The following discussion and analysis of our financial condition and results of operations should be read in conjunction with our financial statements and related notes appearing elsewhere in this Quarterly Report on Form 10-Q and in our Annual Report on Form 10-K for the year ended December 31, 2025, filed with the Securities and Exchange Commission (“SEC”) on February 26, 2026, as amended (the “2025 Annual Report on Form 10-K”). Some of the information contained in this discussion and analysis or set forth elsewhere in this Quarterly Report on Form 10-Q, including information with respect to our plans and strategy for our business, includes forward-looking statements that involve risks and uncertainties. As a result of many factors, including those factors set forth in the “Risk Factors” section of this Quarterly Report on Form 10-Q and the “Risk Factors” section of our 2025 Annual Report on Form 10-K, our actual results could differ materially from the results described in, or implied by, these forward-looking statements. Overview We are a clinical-stage biotechnology company focused on unlocking the broad potential of ribonucleic acid (“RNA”) medicines (also known as oligonucleotides), or those targeting RNA, to transform human health. Our RNA medicines platform, PRISM®, combines multiple RNA medicine modalities, chemistry innovation, and deep insights in human genetics to deliver scientific breakthroughs that treat both rare and common disorders. Our toolkit of RNA-targeting modalities, including RNA interference (“RNAi”) (SpiNA) and RNA editing (AIMers), provides us with unmatched capabilities for designing and sustainably delivering candidates that optimally address disease biology. Our pipeline is focused on our obesity (WVE-007), alpha-1 antitrypsin deficiency (“AATD”) (WVE-006) and PNPLA3 I148M liver disease (WVE-008) programs, and also includes clinical programs for Duchenne muscular dystrophy (“DMD”) and Huntington’s disease (“HD”), as well as several preclinical programs utilizing our versatile RNA medicines platform. We were founded on the recognition that there was a significant, untapped opportunity to use chemistry innovation to tune the pharmacological properties of oligonucleotides. We have more than a decade of experience challenging convention related to oligonucleotide design and pioneering novel chemistry modifications to optimize the pharmacological properties of our molecules. We have seen in clinical trials that these chemistry modifications enhance potency, distribution, and durability of effect of our molecules. Our novel chemistry also allows us to avoid using complex delivery vehicles, such as lipid nanoparticles and viruses, and instead use clinically proven conjugates (e.g., N-acetylgalactosamine or (“GalNAc”)) or free uptake for delivery to a variety of cell and tissue types. We maintain strong and broad intellectual property, including for our novel chemistry modifications. Our best-in-class chemistry capabilities have also unlocked new areas of biology, such as harnessing adenosine deaminases acting on RNA (“ADAR”) enzymes for messenger RNA (“mRNA”) correction and upregulation, selectively silencing a mutant allele, and more. By opening up new areas of biology, we have also opened up new opportunities to slow, stop, or reverse disease and have expanded the possibilities offered through our platform. The inspiration for our multimodal platform is based on the recognition that the biological machinery (i.e., enzymes) needed to address human disease already exists within our cells and can be harnessed for therapeutic purposes with the right tools. We believe that we have built the most versatile toolkit of RNA-targeting modalities in the industry, with multiple means of repairing, restoring, or reducing proteins and designing best-fit solutions based on the unique biology of a given disease target. We are actively advancing programs across modalities, including RNAi (silencing), RNA editing, which uses novel A-to-I RNA editing oligonucleotides (“AIMers”), antisense silencing, and splicing. We have also advanced novel bifunctional modalities designed to silence multiple targets or silence one target while simultaneously editing or upregulating another unique target. 18 We intentionally focus on targeting the transcriptome using oligonucleotides rather than other nucleic acid modalities such as gene therapy and DNA editing. This focus enables us to: •Leverage diversity of expression across cell types by modulating the many regulatory pathways that impact gene expression, including transcription, endogenous RNAi pathways, splicing, and translation; •Address diseases that have historically been difficult to treat with small molecules or biologics; •Access a variety of tissue types or cell types throughout the body and modulate the frequency of dosing for broad distribution in tissues over time; •Avoid the risk of permanent off-target genetic changes and other challenges associated with DNA editing or gene therapy approaches; and •Leverage well-established industry manufacturing processes and regulatory, access, and reimbursement pathways. We are currently prioritizing lead programs that use GalNAc delivery for hepatic and metabolic diseases, each of which has potential to translate powerful human genetic insights into potentially transformational RNA medicines: •WVE-007 is a GalNAc-conjugated siRNA (SpiNA design) targeting inhibin βE (“INHBE”) for obesity; •WVE-006 is a GalNAc-conjugated RNA editing oligonucleotide (AIMer) for AATD; •WVE-008 is a GalNAc-conjugated RNA editing oligonucleotide (AIMer) for PNPLA3 I148M liver disease. Our clinical-stage portfolio also includes WVE-N531, an exon 53 splicing oligonucleotide for DMD, and WVE-003, an allele-selective oligonucleotide designed to lower mutant huntingtin (“mHTT”) protein and preserve healthy, wild-type huntingtin (“wtHTT”) protein. We are also advancing several emerging siRNA and RNA editing programs targeting both hepatic and extra-hepatic tissues. 