4334). Our pipeline also includes a novel, oral broad-spectrum non-nucleoside polymerase inhibitor (NNPI) for the treatment of transplant-related herpesviruses, ABI-7272 (7272), which is currently undergoing studies to enable a regulatory filing, and we have additional research programs against multiple viral and liver disease targets. In December 2025, pursuant to our collaboration with Gilead (the Gilead Collaboration), Gilead exercised its option to license our HPI program for the treatment of recurrent genital herpes, including our long-acting investigational candidates 1179 and 5366. For additional information regarding Gilead's exercise of its option, see "Collaboration and License Agreement-Gilead Sciences, Inc.-Option Exercise."

Our Clinical Programs and Regulatory Filing-Enabling Program

In the second quarter of 2026, we continued to progress each of our investigational product candidates, 5366, 1179, 6250 and 4334.

In addition, we completed a $115.0 million gross financing transaction that we expect to extend funding beyond our planned Phase 2 studies of 6250 in both HDV and CLD.

Recurrent Genital Herpes/HSV-1 and HSV-2

Genital herpes can be caused by either herpes simplex virus type 1 (HSV-1) or herpes simplex virus type 2 (HSV-2). HSV-1 and HSV-2 are acquired by oral or genital contact either during symptomatic or asymptomatic reactivation of the virus. Both viruses replicate in neurons, where they can remain latent for the rest of the individual's life and periodically reactivate, with the virus spreading, replicating and causing disease in epithelial tissues. Initial infection can be asymptomatic or can be marked by serious symptoms, including painful skin lesions, swelling of lymph nodes and urinary problems that can persist for two to three weeks. While genital herpes can be caused by either HSV-1 or HSV-2, recurrences are more likely to be experienced by individuals infected by HSV-2. Genital herpes recurrence can cause painful genital lesions that can lead to increased transmission and debilitate individuals, and symptoms may become more serious with additional episodes. Additional complications include increased risk of HIV infection, as 30% of HIV infections acquired through sexual transmission are attributable to HSV-2 infection. In addition, people with recurrent genital herpes often experience associated psychosocial impacts, including anxiety, concerns about transmission, depression and social stigma. Immunocompromised individuals may experience more severe and prolonged symptoms due to increased recurrence rates.

HPIs are antiviral agents in development for the treatment of recurrent genital herpes, with a clinically-validated mechanism of action. HPIs inhibit the HSV helicase-primase complex, which is a unique viral enzyme complex without a human homolog, consisting of helicase, primase and cofactor subunits. These subunits have functions that are essential for viral DNA replication and are conserved across HSV-1 and HSV-2. Unlike nucleoside analogs, these compounds do not require phosphorylation by the HSV thymidine kinase (TK) and ongoing viral replication to become active drugs. As a result, HPIs are active immediately upon reactivation of latent HSV-1 and HSV-2. Furthermore, HPIs are active against TK-deficient HSV-1 and HSV-2, which is a major mechanism of resistance to nucleoside analogs.

Most people with initial symptomatic genital herpes who are infected with HSV-2 have frequent recurrences, generally between three and 15 per year, impacting over four million people in the United States and France, Germany, Italy and Spain (collectively, the EU4) and the United Kingdom (UK). Currently, there are three antiviral drugs (all nucleoside analogs) that have been approved in the United States and the EU4/UK for the treatment of genital herpes. However, no new drugs have been approved in these regions to treat genital herpes for more than 25 years. In addition to the approved nucleoside analogs, agents such as local anesthetics or analgesics may be used to alleviate local symptoms of minor pain and discomfort.

Nucleoside analogs can be administered as episodic therapy as individual outbreaks arise or daily as chronic suppressive therapy for those with high post-exposure recurrences. However, these agents are only partially effective at controlling the infection or reducing transmission risk. With current nucleoside analog therapies, only one out of three people with recurrent genital herpes with six or more recurrences per year are able to make it through a year of treatment without a recurrence. There are still high titer (greater than 104 HSV-2 DNA copies/mL) shedding episodes under this current standard of care for recurrent genital herpes, which can lead to recurrent episodes and transmission of genital herpes. In addition, nucleoside analogs also carry a high pill burden as a lifelong daily treatment, with doses ranging from one to three times daily. There is also high treatment variability among those taking nucleoside analogs, as many seeking care may not consistently receive suppressive therapy.

Based on the limitations of current therapies, we see a path to advancing the treatment paradigm for people suffering from recurrent genital herpes. To reach that goal, we discovered and began the clinical development of a novel, potent, long-acting HPI for recurrent genital herpes, 5366, which demonstrated low nanomolar potency in vitro against both HSV-1 and HSV-2 clinical isolates and a favorable nonclinical safety profile in the FDA's Good Laboratory Practice (GLP) toxicology studies. In addition, we began development of a second novel, potent, long-acting HPI for genital herpes, 1179, which was in-licensed to us as part of our collaboration with Gilead. As Gilead has exercised its option to exclusively license our HPI program, including 5366 and 1179, development is now in Gilead's sole control following completion of the Phase 1a/b studies of 5366 and 1179. For additional information regarding the option exercise, see "Collaboration and License Agreements-Gilead Sciences, Inc.-Option Exercise."

