Quarterly Report for Quarter Ending September 30, 2026 (Form 10-Q)

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

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 lead pipeline programs include obesity (WVE-007), alpha-1 antitrypsin deficiency ("AATD") (WVE-006), and PNPLA3 I148M liver disease (WVE-008), and we are also advancing 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.

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:

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:

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.

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").

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:

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 fourth quarter 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 ongoing. 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.

The INLIGHT clinical program is also evaluating WVE-007 in combination with tirzepatide as a treatment for obesity and other cardiometabolic indications, including MASH. The placebo-controlled (3:1) Phase 2a combination trial will evaluate 240 mg and 400 mg doses of WVE-007 in combination with weekly tirzepatide compared to tirzepatide alone in individuals living with obesity (BMI 35-50 kg/m2) and type 2 diabetes.

We also expect to initiate a clinical trial of WVE-007 as a maintenance therapy to preserve weight loss following discontinuation of incretin treatment in the fourth quarter 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).

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:

We expect to share data from the 600 mg monthly multidose cohort of RestorAATion-2 in the fourth quarter of 2026.

In October 2026, we announced alignment with the U.S. Food and Drug Administration ("FDA") on key aspects of our planned registrational pathway for WVE-006. Planning is underway for a two-year registrational trial to support potential full approval, with a one-year interim analysis to support potential accelerated approval based on AATD biomarkers.

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 fourth quarter of 2026.

Huntington's disease ("HD") and Duchenne muscular dystrophy ("DMD")

In HD, WVE-003 is our clinical-stage 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). In DMD, WVE-N531 is our clinical-stage compound designed to skip exon 53 within the dystrophin gene - a therapeutic approach that would address approximately 8-10% of DMD cases. We continue partnering discussions for WVE-003 and WVE-N531.

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 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. In September 2026, GSK selected a GalNAc-siRNA candidate to transition into GSK's pipeline, resulting in a $12 million milestone to Wave. With this new hepatic program now transitioning to candidate, our collaboration momentum continues as we have three additional programs rapidly advancing towards candidate selection, all leveraging our proprietary PRISM chemistry.

Recent Developments

On August 7, 2026, as part of the previously announced plan to restructure the Wave Life Sciences group of companies to cause a Delaware corporation to be the parent company of the group (the "Redomiciliation"), Wave Life Sciences, Inc., a Delaware corporation ("Wave-Delaware"), became the ultimate parent company of the Wave Life Sciences group of companies pursuant to a statutory procedure known as a scheme of arrangement under the Companies Act 1967 of Singapore (the "Scheme of Arrangement"). Pursuant to the Scheme of Arrangement, all issued ordinary shares in the capital of Wave Life Sciences Ltd., a public company limited by shares incorporated under the laws of the Republic of Singapore ("Wave-Singapore") as of immediately prior to the effective time of the Scheme of Arrangement were exchanged on a one-for-one basis for newly issued shares of common stock, par value $0.001 per share, of Wave-Delaware, and Wave-Singapore became a wholly owned subsidiary of Wave-Delaware.

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 September 30, 2026 and 2025 was $61.9 million and $53.9 million, respectively. Our net loss for the nine months ended September 30, 2026 and 2025 was $157.4 million and $151.2 million, respectively. As of September 30, 2026 and December 31, 2025, we had an accumulated deficit of $1,483.6 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:

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, 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.

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, stock-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

Following the Redomiciliation, we are a Delaware corporation subject to taxation in the United States and various other jurisdictions, including Singapore, where our wholly owned subsidiary, Wave Life Sciences Pte. Ltd., is incorporated.

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 September 30, 2026 and 2025

Revenue

Revenue for the three months ended September 30, 2026 and 2025 was $13.2 million and $7.6 million, respectively, and is comprised of revenue earned under the GSK Collaboration Agreement.

Research and Development Expenses

(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 $53.8 million for the three months ended September 30, 2026, compared to $45.9 million for the three months ended September 30, 2025. The increase of $8.0 million was due to the following:

General and Administrative Expenses

General and administrative expenses were $25.4 million for the three months ended September 30, 2026, as compared to approximately $18.1 million for the three months ended September 30, 2025. The increase of approximately $7.3 million was primarily driven by increases in compensation-related and other external expenses.