19 Our Current Programs Additional details regarding our lead therapeutic programs are set forth below. Obesity WVE-007 is a GalNAc-siRNA that utilizes our proprietary design (“SpiNA”). WVE-007 is designed to silence INHBE mRNA to induce fat loss by stimulating lipolysis (fat breakdown) while preserving muscle mass to promote and maintain a healthy metabolic profile. There are approximately 175 million people in the United States and Europe, and over one billion people globally, living with obesity, and therapeutic options beyond GLP-1 receptor agonists are needed. GLP-1 receptor agonists lead to weight loss at the expense of muscle, suppress the general reward system, and are associated with a poor tolerability profile and high discontinuation rates. Heterozygous INHBE loss-of-function (“LoF”) human carriers exhibit a healthy metabolic profile, including reduced waist-to-hip ratio and reduced odds of developing type 2 diabetes or coronary artery disease, and reduction of INHBE by 50% or more is expected to promote a healthy metabolic profile. In preclinical diet-induced obesity (“DIO”) mouse models, a single dose of our INHBE GalNAc-siRNA has demonstrated highly potent and durable INHBE silencing (and >70% Activin E reductions), supporting once or twice a year subcutaneous dosing in humans. Weight loss was driven by visceral fat loss, and muscle mass was preserved in the mice, which is consistent with the profile of human INHBE LoF carriers. In DIO mice studies, a single dose of our INHBE GalNAc-siRNA led to a weight loss effect that was similar to daily subcutaneous injections of semaglutide for 28 days. We also observed a decrease in high fat diet-induced expansion of visceral adipose mass. This reduction of visceral fat mass was associated with significant shrinkage of adipocyte enlargement induced by a high fat diet compared with phosphate-buffered saline (“PBS”) treatment. Collectively, these results support the promotion of healthy adipose tissue with this mechanism of action, while muscle mass was preserved. In a head-to-head study in DIO mice, treatment with our INHBE GalNAc-siRNA prior to cessation of semaglutide treatment curtailed expected rebound weight gain. When administered as an add-on to semaglutide, a single dose of our INHBE GalNAc-siRNA doubled the weight loss observed with semaglutide alone, and this effect was sustained throughout the duration of the preclinical study. In preclinical studies, we have also observed that infiltration of macrophages into visceral adipose was significantly decreased by a single dose of INHBE GalNAc-siRNA compared with PBS controls. INHBE GalNAc-siRNA also significantly reduced proinflammatory M1 macrophage (CD11c positive) while sustaining levels of anti-inflammatory M2 macrophages in visceral fat, indicating an overall shift away from a pro-inflammatory state. Further, RNA sequencing data from subcutaneous adipose tissue indicates that INHBE GalNAc-siRNA leads to the upregulation of genes promoting insulin sensitivity, fatty acid utilization and beiging of white adipose, while downregulating adipose inflammation and fibrosis pathways. RNA sequencing data from visceral adipose tissue demonstrate that our INHBE GalNAc-siRNA increased glucose and fatty acid utilization, and reduced inflammation and fibrosis in adipose tissue. The INLIGHT™ trial is our first-in-human clinical study of WVE-007 in individuals living with obesity. The Phase 1 single ascending dose (“SAD”) portion of the INLIGHT trial includes otherwise healthy adults living with overweight or obesity to assess safety, tolerability, pharmacokinetics (“PK”), Activin E, body weight, biomarkers and body composition as measured by Dual-Energy X-ray Absorptiometry (“DEXA”). 20 In December 2025, we announced positive interim data from the ongoing Phase 1, SAD portion of the INLIGHT trial, including three-month follow-up from the single subcutaneous 240 mg dose cohort in 32 individuals. These data demonstrated improvements in body composition including reduction in visceral fat, reduction in total fat mass, and preservation of muscle as measured by DEXA. Additionally, we shared that we observed consistent and durable serum Activin E reductions across participants, which support WVE-007’s potential for once or twice-yearly dosing. WVE-007 was generally safe and well tolerated across all dose levels (75 mg, 240 mg, 400 mg, and 600 mg). In March 2026, we announced additional interim data from the Phase 1, SAD portion of the INLIGHT trial. Participants had an average BMI of 32 kg/m², a population with less fat and lower BMI than those in Phase 2 and 3 obesity studies. Key highlights from the update in March 2026 include: -At six-month follow-up, a single 240 mg dose of WVE-007 demonstrated significant placebo-adjusted reductions in visceral fat (-14%; p<0.05) and total fat (-5%), stabilization of lean mass (+2%), and reductions in waist circumference (-3%) and body weight (-1%). -The 400 mg cohort had a leaner baseline body composition, with lower BMI and more participants (10 out of 24 individuals) with healthy levels of visceral fat (≤500 g). A post-hoc analysis of the three-month 400 mg cohort results demonstrated robust and statistically significant average reduction in visceral fat (-7.8%, p<0.05) in individuals with higher baseline visceral fat (>500g), emphasizing the impact of baseline body composition on therapeutic effect. -Consistent, durable, and dose-dependent serum Activin E reductions sustained through at least seven months continue to support WVE-007’s potential for once or twice-yearly dosing, with a mean maximum reduction of up to 88%. -WVE-007 was generally safe and well tolerated across all dose levels (75 mg, 240 mg, 400 mg, and 600 mg). The INLIGHT clinical trial is currently ongoing with 240 mg (n=32), 400 mg (n=32), and 600 mg (n=32) cohorts fully dosed. The INLIGHT trial is ongoing at multiple trial sites including in the United States, following clearance of an Investigational New Drug (“IND”) application. Additional data from the INLIGHT trial, including data from the 600 mg Phase 1 SAD cohort, are expected in the second half of 2026. Dosing in the Phase 2a multidose portion of the INLIGHT trial of WVE-007 (INHBE GalNAc-siRNA) in individuals with higher BMI (35-50 kg/m2) with and without type 2 diabetes is underway. This placebo-controlled (3:1) Phase 2a study includes multiple assessments over a 12-month period, including body weight, waist circumference, body composition (MRI and DEXA), liver fat (MRI-PDFF), HbA1c, lipid levels, CRP, and muscle function. The results will inform further development of WVE-007 in obesity, as well as metabolic dysfunction-associated steatohepatitis (“MASH”), type 2 diabetes, and other cardiometabolic diseases. The first assessment in this portion of the trial is planned for three months after participants have received their first dose. We expect to initiate combination and maintenance trials of WVE-007 in the second half of 2026. Alpha-1 antitrypsin deficiency (“AATD”) Our AATD program uses our novel GalNAc-conjugated AIMers (RNA editing oligonucleotides) and endogenous ADAR enzymes to correct a single base in the mutant SERPINA1 mRNA. By correcting the single RNA base mutation that causes a majority of AATD cases with the Pi*ZZ genotype (approximately 200,000 in the United States and Europe), RNA editing may provide an ideal approach for increasing circulating levels of wild-type AAT protein and reducing mutant protein aggregation in the liver, thus simultaneously addressing both the lung and liver manifestations of the disease. WVE-006 does not require lipid nanoparticle (“LNP”) delivery, which may be associated