We reported interim data from the Phase 1b portion of the 5366 study in August 2025, focused on two different oral doses of 5366 administered on a once-weekly basis. For the powered antiviral endpoint, HSV-2 shedding rate, highly

potent antiviral activity was observed with a 94% reduction compared to placebo (p<0.01) over the 29-day evaluation period in the cohort evaluating a 350 mg weekly dose. This reduction exceeded our target for the study of an 80-85% reduction in the rate of HSV-2 shedding. For a secondary clinical endpoint of virologically confirmed genital lesion rate, a 97% reduction compared to placebo (p<0.05) was observed with the 350 mg weekly dose. The rate of genital swabs with high viral load (i.e., >104 copies/mL HSV DNA), a potential surrogate for HSV-2 transmission and a secondary endpoint, was reduced by 98% compared to placebo (p<0.05) in this cohort.

We reported additional interim data from the Phase 1b portion of the 5366 study in December 2025, which included data from a monthly oral dosing regimen. In the 5366 monthly dose cohort, potent antiviral activity was observed, with a 76% reduction in HSV-2 shedding rate compared to placebo (p<0.01) over the 29-day evaluation period. The majority of positive swabs (89%) were collected in the last two weeks of the evaluation period when drug levels were declining. We observed an 88% reduction in virologically confirmed genital lesion rate (p=0.01), along with an 81% reduction in the number of samples with high viral load (p<0.01) compared to placebo in the monthly dose cohort.

Across the two weekly oral dose cohorts and the monthly oral dose cohort of the Phase 1b study, 5366 demonstrated a pharmacokinetic (PK) profile that continues to support once-weekly and potentially once-monthly dosing.

5366 was observed to be well-tolerated at all dose levels tested in the Phase 1b portion of the study. The two weekly oral cohorts as well as the monthly oral cohort are complete and unblinded safety data has been reported. Across all cohorts, the proportion of participants reporting treatment-emergent adverse events (AEs) was similar between 5366 and placebo recipients, and all were Grade 1 or Grade 2. One Grade 3 AE was reported, hypertriglyceridemia, in a participant with relevant medical history who had Grade 4 elevated triglycerides pre-dose on Day 1. This AE resulted in study discontinuation but was not considered treatment related. The proportion of participants reporting treatment-emergent lab abnormalities was similar in 5366 and placebo recipients with the majority being Grade 1 or Grade 2. There were three participants with treatment-emergent Grade 3 lab abnormalities across all cohorts, all of which are considered unrelated to assigned treatment; one participant with exercise-associated elevation in creatine kinase (150/30 mg QW); one participant with an elevation of cholesterol in the follow up period, which participant had a Grade 2 elevation at baseline (350 mg QW); and one participant, who was dosed with placebo, with decreased neutrophils. There did not appear to be a dose-response relationship in either the frequency or severity of the treatment-emergent AEs or lab abnormalities. No serious AEs have been reported to date.

All participants in the Phase 1b portion of the 5366 study have completed dosing and follow up. The observed PK profile continues to support once-weekly dosing and the potential for once-monthly oral dosing regimens. Additionally, all chronic toxicology studies have been completed. With these data, 5366 is ready to move into a Phase 2 clinical study; however, 5366 development is in Gilead's sole control and Gilead does not intend to develop 5366 further at this time.

The 5366 data reported in August and December 2025 were presented in an oral presentation and two poster presentations at the Congress of the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) in Munich, Germany in April 2026.

We also conducted a Phase 1a/b clinical study of 1179, a structurally-differentiated HPI, which has single digit nanomolar potency against HSV-1 and HSV-2 and a nonclinical PK and safety profile that is supportive of a potential long-acting treatment by once-weekly oral administration. We reported interim data from two oral weekly dose cohorts in the Phase 1b portion of the 1179 study in December 2025. For the powered antiviral endpoint, HSV-2 shedding rate, highly potent antiviral activity was observed with a 98% reduction in HSV-2 shedding rate compared to placebo (p<0.01) over the 29-day evaluation period in the 50 mg weekly dose cohort. This reduction exceeded our target for the study of an 80-85% reduction in HSV-2 shedding rate. Further, data revealed a 91% reduction in virologically confirmed lesion rate compared to placebo (p<0.01) with the 50 mg weekly dose. There was also a >99% reduction in the number of samples with high viral load, a potential surrogate for HSV-2 transmission and a secondary endpoint.