Other Income, Net

Other income, net for the three months ended September 30, 2026 and 2025 was $4.1 million and $2.5 million, respectively, and consisted primarily of interest income on cash, cash equivalents and marketable securities.

Income Tax Benefit

During the three months ended September 30, 2026 and 2025, we recorded no income tax benefit or provision. We maintained a full valuation allowance for the three months ended September 30, 2026 and 2025 in all jurisdictions due to uncertainty regarding future taxable income.

Comparison of the nine months ended September 30, 2026 and 2025

Revenue

Revenue for the nine months ended September 30, 2026 and 2025 was $53.7 million and $25.5 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, and the $12.0 million milestone in the nine months ended September 30, 2026.

Research and Development Expenses

(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 $152.6 million for the nine months ended September 30, 2026, compared to $130.0 million for the nine months ended September 30, 2025. The increase of $22.6 million was due to the following:

General and Administrative Expenses

General and administrative expenses were $72.2 million for the nine months ended September 30, 2026, as compared to approximately $54.4 million for the nine months ended September 30, 2025. The increase of approximately $17.8 million was primarily driven by increases in compensation-related and other external expenses.

Other Income, Net

Other income, net for the nine months ended September 30, 2026 and 2025 was $13.8 million and $7.7 million, respectively, and consisted primarily of interest income on cash, cash equivalents and marketable securities.

Income Tax Benefit

During the nine months ended September 30, 2026 and 2025, we recorded no income tax benefit or provision. We maintained a full valuation allowance for the nine months ended September 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 common stock and other securities, collaborations with third parties and private placements of debt and equity securities. Through September 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 common stock 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 September 30, 2026, we had cash and cash equivalents totaling $197.3 million, marketable securities of $233.4 million, restricted cash of $3.8 million and an accumulated deficit of $1,483.6 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 September 30, 2026 total approximately $64.4 million, of which approximately $2.0 million is related to payments in 2026 and approximately $62.4 million is related to payments beyond 2026.

On November 12, 2024, Wave-Singapore filed a shelf registration statement on Form S-3ASR with the SEC, which we refer to as the "2024 WKSI Shelf," covering the offering, issuance and sale from time to time of an indeterminate amount of common stock, debt securities, warrants, rights and/or units. In connection with the Redomiciliation, Wave-Delaware, as successor to Wave-Singapore, filed Post-Effective Amendment No. 1 to the 2024 WKSI Shelf pursuant to Rule 414(d) under the Securities Act to adopt the 2024 WKSI Shelf as its own. The 2024 WKSI Shelf includes a prospectus covering the offer and sale of up to $250.0 million of our common stock pursuant to our "at-the-market" equity program through Jefferies LLC, as sales agent, under the Amended and Restated Open Market Sale Agreement, dated August 7, 2026. For the three and nine months ended September 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:

Operating Activities

During the nine months ended September 30, 2026, operating activities used $173.3 million of cash, due to our net loss of $157.4 million and changes in operating assets and liabilities of $52.4 million, partially offset by non-cash charges of $36.5 million. The largest changes in operating assets and liabilities were the $30.8 million decrease in deferred revenue and the $10.7 million increase in accounts receivable.

During the nine months ended September 30, 2025, operating activities used $153.7 million of cash, due to our net loss of $151.2 million and changes in operating assets and liabilities of $26.7 million, partially offset by non-cash charges of $24.2 million. The largest changes in operating assets and liabilities were the $13.9 million decrease in deferred revenue and the $8.6 million increase in accounts receivable.

Investing Activities

During the nine months ended September 30, 2026, investing activities used $234.8 million of cash, which was primarily related to purchases of marketable securities.

During the nine months ended September 30, 2025, investing activities used $0.7 million of cash, related to purchases of property and equipment.

Financing Activities

During the nine months ended September 30, 2026, net cash provided by financing activities was $3.3 million, which was primarily due to $2.4 million in proceeds from the exercise of stock options.

During the nine months ended September 30, 2025, net cash provided by financing activities was $48.5 million, which was primarily due to $42.6 million in net proceeds from sales under our "at-the-market" equity program and $5.1 million in proceeds from the exercise of stock 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:

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:

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 stockholders will be diluted, and the terms may include liquidation or other preferences that adversely affect the rights of our stockholders. 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 stockholders' 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.