with systemic and liver toxicities, and comes without the risk of irreversible, collateral bystander edits and indels, which are associated with DNA base editing. WVE-006 is first-in-class in AATD and is the most advanced program currently in clinical development using an oligonucleotide to harness an endogenous enzyme for RNA editing. Preclinical data show that treatment with WVE-006 resulted in serum AAT protein levels of up to 30 µM (7-fold increase) in an established AATD mouse model (NSG-PiZ). WVE-006 also led to restoration of approximately 50% wild-type M-AAT protein in serum and a 3-fold increase in neutrophil elastase inhibition activity, indicating that the restored M-AAT protein was functional. Our AATD AIMers are highly specific to SERPINA1 RNA in vitro and in vivo based on transcriptome-wide analyses. Our RestorAATion clinical program investigating WVE-006 as a treatment for AATD is comprised of two parts: RestorAATion-1, a study of healthy volunteers, and RestorAATion-2, a Phase 1b/2a open label study designed to evaluate the safety, tolerability, pharmacodynamics and pharmacokinetics of WVE-006 in patients with AATD. The trial includes both single ascending dose and multiple ascending dose portions. The RestorAATion-2 clinical trial is fully enrolled and dosing is complete in all cohorts (200 mg, 400 mg, and 600 mg). 21 We have shared interim data from the 200 mg and 400 mg single and multidose cohorts, as well as data from the 600 mg single dose cohort of RestorAAtion-2. Key highlights include: -Robust, dose-dependent reductions of circulating, mutant Z-AAT from baseline: 70.5% in the 200 mg biweekly dose cohort (seven doses) and 67.7% in the 400 mg monthly dose cohort (four doses). -Robust, dose-dependent restoration of wild-type M-AAT protein (canonical M-AAT) as a percentage of total circulating AAT: 64.4% in the 200 mg biweekly dose cohort (seven doses) and 58.7% in the 400 mg monthly dose cohort (four doses). -Restoration of dynamic AAT response: Three instances of dynamic and rapid production of serum AAT protein due to acute phase responses were observed across RestorAATion-2 as indicated by concurrent C-reactive protein (CRP) and AAT elevation; this included a total AAT level of 20.6 µM and M-AAT level of 10.3 µM observed in one individual during an acute phase response due to a kidney stone following a single 200 mg dose of WVE-006. Across all available RestorAATion-2 data, CRP increases were strongly correlated with increases in AAT (r=0.73, p<0.001, n=19). -Safety and durability: Data support monthly subcutaneous dosing, with editing sustained at least three months following the last dose in both the 200 mg and 400 mg multidose cohorts. WVE-006 continued to be well tolerated with a favorable safety profile. All adverse events (AEs) were mild to moderate in intensity, and there were no SAEs or clinically meaningful liver function test elevations. We expect to share data from the 600 mg monthly multidose cohort of RestorAATion-2 in the second half of 2026. Our request for a meeting regarding a potential accelerated approval pathway for WVE-006 was granted by the U.S. Food and Drug Administration (“FDA”). The meeting is scheduled for the end of summer 2026. PNPLA3 I148M liver disease To effectively address the manifestations of PNPLA3 I148M liver disease, we use our novel RNA editing approach and have advanced WVE-008, a GalNAc-conjugated AIMer, as our clinical candidate. PNPLA3 I148M is a genetic driver of liver disease, including metabolic dysfunction-associated fatty liver disease (“MAFLD”), MASH, and alcoholic steatohepatitis (“ASH”). There are an estimated nine million homozygous PNPLA3 I148M individuals with liver disease in the United States and Europe. Homozygous carriers have a near nine-fold higher risk of liver-related death compared to non-carriers. Additionally, homozygous PNPLA3 I148M carriers with MASH may experience more severe disease with faster progression to advanced fibrosis and end-stage liver disease. The PNPLA3 protein plays a critical role in hepatic lipid metabolism by balancing triglyceride storage and secretion, and supporting lipid remodeling, lipid mobilization, and retinol metabolism. The PNPLA3 I148M variant leads to a gain-of-function and contributes to liver disease by aggravating steatosis, inflammation, fibrosis, and ballooning. Therapeutic approaches aimed at silencing PNPLA3 may address liver fat accumulation, but they provide limited benefit in restoring retinol metabolism; fibrosis, ballooning, and inflammation are expected to persist. In contrast, an RNA editing approach to restore, rather than silence, PNPLA3 function in homozygous PNPLA3 I148M carriers should address liver disease by restoring lipid metabolism and reversing steatosis, fibrosis, ballooning, and inflammation. In preclinical studies, we have demonstrated that our PNPLA3 GalNAc-AIMer restores functional PNPLA3 protein and decreases lipid accumulation. We expect to file a clinical trial application for WVE-008 in the second half of 2026. Duchenne muscular dystrophy (“DMD”) In DMD, we are advancing WVE-N531, which is designed to skip exon 53 within the dystrophin gene – a therapeutic approach that would address approximately 8-10% of DMD cases. WVE-N531 is designed to cause the cellular splicing machinery to skip over exon 53 during pre-mRNA processing, which restores the dystrophin mRNA reading frame and enables production of a truncated, but functional, dystrophin protein. Exon skipping produces dystrophin from the endogenous dystrophin gene (not micro or mini dystrophin expressed from a foreign vector), under the control of native gene-regulatory elements, resulting in physiological control over its expression. WVE-N531 is our first splicing candidate incorporating PN backbone (“PN”) chemistry to be assessed in the clinic. In the third quarter of 2024, the FDA granted Rare Pediatric Disease Designation and Orphan Drug Designation to WVE-N531. FORWARD-53, the Phase 1b/2a proof-of-concept, open label trial of WVE-N531 included “Part A,” in which 3 boys received 3 doses of WVE-N531 at 10 mg/kg every two weeks and “Part B,” in which 11 boys initially received 10 mg/kg every two weeks for 48 weeks. In “Part B”, biopsy data was gathered from eight boys after 24 and 48 weeks, as well as safety and functional outcome assessments for all participants. Key results from the study included: -WVE-N531 uptake in myogenic stem cells, which are integral to muscle regeneration, and in myofibers; -Mean WVE-N531 skeletal muscle concentrations of ~41,000 ng/g and a 61-day tissue half-life support monthly dosing; 22 -Statistically significant and clinically meaningful improvement of 3.8 seconds in Time-to-Rise vs. natural history with largest effect observed relative to any approved dystrophin restoration therapy at 48 weeks; additional