Across both oral weekly dose cohorts, 1179 demonstrated a PK profile that continues to support once-weekly dosing. 1179 was observed to be well-tolerated at both doses. Overall, the proportion of participants reporting treatment-emergent AEs was similar between 1179 and placebo recipients. Of the treatment-emergent AEs reported, the majority were Grade 1 or Grade 2. The most common AEs were upper respiratory tract infection and headache. There have been no serious AEs reported to date. One Grade 3 AE of migraine was reported in a participant enrolled in the 50 mg/placebo cohort.

All participants in the Phase 1b portion of the 1179 study have completed dosing and follow up. With these data, 1179 can move directly into a Phase 2 study for a once-weekly treatment regimen, subject to the completion of chronic toxicology studies, which are underway. The 1179 data reported in December 2025 was presented in a poster presentation at ESCMID in April 2026.

In December 2025, Gilead exercised its option early to license our HPI program for the treatment of recurrent genital herpes, including 5366 and 1179. We received Gilead's clinical development plan and budget for the HPI program in June 2026. The plan indicates that 1179 has been selected to advance, with a Phase 2 clinical study in participants with recurrent genital herpes expected to initiate by the end of 2026. Gilead is also considering the possible evaluation of 1179 as part of a combination strategy with HIV PrEP. Our decision regarding the Profit-Share (as defined below) will be made after receipt and review of Gilead's commercial cost estimates, which will complete the opt-in package. For more information regarding Gilead's exercise of its option, see "Collaboration and License Agreement-Gilead Sciences, Inc.-Option Exercise."

Our Liver Disease Programs

HDV and HBV

The World Health Organization (WHO) estimates that 240 million people worldwide were chronically infected with HBV as of 2024, and 0.9 million new infections occur each year. HBV is a leading global cause of chronic liver disease and liver transplants, and the WHO estimates that 1.1 million people died in 2024 from HBV, mostly due to cirrhosis and hepatocellular carcinoma (primary liver cancer). Of the 240 million people living with chronic HBV infection, only approximately 65 million, or 27%, were aware of their infection, and only approximately 10 million, or 4%, of those diagnosed received treatment. HBV is a highly prevalent disease that infects almost three times the number of people infected with hepatitis C virus and HIV infections combined, according to the WHO.

HDV is a "satellite virus" of HBV because it can only infect people (1) who are already infected with HBV or (2) at the same time as a person is infected with HBV. HDV affects a subset of approximately 12 million HBV infected people. These individuals infected with HDV, which comprise an estimated nearly 5% of hepatitis B surface antigen (HBsAg) positive individuals, experience a substantially increased disease burden, as they account for 18% of cirrhosis and 20% of hepatocellular carcinoma associated with HBV. HDV is considered the most severe form of hepatitis, as 70% of individuals infected with HDV progress to cirrhosis within ten years. While HDV is less prevalent in the United States, it is a significant and serious health problem with inadequate treatment in many parts of Europe, Africa, the Middle East, East Asia and parts of South America. HDV may be significantly underdiagnosed, because there were no HDV-targeted therapies approved until very recently, and the first HDV-targeted therapy is only approved in the European Economic Area (EEA), the UK, Switzerland, Australia, Canada and the United States. HDV is known to accelerate disease progression and increase the incidence of liver cirrhosis and liver cancer, which results in higher morbidity and mortality rates than HBV alone.

The current standard of care treatment for HDV is off-label pegylated interferon-α (IFN-α) injected weekly or, in the EEA, the UK, Switzerland, Australia, Canada and the United States, a large, complex peptide inhibitor that requires daily injections, bulevirtide. We believe a safe and effective oral small molecule entry inhibitor would be a significant innovation for people living with HDV, who face a significant and immediate disease burden.

The current standard of care for chronic HBV infection, nucleos(t)ide analog reverse transcriptase inhibitors (NrtIs), are taken life-long and reduce, but do not eliminate, the virus and result in very low cure rates. No new mechanisms of action (MOA) have been approved for the treatment of chronic HBV infection in over 25 years. The focus of our HBV program is to improve outcomes and increase the number of patients diagnosed and treated through the development of finite and curative therapies targeting an orthogonal MOA.

HDV Entry Inhibitor

HDV is a small RNA virus that encodes just two viral proteins and relies on host enzymes as well as the HBsAg from HBV to replicate, which limits the number of HDV-specific antiviral targets. Similar to HBV, HDV utilizes HBsAg to enter hepatocytes by binding the cellular transmembrane protein, NTCP. NTCP is highly expressed on human hepatocytes, where it serves as one of several proteins involved in the transport of bile acids. The binding of specific small or large molecules to NTCP has been shown to effectively inhibit the interaction of HBsAg with NTCP, which

prevents HBV and HDV from infecting hepatocytes.