functional benefits observed in other outcome measures including North Star Ambulatory Assessment (“NSAA”); -First-ever demonstration of substantial improvements in muscle health with exon skipping – statistically significant reduction in fibrosis driven by decreases in inflammation and necrosis, coupled with transition from regenerative to mature muscle; decreases in creatine kinase and circulating inflammatory biomarkers; -Dystrophin expression stabilized between 24 and 48 weeks and averaged 7.8% with 88% of boys above 5% average dystrophin; and -WVE-N531 was generally safe and well-tolerated with no SAEs observed. All participants in FORWARD-53 elected to advance to the extension portion of the clinical trial, which is currently ongoing with boys receiving monthly doses of WVE-N531. To augment monthly data and ensure a monthly regimen at a potential launch, we expanded FORWARD-53 to include additional boys on a monthly dosing regimen. We are evaluating the evolving regulatory and commercial landscape in DMD and exploring potential partnerships in advance of filing a New Drug Application (“NDA”). Huntington’s disease (“HD”) WVE-003 is our stereopure allele-selective oligonucleotide that incorporates our proprietary PN chemistry and is designed to selectively target rs362273, a variant of the single nucleotide polymorphism (“SNP”), “mHTT SNP3”, associated with the disease-causing mHTT mRNA transcript within the HTT gene (Iwamoto et al., MTNA). Targeting mRNA through SNP3 allows us to lower expression of transcript from the mutant allele, while leaving the healthy transcript relatively intact, thereby preserving wild-type (healthy) huntingtin (“wtHTT”) protein, which is important for neuronal function. Approximately 40% of the HD population carries SNP3 according to published literature (Carroll et al., Molecular Therapy, 2011), and up to 80% of HD may be addressed in the future with other SNP-targeted candidates. SELECT-HD was a global, multicenter, randomized, double-blind, placebo-controlled Phase 1b/2a clinical trial to assess the safety and tolerability of WVE-003 in people with a confirmed diagnosis of HD who were in the early stages of the disease and carry SNP3 in association with their cytosine adenine guanine (“CAG”) expansion. Additional objectives included assessing PK and exploratory pharmacodynamics and clinical endpoints. In June 2024, we announced positive clinical data from the SELECT-HD study. Results from the multi-dose portion of the trial, which evaluated three doses of 30 mg WVE-003 administered every eight weeks, showed clear translation of target engagement to clinic with statistically significant, potent, durable and allele-selective reductions in cerebrospinal fluid (“CSF”) mHTT of up to a mean 46%, with preservation of wtHTT protein. The multi-dose cohort also revealed a statistically significant correlation between mHTT reduction and slowing of caudate atrophy, indicating a potential benefit of allele-selective mHTT reductions. Caudate atrophy, as measured by MRI, is a well-characterized measure of disease progression in HD. In the multi-dose cohort, WVE-003 was generally safe and well-tolerated, with mild-to-moderate adverse events (“AEs”) and no SAEs. In November 2024, five months after a patient completed their final safety visit, an SAE was reported that we assessed to be not related to WVE-003. Following our positive clinical results, we initiated engagement with the FDA. In November 2024, we received supportive initial feedback from the FDA, who recognize the severity of HD and are receptive to and engaged with us regarding a potential pathway to accelerated approval. The FDA is open to our plan to evaluate biomarkers, including caudate atrophy, as an endpoint to assess HD progression with the potential to predict clinical outcomes. Also in November 2024, the FDA granted Orphan Drug Designation to WVE-003. We have prepared an IND application for a potentially registrational Phase 2/3 study of WVE-003 and would plan to submit it in conjunction with a prospective strategic partner. Discovery Pipeline We are advancing new targets across multiple disease areas to expand our pipeline of wholly owned programs. Our compelling preclinical data demonstrate that our oligonucleotides can distribute to various tissues and cells without complex delivery vehicles, enabling us to address a wide variety of diseases. Within RNA editing, we have demonstrated clinically that we can address monogenic diseases by correcting the disease-causing mutation, as evidenced by restoration of healthy protein function for the treatment of AATD. Beyond correction, we have preclinical data demonstrating our ability to increase the stability of the mRNA transcript to upregulate protein levels. Within RNAi, we have shared preclinical data which show that our SpiNA designs enable RNAi-mediated silencing by further improving Ago2 loading and pharmacokinetics, leading to increased potency and durability compared to industry benchmarks. With our SpiNA designs, our preclinical data demonstrate we can silence targets in extra-hepatic tissues including adipose, skeletal muscle, heart, central nervous system (“CNS”), and kidney. We are utilizing a combination of human genetics and artificial intelligence (“AI”) for target discovery and oligonucleotide design, and we have initiated a number of 23 preclinical RNA editing and RNAi programs supported by evidence from human genetics, that leverage easily accessible biomarkers, offer efficient paths to proof-of-concept in humans, and represent meaningful commercial opportunities. We have applied learnings from across our platform and chemistry optimization to investigate new bifunctional modalities which combine RNAi and RNA editing or dual RNAi silencing into a single oligonucleotide construct. These constructs are designed to silence multiple targets or silence one target while simultaneously editing or upregulating another distinct target. We demonstrated the ability of a single bifunctional oligonucleotide to engage in silencing and editing in vivo in mice using a GalNAc-conjugated oligonucleotide that is designed to edit UGP2 and silence TTR. In a separate preclinical study, we also demonstrated that we were able to upregulate low-density lipoprotein receptor and silence PCSK9 using a single construct in primary human hepatocytes. Through our collaboration with GlaxoSmithKline Intellectual Property (No. 3) (“GSK”), we are actively working on multiple target validation programs as GSK-partnered programs, for which all of our costs and expenses are prepaid by GSK. GSK has selected four programs, across multiple modalities in both hepatic and extra-hepatic tissues, to advance to development candidates following achievement of target validation, which have resulted in additional payments to us under the collaboration. Recent