The inhibition of HBV and HDV infection by molecules that bind NTCP has been demonstrated in vitro, in animal models and clinically. Notably, bulevirtide, a peptide inhibitor of NTCP, is the only approved therapy for HDV. 6250 has the same clinically-validated MOA as bulevirtide. The binding of HBV/HDV entry inhibitors to NTCP has also been shown to inhibit the transport of certain bile acids into cells, which results in plasma elevations of bile acids; this effect has been well-tolerated clinically and may serve as a biomarker of pharmacologically active concentrations of drug in the plasma.

We believe a safe and effective oral small molecule entry inhibitor would be a significant innovation for people living with HDV and could significantly improve treatment uptake and diagnosis rates, especially when compared with currently available injectable products.

Top-line clinical data, including PK, biomarker and safety data for the Phase 1a study of 6250 was presented at the European Association for the Study of the Liver Congress that took place in Barcelona, Spain in May 2026. Across all cohorts , a mean half-life of approximately four days was observed for 6250 when dosed orally, supporting the once-daily oral dosing profile target. Given this half-life, accumulation was observed in the multiple-dose cohorts with exposures on the last day of dosing generally reaching six- to eight-fold higher than the exposure seen after the first dose.

Dose-dependent elevations of total serum bile acids (TBAs) were observed for both the 5 mg and 25 mg single-dose cohorts, indicative of NTCP target engagement. In the highest single-dose cohort of 25 mg, coproporphyrin I (CP-1), a biomarker for off-target engagement of the organic anion transporters, OATP1B1 and/or OATP1B3, was also elevated. CP-1 elevation was not noted at the other doses.

Given the predicted 6250 accumulation driven by the long half-life and the observed elevations of TBAs for the single-dose cohorts, doses at and below 1 mg daily were selected for the multiple-dose cohorts to characterize the lower end of the dose-response curve. Elevation of TBAs was observed for both the 0.2 mg and 1 mg daily multiple-dose cohorts at levels similar to or greater than those seen with steady-state dosing of bulevirtide, consistent with the respective 6250 exposures. Minimal TBA elevation was observed in the 0.05 mg daily multiple-dose cohort.

Treatment-emergent AEs and laboratory abnormalities were all Grade 1 or 2 in severity with the majority being Grade 1. There were no serious AEs in any dose cohort. No protocol defined stopping criteria were met. There were no clinically significant electrocardiogram abnormalities or patterns of AEs noted.

One Grade 2 alanine transminase (ALT) elevation was observed in the cohort evaluating the highest single-dose level of 25 mg. In this cohort, off-target engagement of other liver transporters was also seen as indicated by elevated CP-1 levels. Grade 1 ALT elevations were observed at a low frequency across the other cohorts, including placebo. All ALT elevations were self-limited, and none were accompanied with elevations in bilirubin or other markers of liver injury. The elevations resolved in the study period with ongoing drug exposure due to 6250's four-day half-life.

All participants in the Phase 1a study have completed dosing and follow up. The chronic toxicology studies to enable longer term dosing are complete, and we are preparing for Phase 2 clinical studies, with Phase 2 initiation expected in the fourth quarter of 2026. In addition, we expect to initiate additional Phase 1 pharmacology studies to support labeling anticipated to start in the fourth quarter of 2026.

Capsid Assembly Modulator

HBV is a DNA virus that infects hepatocytes and establishes a reservoir of covalently closed circular DNA (cccDNA), a unique viral DNA moiety that resides in the nucleus of HBV-infected hepatocytes and is associated with viral persistence and chronic infection. No currently approved oral therapies target cccDNA activity directly. As a result, we have worked to discover and develop compounds targeting the core protein, a viral protein involved in numerous aspects of the HBV replication cycle, including the generation of HBV cccDNA.

A benchmark for therapeutic agents aiming to decrease cccDNA levels is the use of several key viral antigens as surrogate biomarkers of active cccDNA. The same biomarkers can be used in both primary human hepatocytes and infected individuals. On this basis, our next-generation CAM, 4334, has shown nonclinical proof of principle. In a

variety of cell culture models, 4334 has demonstrated the ability to reduce production of HBV DNA levels as well as the surrogate markers for cccDNA establishment: HBV e antigen (HBeAg), HBV core-related antigen (HBcrAg) and HBV pre-genomic RNA (pgRNA).

As a next-generation CAM, 4334 was optimized to potently disrupt viral replication (MOA #1) and prevent the establishment and replenishment of new cccDNA (MOA #2). In contrast, while active against MOA #1, first-generation CAMs have not demonstrated adequate potency to sufficiently block MOA #2. Further, the current standard of care, NrtIs, impacts the viral life cycle after establishment of cccDNA and can only inhibit production of new viral particles, and it does so incompletely. The chemical scaffold of 4334 is novel and distinct from all our prior CAM candidates.

We believe that 4334 has a best-in-class nonclinical profile, with single-digit nanomolar potency against MOA #1 and MOA #2, pan-genotypic activity, an improved resistance profile and a favorable safety profile. Through mechanistic studies presented at multiple conferences, we have demonstrated that 4334 promotes the formation of empty capsids by acceleration of capsid assembly, prevents the formation of cccDNA by disrupting incoming capsids, and prematurely disrupts capsids containing duplex linear DNA, the precursor for integrated HBV DNA.

A Phase 1a study demonstrated that 4334 was well-tolerated when administered orally as single or multiple doses. During the second quarter of 2024, we dosed our first participant in a Phase 1b clinical study of 4334. We reported interim clinical results from the initial 150 mg cohort in December 2024, and topline clinical results, including a subsequent 400 mg cohort in June 2025. In both the 150 mg and 400 mg cohorts, 4334 continued to show a half-life supportive of once-daily oral dosing. In addition, results for both cohorts indicated that 4334 maintained clinical exposures multiple folds above those anticipated to be required for potent viral activity and inhibition of cccDNA formation. Mean declines in HBV DNA of 2.9 log10 IU/mL and 3.2 log10 IU/mL were observed over 28 days in a population of predominately HBeAg negative participants receiving 150 mg and 400 mg, respectively. Among the subset of participants with detectable HBV RNA at baseline, mean declines of 2.5 log10 U/mL and 2.3 log10 U/mL were observed over 28 days in the participants receiving 150 mg and 400 mg, respectively. As anticipated, limited changes in viral antigens were observed for the study population over the 28-day treatment period. These antiviral data are consistent with the high potency seen preclinically for 4334. The safety data also demonstrated that 4334 was well-tolerated with a favorable safety profile observed. The 400 mg cohort was the final cohort for this Phase 1b study and final data was presented at the American Association for the Study of Liver Disease, The Liver Meeting® in November 2025.

In March 2026, Gilead declined to either exercise its option to license 4334 or defer its option until completion of Phase 2 studies. As a result, we retain full control of 4334, including the right to evaluate partnering opportunities for 4334 outside of the Gilead Collaboration. We are actively evaluating partnering opportunities for 4334 and do not plan to advance 4334 further without a partner.

PBC and PSC

PBC and PSC are chronic, autoimmune CLDs characterized by impaired bile flow, accumulation of bile acids in the liver and progressive liver damage. Clinical symptoms for both PBC and PSC include itch and fatigue, with development of fibrosis and cirrhosis as the diseases progress.

PBC affects intrahepatic bile ducts, with complications including cirrhosis and hepatocellular carcinoma. PBC is also associated with Sjogren's Syndrome. There are approximately 150,000 adults diagnosed with PBC in the United States, and approximately 40% of patients fail first line therapy. There are multiple therapies available for the treatment of PBC; however, a significant percentage of individuals have an inadequate response to these treatments, and there remains an unmet medical need for improved treatment of PBC.

PSC affects intrahepatic and extrahepatic bile ducts, and has complications including cirrhosis, cholangiocarcinoma and cholangitis. PSC is also associated with inflammatory bowel disease. There are approximately 30,000 adults diagnosed with PSC in the United States. The ten-year overall mortality rate for PSC patients is approximately 35%. We believe there is a significant unmet medical need for the management of PSC as there are currently no approved therapies.

Nonclinical data with 6250 demonstrate potent inhibition of bile acid uptake in liver cells, a mechanism directly

relevant to CLD, where bile acid accumulation drives liver inflammation and liver injury. In addition, animal studies as well as the Phase 1a study with 6250 demonstrated elevations in serum bile acids, which we believe to be a biomarker for NTCP engagement that reflects reductions of bile acids in the liver.

In May 2026, we announced that we expanded 6250 clinical development beyond HDV into CLD, targeting PBC and PSC. Further, we conducted a pre-IND meeting with the FDA to discuss our planned development of 6250 in CLD. Official meeting minutes support advancement of the CLD program. We are preparing for Phase 2 clinical studies, with Phase 2 initiation expected in the first quarter of 2027.

Transplant-Associated Herpesviruses

In a transplant setting, when patients are experiencing immunosuppression, they are at high risk of uncontrolled viral replication and severe disease brought on by one or more herpesviruses, including cytomegalovirus (CMV), HSV-1, HSV-2, varicella zoster virus (VZV) and Epstein-Barr virus (EBV). Each of these herpesviruses are highly prevalent, as approximately (1) 60% of transplant patients are CMV-positive; (2) 60% of transplant patients are HSV-positive; (3) 80% of transplant patients are VZV-positive and (4) 45% of transplant patients are EBV-positive. These viruses establish lifelong latent infections and frequently reactivate in transplant patients due to the use of immunosuppressive drugs following transplantation. These uncontrolled herpesvirus infections increase the risk of severe disease and serious complications, including organ rejection, graft loss and death, and impacted approximately 95,000 people receiving transplants in 2021 in the United States and Europe.