Developments As previously disclosed on April 15, 2026, Wave Life Sciences Ltd., a public company limited by shares incorporated under the laws of the Republic of Singapore (“Wave-Singapore”), announced that it has decided to restructure its corporate group to cause the parent company of the group to be a Delaware corporation (the “Redomiciliation”). On June 22, 2026, we obtained the requisite shareholder approval required in connection with the Redomiciliation to the United States by way of the implementation of a statutory procedure known as a scheme of arrangement under Section 210 of the Companies Act 1967 of Singapore (the “Scheme of Arrangement”). On July 14, 2026, the Scheme of Arrangement was approved by the High Court of the Republic of Singapore. We expect the Redomiciliation to take effect in August 2026. Under U.S. GAAP, the Scheme of Arrangement required for the Redomiciliation will be accounted for consistent with a reorganization of entities under common control. On June 29, 2026, we entered into an amendment to extend the term of our lease for our manufacturing facility in Lexington, Massachusetts. We leveraged market conditions to secure our existing, state-of-the-art, oligonucleotide space through at least January 2038. In addition to manufacturing space, the Lexington facility includes additional laboratory and office space. This facility supplements our existing Cambridge, Massachusetts laboratory and office space headquarters and enhances our ability to secure drug substance for current and future development activities. 24 Financial Operations Overview We have never been profitable, and since our inception, we have incurred significant operating losses. Our net loss for the three months ended June 30, 2026 and 2025 was $69.4 million and $50.5 million, respectively. Our net loss for the six months ended June 30, 2026 and 2025 was $95.4 million and $97.3 million, respectively. As of June 30, 2026 and December 31, 2025, we had an accumulated deficit of $1,421.7 million and $1,326.2 million, respectively. We expect to continue to incur significant expenses and operating losses for the foreseeable future. Revenue We recognize collaboration revenue under the GSK Collaboration Agreement (as defined in Note 7 in the notes to our unaudited consolidated financial statements appearing elsewhere in this Quarterly Report on Form 10-Q), which became effective in January 2023. We have not generated any product revenue since our inception and do not expect to generate any revenue from the sale of products for the foreseeable future. Operating Expenses Our operating expenses since inception have consisted primarily of research and development expenses and general and administrative expenses. Research and Development Expenses Research and development expenses consist primarily of costs incurred for our research activities, including our discovery efforts, and the development of our product candidates, which include: •compensation-related expenses, including employee salaries, bonuses, share-based compensation expense and other related benefits expenses for personnel in our research and development organization; •expenses incurred under agreements with third parties, including contract research organizations (“CROs”) that conduct research, preclinical and clinical activities on our behalf, as well as contract manufacturing organizations (“CMOs”) that manufacture drug product for use in our preclinical studies and clinical trials; •expenses incurred related to our internal manufacturing of drug substance for use in our preclinical studies and clinical trials; •expenses related to compliance with regulatory requirements; •expenses related to third-party consultants; •research and development supplies and services expenses; and •facility-related expenses, including rent, maintenance and other general operating expenses. We recognize research and development costs as incurred. We recognize external development costs based on an evaluation of the progress to completion of specific tasks using information provided to us by our vendors. Payments for these activities are based on the terms of the individual agreements, which may differ from the pattern of costs incurred, and are reflected in our financial statements as prepaid or accrued expenses. Our primary research and development focus has been the development of our RNA medicines platform, PRISM. We are using PRISM, which combines multiple modalities, chemistry innovation and deep insights in human genetics, to deliver scientific breakthroughs that treat both rare and common disorders, and advance our pipeline of RNA medicines. Our research and development expenses consist primarily of expenses related to our CROs, CMOs, consultants, other external vendors and fees paid to global regulatory agencies to conduct our clinical trials, in addition to compensation-related expenses, internal manufacturing expenses, facility-related expenses and other general operating expenses. These expenses are incurred in connection with research and development efforts and our preclinical studies and clinical trials. We track certain external expenses on a program-by-program basis. However, we do not allocate compensation-related expenses, internal manufacturing expenses, equipment repairs and maintenance expenses, facility-related expenses or other operating expenses to specific programs. These expenses, which are not allocated on a program-by-program basis, are included in the “Other research and development expenses(1), including PNPLA3, additional preclinical programs, PRISM” category along with other external expenses related to our discovery and development programs, as well as platform development and identification of potential drug discovery candidates. 25 Product candidates in later stages of clinical development generally have higher development costs than those in earlier stages of clinical development, primarily due to the increased size and duration of later-stage clinical trials. We expect to continue to incur significant research and development expenses in the foreseeable future as we continue to manage our existing clinical trials, initiate additional clinical trials for certain product candidates, pursue later stages of clinical development for certain product candidates, maintain our manufacturing capabilities and continue to discover and develop additional product candidates in multiple therapeutic areas. General and Administrative Expenses General and administrative expenses consist primarily of compensation-related expenses, including salaries, bonuses, share-based compensation and other related benefits costs for personnel in our executive, finance, corporate, legal and administrative functions, as well as compensation-related expenses for our board of directors. General and administrative expenses