While there are approved antivirals that are administered in a transplant setting, currently approved antivirals are not active against a broad spectrum of transplant-associated herpesviruses and pose the risk of potentially serious side effects and drug-drug interactions. As a result of these limitations, we identified an opportunity to develop an oral, broad-spectrum NNPI for transplant-associated herpesvirus infections, which could greatly advance treatment.

7272, our development candidate in our NNPI program, is currently in regulatory filing-enabling nonclinical studies.

Research Programs

In addition to our investigational therapy programs that have nominated development candidates and have advanced into clinical studies or regulatory-filing enabling studies, our research team continues to actively focus on proprietary research to discover and nominate novel molecules to treat serious viral and liver diseases.

Collaboration and License Agreement

Gilead Sciences, Inc.

In October 2023, we entered into an Option, License and Collaboration agreement (the Gilead Collaboration Agreement) with Gilead pursuant to which Gilead (1) exclusively licensed to us its HPI program and its NNPI program, while retaining opt-in rights to these programs, and (2) has an option to take an exclusive license, on a program-by-program basis, to all of our other current and future pipeline programs. During the 12-year collaboration term (subject to payment of certain extension fees) and for a specified period thereafter, Gilead may exercise its opt-in rights, on a program-by-program basis, at one of two timepoints-completion of a certain Phase 1 study or, upon payment of a deferral fee and completion of a certain Phase 2 study for the first product within the program-upon payment of an opt-in fee ranging from $45.0 million to $125.0 million per program depending on the type of program and when the option is exercised. Pursuant to the Gilead Collaboration Agreement, Gilead made an $84.8 million upfront cash payment to us. In December 2024, we and Gilead entered into the First Amendment to the Gilead Collaboration Agreement, which restructured the timing of specific options exercisable and the fees payable to us under the terms of the Gilead Collaboration Agreement due to an agreed upon development plan for 6250. To facilitate this development plan, (1) we received a payment of $10.0 million from Gilead and (2) the opt-in fee payable by Gilead in connection with 6250 was restructured, though it remains in the range of opt-in fees detailed above. The $10.0 million payment received in connection with the First Amendment to the Gilead Collaboration Agreement was creditable towards future collaboration-related payments payable by Gilead and was applied toward Gilead's opt-in fee paid for the HPI program in December 2025.

If Gilead exercises its opt-in right to any current or future program under the collaboration, we are eligible to receive up to $330.0 million in potential regulatory and commercial milestones on that program, in addition to royalties ranging from the high single-digits to high teens, depending on the clinical stage of the program at the time of the opt-in. Following Gilead's exercise of its option for each program, we may opt-in to cover 40% of the research and

development costs in the United States and share 40% of the profits and operating loss in the United States for products within the program in lieu of receiving milestones and royalties for that program in the United States, unless we later opt out of the cost/profit share for the program. Prior to Gilead's potential exercise of its opt-in, we are primarily responsible for all discovery, research and development on both our programs and the two Gilead-contributed programs. Following Gilead's opt-in, Gilead will control the further discovery, research, development and commercialization on any optioned programs, and is responsible for all related costs unless we opt in to share 40% of all costs and profits in the United States. During the term, Gilead will continue to support the collaboration through extension fees of $75.0 million in each of the third, fifth and seventh anniversaries of the collaboration.

The Gilead Collaboration Agreement is subject to termination by either party for the other party's uncured, material breach or insolvency. Subject to certain limitations, we and Gilead both have certain termination for convenience rights, upon sufficient prior written notice, with respect to programs that one party in-licenses from the other (subject to Gilead's option rights), and with respect to Gilead, for programs it has option rights to (subject to certain time limitations with respect to existing Company programs). Gilead also has a right to terminate the collaborative activities under the Gilead Collaboration Agreement at certain specified points during the collaboration term. Other customary termination rights are further provided in the Gilead Collaboration Agreement.

Also in October 2023, we and Gilead entered into a Common Stock Purchase Agreement and an Investor Rights Agreement (together, the Gilead Equity Agreements), which were both amended in June 2024. The Gilead Equity Agreements include a three-year standstill provision and a two-year lockup provision (which has expired), each with customary exceptions, and provide Gilead with certain other stock purchase rights and registration rights, as well as the right to designate two directors (or, alternatively, board observers at Gilead's election) to our board of directors. In December 2023, Gilead designated Tomas Cihlar, Ph.D. to serve on our board of directors, and in March 2024, Gilead designated Robert D. Cook II to serve on our board of directors.

As of June 30, 2026, Gilead held (1) approximately 25.1% of our outstanding common stock, (2) a warrant to purchase up to 179,500 shares of our common stock at a price of $17.00 per share, which was acquired in a financing transaction in 2024 (the 2024 Warrant), (3) a Class A warrant to purchase up to 1,147,960 shares of our common stock at a price of $21.60 per share (Class A Warrant), which was acquired in a financing transaction in 2025 (the 2025 Financing) and (4) a Class B Warrant to purchase up to 1,147,960 shares of our common stock at a price of $21.60 per share (Class B Warrant), which was also acquired in the 2025 Financing. The 2024 Warrant is exercisable and expires on June 18, 2029. The Class A Warrant is also exercisable and expires on or prior to the earlier of (a) August 11, 2030 (five years from the date of issuance) and (b) the date that is 30 days after the public announcement that we have completed enrollment of at least 200 patients for our Phase 2 clinical study evaluating 5366 versus valacyclovir. The Class B Warrant is exercisable between November 15, 2026 and December 31, 2026, provided that if, prior to November 15, 2026, we publicly announce that we have received at least $75.0 million in the aggregate of non-dilutive capital in connection with a collaboration agreement, then the Class B Warrant automatically terminates in full.

Option Exercise

In December 2025, Gilead exercised its option to exclusively license our HPI program for the treatment of recurrent genital herpes, including 5366 and 1179. This is the first program that Gilead will advance under the Gilead Collaboration.

Under the terms of the Gilead Collaboration Agreement, we received a net $35 million payment in connection with Gilead's exercise of our HPI program. The net $35 million payment reflects a $45 million option fee, net of $10 million in accelerated funding that we received under the First Amendment to the Gilead Collaboration Agreement, which was creditable against future payments. Gilead received an exclusive license to 5366 and 1179 and will have the sole right and responsibility for further clinical development and commercialization of the HPI program.

We received Gilead's clinical development plan and budget for the HPI program in June 2026. The plan indicates that 1179 has been selected to advance, with a Phase 2 clinical study in participants with recurrent genital herpes expected to initiate by the end of 2026. Gilead is also considering the possible evaluation of 1179 as part of a combination strategy with HIV PrEP. Our decision regarding whether to exercise our right to opt in to share 40% of all costs and profits in the United States (the Profit-Share) in lieu of receiving milestones and royalties for that program in the United States will be made after receipt and review of Gilead's commercial cost estimates, which will complete the opt-in package. If we opt in to the Profit-Share, we remain eligible to receive up to $280 million in regulatory and

commercial milestones, as well as tiered royalties on net sales ranging from the high single-digits to low teens.

Results of Operations

Comparison of the Three Months Ended June 30, 2026 and 2025

Collaboration Revenue

The following table summarizes the period-over-period changes in our collaboration revenue (in thousands, except for percentages):

Collaboration revenue was $13.4 million for the three months ended June 30, 2026 compared to $9.6 million for the same period in 2025. The $3.7 million increase reflects the timing of activities performed and progress toward completion of services under the Gilead Collaboration Agreement, and includes a $5.1 million cumulative catch-up adjustment recognized during the three months ended June 30, 2026 related to updated estimates of future activities under the collaboration.

Research and Development Expenses

Research and development expenses consist primarily of employee-related expenses, fees paid to contract research organizations and contract manufacturing organizations, lab supplies and other third-party expenses that support our research and discovery, nonclinical and clinical activities. External program costs represent a significant portion of our research and development expenses, which we track by product candidate once it has been nominated. We use our employee and infrastructure resources, as well as certain third-party costs, across multiple research and development programs, and we do not specifically allocate these costs to our programs.

The following table summarizes the period-over-period changes in our research and development expenses (in thousands, except for percentages):

Research and development expenses were $14.9 million for the three months ended June 30, 2026 compared to $16.1 million for the same period in 2025. The $1.2 million decrease was primarily driven by lower external program expenses, particularly for 5366, reflecting the completion of clinical trials and lower manufacturing and toxicology study costs, partially offset by increases in our research and discovery efforts and higher employee-related expenses

due to increased headcount, annual salary adjustments and stock-based compensation expense related to performance-based restricted stock units granted in mid-2025.

General and Administrative Expenses

General and administrative expenses consist primarily of salaries and other related costs for personnel in executive, finance, accounting, business development, information technology, legal and human resources functions. Other significant costs include facility costs not otherwise included in research and development expenses, insurance costs, legal fees relating to patents and corporate matters and fees for accounting and consulting services.

The following table summarizes the period-over-period changes in our general and administrative expenses (in thousands, except for percentages):

General and administrative expenses were $4.8 million for the three months ended June 30, 2026 compared to $4.6 million for the same period in 2025. The $0.2 million increase was primarily driven by higher stock-based compensation expense associated with performance-based restricted stock units granted in mid-2025, partially offset by lower professional fees related to patent filings.

Interest and Other Income, Net

Interest income consists of interest earned on our cash and cash equivalents and available-for-sale marketable securities.