also include legal fees; expenses associated with being a public company; professional fees for accounting, auditing, tax and consulting services; insurance costs; travel expenses; other operating costs; and facility-related expenses. Other Income, Net Other income, net is comprised primarily of interest income on cash, cash equivalents and marketable securities and, refundable tax credits from tax authorities. We recognize refundable tax credits when there is reasonable assurance that we will comply with the requirements of the refundable tax credit and that the refundable tax credit will be received. Income Taxes We are a Singapore multi-national company subject to taxation in the United States and various other jurisdictions. Critical Accounting Policies and Significant Judgments and Estimates Our consolidated financial statements are prepared in accordance with generally accepted accounting principles in the United States of America. The preparation of our financial statements and related disclosures requires us to make estimates and assumptions that affect the reported amount of assets, liabilities, revenue, costs and expenses and related disclosures. Management considers many factors in selecting appropriate financial accounting policies and in developing the estimates and assumptions that are used in the preparation of the financial statements. Management must apply significant judgment in this process. We believe that our revenue recognition policy, particularly (a) assessing the number of performance obligations; (b) determining the transaction price; (c) allocating the transaction price to the performance obligations in the contract; and (d) determining the pattern over which performance obligations are satisfied, including estimates to complete performance obligations, and the assumptions and estimates used in our analysis of contracts with CROs and CMOs to estimate the contract expense, involve a greater degree of judgment, and therefore we consider them to be our critical accounting policies. We evaluate our estimates and assumptions on an ongoing basis. Our actual results may differ from these estimates under different assumptions and conditions. Results of Operations Comparison of the three months ended June 30, 2026 and 2025 Three Months Ended June 30, 2026 2025 Change (in thousands) Revenue $ 2,272 $ 8,699 $ (6,427 ) Operating expenses: Research and development 51,293 43,469 7,824 General and administrative 24,781 17,989 6,792 Total operating expenses 76,074 61,458 14,616 Loss from operations (73,802 ) (52,759 ) (21,043 ) Total other income, net 4,447 2,290 2,157 Loss before income taxes (69,355 ) (50,469 ) (18,886 ) Income tax benefit — — — Net loss $ (69,355 ) $ (50,469 ) $ (18,886 ) 26 Revenue Revenue for the three months ended June 30, 2026 and 2025 was $2.3 million and $8.7 million, respectively, and is comprised of revenue earned under the GSK Collaboration Agreement. Research and Development Expenses Three Months Ended June 30, 2026 2025 Change (in thousands) INHBE program $ 6,870 $ 3,515 $ 3,355 AATD program 2,989 1,846 1,143 DMD program 3,953 2,681 1,272 HD program 157 789 (632 ) Other research and development expenses(1), including PNPLA3, additional preclinical programs, PRISM 37,324 34,638 2,686 Total research and development expenses $ 51,293 $ 43,469 $ 7,824 (1) Includes expenses related to other research and development programs, identification of potential drug discovery candidates, compensation-related expenses, internal manufacturing expenses, equipment repairs and maintenance expense, facility-related expenses, and other operating expenses, which are not allocated to specific programs. Research and development expenses were $51.3 million for the three months ended June 30, 2026, compared to $43.5 million for the three months ended June 30, 2025. The increase of approximately $7.8 million was due to the following: •an increase of $3.4 million in external expenses related to our INHBE program, including WVE-007 (RNAi); •an increase of $1.1 million in external expenses related to our AATD program, WVE-006 (RNA editing); •an increase of $1.3 million in external expenses related to our DMD program, including WVE-N531 (splicing); •a decrease of $0.6 million in external expenses related to our HD program, including WVE-003 (silencing); and •an increase of approximately $2.7 million in other research and development expenses, including PNPLA3, additional preclinical programs, PRISM, and internal and external research and development expenses that are not allocated on a program-by-program basis or are related to other discovery and development programs, and the identification of potential drug discovery candidates. This is mainly due to increases in compensation-related expenses, partially offset by decreases in other external research and development expenses. General and Administrative Expenses General and administrative expenses were $24.8 million for the three months ended June 30, 2026, as compared to approximately $18.0 million for the three months ended June 30, 2025. The increase of approximately $6.8 million was primarily driven by increases in compensation-related and other external expenses. Other Income, Net Other income, net for the three months ended June 30, 2026 and 2025 was $4.4 million and $2.3 million, respectively, and consisted primarily of interest income on cash, cash equivalents and marketable securities. Income Tax Benefit During the three months ended June 30, 2026 and 2025, we recorded no income tax benefit or provision. We maintained a full valuation allowance for the three months ended June 30, 2026 and 2025 in all jurisdictions due to uncertainty regarding future taxable income. 27 Comparison of the six months ended June 30, 2026 and 2025 Six Months Ended June 30, 2026 2025 Change (in thousands) Revenue $ 40,518 $ 17,874 $ 22,644 Operating expenses: Research and development 98,733 84,091 14,642 General and administrative 46,884 36,346 10,538 Total operating expenses 145,617 120,437 25,180 Loss from operations (105,099 ) (102,563 ) (2,536 ) Total other income, net 9,657 5,216 4,441 Loss before income taxes (95,442 ) (97,347 ) 1,905 Income tax benefit — — — Net loss $ (95,442 ) $ (97,347 ) $ 1,905 Revenue Revenue for the six months ended June 30, 2026 and 2025 was $40.5 million and $17.9 million, respectively, and is comprised of revenue earned under the GSK Collaboration Agreement. The year-over-year change in revenue was primarily driven by the recognition of the remaining deferred revenue related to the AATD performance obligation ($35.9 million), which was fully satisfied upon the termination of the AATD license, in the six months ended June 30, 2026. Research and Development Expenses Six Months Ended June 30, 2026 2025 Change (in thousands) INHBE program $ 11,706 $ 6,054 $ 5,652 AATD program 