The following table summarizes the period-over-period changes in our interest and other income, net (in thousands, except for percentages):

Interest and other income, net was $2.5 million for the three months ended June 30, 2026, compared to $0.9 million for the same period in 2025. The $1.6 million increase was primarily due to a larger portfolio balance resulting from the investment of cash proceeds from financing transactions completed in August 2025 and May 2026 and the collaboration transaction completed in December 2025.

Comparison of the Six Months Ended June 30, 2026 and 2025

Collaboration Revenue

The following table summarizes the period-over-period changes in our collaboration revenue (in thousands, except for percentages):

Collaboration revenue was $21.6 million for the six months ended June 30, 2026 compared to $19.0 million for the same period in 2025. The $2.5 million increase reflects the timing of activities performed and progress toward completion of services under the Gilead Collaboration Agreement, and includes a $5.1 million cumulative catch-up adjustment recognized during the six months ended June 30, 2026 related to updated estimates of future activities under the collaboration.

Research and Development Expenses

The following table summarizes the period-over-period changes in our research and development expenses (in thousands, except for percentages):

Research and development expenses were $29.8 million for the six months ended June 30, 2026 compared to $31.0 million for the same period in 2025. The $1.2 million decrease was primarily driven by lower external program expenses, particularly for 5366, reflecting the completion of clinical trials and lower manufacturing and toxicology study costs, partially offset by increases in our research and discovery efforts and higher employee-related expenses due to increased headcount, annual salary adjustments and stock-based compensation expense related to performance-based restricted stock units granted in mid-2025.

General and Administrative Expenses

The following table summarizes the period-over-period changes in our general and administrative expenses (in thousands, except for percentages):

General and administrative expenses were $9.5 million for the six months ended June 30, 2026 compared to $9.1 million for the same period in 2025. The $0.4 million increase was primarily driven by higher stock-based compensation expense associated with performance-based restricted stock units granted in mid-2025, partially offset by lower professional fees related to patent filings.

Interest and Other Income, Net

The following table summarizes the period-over-period changes in our interest and other income, net (in thousands, except for percentages):

Interest and other income, net was $4.8 million for the six months ended June 30, 2026, compared to $2.0 million for the same period in 2025. The $2.8 million increase was primarily due to a larger portfolio balance resulting from the investment of cash proceeds from financing transactions completed in August 2025 and May 2026 and the collaboration transaction completed in December 2025.

Liquidity and Capital Resources

Sources of Liquidity

As a result of our significant research and development expenditures and the lack of any FDA-approved products to generate product sales revenue, we have not been profitable and have generated operating losses since we were incorporated in October 2005. We have funded our operations through June 30, 2026 principally through equity financings, raising an aggregate of $929.8 million in net proceeds, and strategic collaborations, raising an aggregate of $236.2 million.

Cash Flows for the Six Months Ended June 30, 2026 and 2025

The following table summarizes our cash flow activities (in thousands):

Operating Activities

Net cash used in operating activities was $37.6 million for the six months ended June 30, 2026, compared to $40.2 million for the same period in 2025. The decrease was primarily attributable to lower clinical development expenditures resulting from the completion of multiple clinical trials, as well as approximately $1.5 million received under the letter agreement we entered into with Gilead in July 2025.

Investing Activities

Net cash used in investing activities was $97.5 million for the six months ended June 30, 2026, compared to net cash provided by investing activities of $23.6 million for the same period in 2025. The change was primarily due to our purchases of marketable securities following the underwritten offering in May 2026, as we invested the $108.1 million net proceeds received from the offering.

Financing Activities

Net cash provided by financing activities was $108.9 million for the six months ended June 30, 2026, compared to $2.3 million for the same period in 2025. The increase was primarily attributable to the net proceeds received from the underwritten offering in May 2026, which exceeded the proceeds received from sales of common stock under the Company's "at-the-market" offering program during 2025.

Funding Requirements

We expect our future operating expenses to increase over the coming years as we continue to expand our pipeline and advance our candidates. We monitor our cash needs and the status of the capital markets on a continuous basis. From time to time, we opportunistically raise capital and have done so numerous times since our initial public offering by issuing equity securities. We expect to continue to raise capital when and as needed and at the time and in the manner most advantageous to us.

As of June 30, 2026, we held cash, cash equivalents and marketable securities of $320.4 million, which based on our current operating plan, we believe will be sufficient to fund our operating requirements into late 2028. We believe our cash runway will extend into 2029 with the receipt of the $75.0 million extension fee due from Gilead in the fourth quarter of 2026, following the third anniversary of the Gilead Collaboration Agreement. We have based our estimate

on assumptions that may prove to be wrong, and we may utilize our available capital resources sooner than we currently expect.

Our future capital requirements will depend on many factors, including:

Critical Accounting Estimates

Our critical accounting policies and significant estimates are detailed in our 2025 Annual Report. There have been no material changes to our significant estimates from those previously disclosed in our 2025 Annual Report.