4,739 3,292 1,447 DMD program 8,091 5,719 2,372 HD program 220 1,956 (1,736 ) Other research and development expenses(1), including PNPLA3, additional preclinical programs, PRISM 73,977 67,070 6,907 Total research and development expenses $ 98,733 $ 84,091 $ 14,642 (1) Includes expenses related to other research and development programs, identification of potential drug discovery candidates, compensation-related expenses, internal manufacturing expenses, equipment repairs and maintenance expense, facility-related expenses, and other operating expenses, which are not allocated to specific programs. Research and development expenses were $98.7 million for the six months ended June 30, 2026, compared to $84.1 million for the six months ended June 30, 2025. The increase of approximately $14.6 million was due to the following: •an increase of $5.7 million in external expenses related to our INHBE program, including WVE-007 (RNAi); •an increase of $1.4 million in external expenses related to our AATD program, WVE-006 (RNA editing); •an increase of $2.4 million in external expenses related to our DMD program, including WVE-N531 (splicing); •a decrease of $1.7 million in external expenses related to our HD program, including WVE-003 (silencing); and •an increase of approximately $6.9 million in other research and development expenses, including PNPLA3, additional preclinical programs, PRISM, and internal and external research and development expenses that are not allocated on a program-by-program basis or are related to other discovery and development programs, and the identification of potential drug discovery candidates. This is mainly due to increases in compensation-related expenses, partially offset by decreases in other external research and development expenses. 28 General and Administrative Expenses General and administrative expenses were $46.9 million for the six months ended June 30, 2026, as compared to approximately $36.3 million for the six months ended June 30, 2025. The increase of approximately $10.6 million was primarily driven by increases in compensation-related and other external expenses. Other Income, Net Other income, net for the six months ended June 30, 2026 and 2025 was $9.7 million and $5.2 million, respectively, and consisted primarily of interest income on cash, cash equivalents and marketable securities. Income Tax Benefit During the six months ended June 30, 2026 and 2025, we recorded no income tax benefit or provision. We maintained a full valuation allowance for the six months ended June 30, 2026 and 2025 in all jurisdictions due to uncertainty regarding future taxable income. Liquidity and Capital Resources Since our inception, we have not generated any product revenue and have incurred recurring net operating losses. To date, we have primarily funded our operations through public and other registered offerings of our ordinary shares and other securities, collaborations with third parties and private placements of debt and equity securities. Through June 30, 2026, we have received an aggregate of approximately $2,086.7 million in net proceeds from these transactions, consisting of approximately $1,450.5 million in net proceeds from public and other registered offerings of our ordinary shares and other securities, $546.9 million from our collaborations and $89.3 million in net proceeds from private placements of our debt and equity securities. As of June 30, 2026, we had cash and cash equivalents totaling $368.0 million, marketable securities of $122.6 million, restricted cash of $3.8 million and an accumulated deficit of $1,421.7 million. We expect that our existing cash, cash equivalents and marketable securities will be sufficient to fund our operations for at least the next twelve months from the issuance date of these financial statements. We have based this expectation on assumptions that may prove to be incorrect, and we may use our available capital resources sooner than we currently expect. In addition, we may elect to raise additional funds before we need them if the conditions for raising capital are favorable due to market conditions or strategic considerations, even if we expect we have sufficient funds for our current or future operating plans. Our operating lease commitments as of June 30, 2026 total approximately $65.3 million, of which approximately $2.9 million is related to payments in 2026 and approximately $62.4 million is related to payments beyond 2026. On November 12, 2024, we filed a shelf registration statement on Form S-3ASR with the SEC for which we registered for sale an indeterminate amount of any combination of our ordinary shares, debt securities, warrants, rights and/or units from time to time and at prices and on terms that we may determine, which we refer to as the “2024 WKSI Shelf”. Our 2024 WKSI Shelf includes a prospectus covering up to an aggregate of $250.0 million in ordinary shares that we are able to issue and sell from time to time, through Jefferies LLC acting as our sales agent, pursuant to the Open Market Sale Agreement, dated May 10, 2019, as amended by Amendment No. 1, dated as of March 2, 2020, Amendment No. 2, dated as of March 3, 2022, and Amendment No. 3, dated November 12, 2024, for our “at-the-market” equity program. For the three and six months ended June 30, 2026, we made no sales under our “at-the-market" equity program. Adequate additional financing may not be available to us on acceptable terms, or at all. Our inability to raise capital as and when needed would have a negative impact on our financial condition and our ability to pursue our business strategy. We will need to generate significant revenue to achieve profitability, and we may never do so. Cash Flows The following table summarizes our cash flow activity: Six Months Ended June 30, 2026 2025 (in thousands) Net cash used in operating activities $ (113,135 ) $ (109,051 ) Net cash used in investing activities (123,892 ) (471 ) Net cash provided by financing activities 2,857 15,848 Effect of foreign exchange rates on cash, cash equivalents, and restricted cash 119 101 Net decrease in cash, cash equivalents, and restricted cash $ (234,051 ) $ (93,573 ) 29 Operating Activities During the six months ended June 30, 2026, operating activities used $113.1 million of cash, due to our net loss of $95.4 million, by changes in operating assets and liabilities of $42.1 million and non-cash charges of $24.4 million. The largest changes in operating assets and liabilities were the $29.6 million decrease in deferred revenue and the $8.3 million decrease in accrued expenses and other current liabilities. During the six months ended June 30, 2025, operating activities used $109.1 million of cash, due to our net loss of $97.3 million and changes in operating assets and liabilities of $27.2 million, offset by non-cash charges of $15.5 million. The largest changes in operating assets and liabilities were the $16.3 million decrease in deferred revenue and the $8.1 million decrease in accrued expenses and other current liabilities. Investing Activities During the six months ended June 30, 2026, investing activities used $123.9 million of cash, which was primarily related to purchases of marketable securities. During the six months ended June 30, 2025, investing activities used $0.5 million of cash, related to purchases of property and equipment. Financing Activities During the six months ended June 30, 2026, net cash provided by financing activities was $2.9 million, which was primarily due to $2.3 million in proceeds from the exercise of share options. During the six months ended June 30, 2025, net cash provided by financing activities was $15.8 million, which was primarily due to $12.4 million in net proceeds from sales under our “at-the-market” equity program and $3.0 million in proceeds from the exercise of share options. Funding Requirements We expect to continue to incur significant expenses in connection with our ongoing research and development activities and our internal cGMP manufacturing activities. Furthermore, we anticipate that our expenses will continue to vary if and as we: •continue to conduct our clinical trials evaluating our product candidates in patients; •conduct research and preclinical development of discovery targets and advance additional programs into clinical development; •file clinical trial applications with global regulatory agencies and conduct clinical trials for our programs; •make strategic investments in continuing to innovate our research and development platform, PRISM, and in optimizing our manufacturing processes and formulations; •maintain our manufacturing capabilities through our internal facility and our CMOs; •maintain our intellectual property portfolio and consider the acquisition of complementary intellectual property; •seek and obtain regulatory approvals for our product candidates; •respond to the impacts of local and global health epidemics, geopolitical conflicts, global economic uncertainty, rising inflation, tariffs, rising interest rates or market disruptions on our business; and •establish and build capabilities to market, distribute and sell our product candidates. 30 We may experience delays or encounter issues with any of the above, including but not limited to failed studies, complex results, safety issues or other regulatory challenges. Because of the numerous risks and uncertainties associated with the development of drug candidates and because the extent to which we may enter into collaborations with third parties for development of product candidates is unknown, we are unable to estimate the amounts of future capital outlays and operating expenses associated with completing the research and development for our therapeutic programs. Our future capital requirements for our therapeutic programs will depend on many factors, including: •the progress, results and costs of conducting research and continued preclinical and clinical development for our therapeutic programs and future potential pipeline candidates; •the number and characteristics of product candidates and programs that we pursue; •the cost of manufacturing clinical supplies of our product candidates; •whether and to what extent milestone events are achieved under our collaboration with GSK or any potential future licensee or collaborator; •the costs, timing and outcome of regulatory review of our product candidates; •our ability to obtain marketing approval for our product candidates; •the impacts of local and global health epidemics, geopolitical conflicts, global economic uncertainty, tariffs, rising inflation, rising interest rates or market disruptions on our business; •the costs and timing of future commercialization activities, including manufacturing, marketing, sales and distribution, for any of our product candidates for which we receive marketing approval; •market acceptance of our product candidates, to the extent any are approved for commercial sale, and the revenue, if any, received from commercial sales of our product candidates for which we receive marketing approval; •the costs and timing of preparing, filing and prosecuting patent applications, maintaining and enforcing our intellectual property rights and defending any intellectual property-related claims; •the effect of competing technological and market developments; and •the extent to which we acquire or invest in businesses, products and technologies, including entering into licensing or collaboration arrangements for product candidates. Identifying potential product candidates and conducting preclinical testing and clinical trials is a time-consuming, expensive and uncertain process that takes years to complete, and we may never generate the necessary data or results required to obtain marketing approval and achieve product sales. In addition, our product candidates, if approved, may not achieve commercial success. Our product revenue, if any, will be derived from sales of products that we do not expect to be commercially available for many years, if ever. Accordingly, we will need to obtain substantial additional funds to achieve our business objectives. Adequate additional funds may not be available to us on acceptable terms when we need them, or at all. We do not currently have any committed external source of funds, except for possible future payments from GSK under our collaboration with them. To the extent that we raise additional capital through the sale of equity or convertible debt securities, the ownership interest of our existing shareholders will be diluted, and the terms may include liquidation or other preferences that adversely affect the rights of our shareholders. Additional debt financing and preferred equity financing, if available, may involve agreements that include covenants limiting or restricting our ability to take specific actions, such as incurring additional debt, making capital expenditures or declaring dividends and may require the issuance of warrants, which could potentially dilute our shareholders’ ownership interests. If we raise additional funds through collaborations, strategic alliances or licensing arrangements with third parties, we may have to relinquish valuable rights to our technologies, future revenue streams, research programs or product candidates or grant licenses on terms that may not be favorable to us. If we are unable to raise additional funds through equity or debt financings when needed, we may be required to delay, limit, reduce or terminate our product development programs or any future commercialization efforts or grant rights to develop and market product candidates that we would otherwise prefer to develop and market ourselves. 31