Form 8-K

8-K — Wave Life Sciences Ltd.

Accession: 0001193125-26-324917

Filed: 2026-07-30

Period: 2026-07-30

CIK: 0001631574

SIC: 2834 (PHARMACEUTICAL PREPARATIONS)

Item: Results of Operations and Financial Condition

Item: Regulation FD Disclosure

Item: Financial Statements and Exhibits

Documents

8-K — d177737d8k.htm (Primary)

EX-99.1 (d177737dex991.htm)

EX-99.2 (d177737dex992.htm)

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8-K

8-K (Primary)

Filename: d177737d8k.htm · Sequence: 1

8-K

7 Straits View #12-00 false 0001631574 0001631574 2026-07-30 2026-07-30

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

Form 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d)

of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): July 30, 2026

WAVE LIFE SCIENCES LTD.

(Exact name of registrant as specified in its charter)

Singapore

001-37627

98-1356880

(State or other jurisdiction

of incorporation)

(Commission

File Number)

(IRS Employer

Identification No.)

7 Straits View #12-00, Marina One East Tower

Singapore

018936

(Address of principal executive offices)

(Zip Code)

Registrant’s telephone number, including area code: +65 6236 3388

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2. below):

☐

Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐

Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐

Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐

Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company ☐

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

Securities registered pursuant to Section 12(b) of the Act:

Title of each class

Trading

symbol

Name of each exchange

on which registered

$0 Par Value Ordinary Shares

WVE

The Nasdaq Global Market

Item 2.02

Results of Operations and Financial Condition.

On July 30, 2026, Wave Life Sciences Ltd. (the “Company”) announced its financial results for the quarter ended June 30, 2026. The full text of the press release issued in connection with the announcement is furnished as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated by reference herein.

Item 7.01

Regulation FD Disclosure.

From time to time, the Company presents and/or distributes slides and presentations to the investment community to provide updates and summaries of its business. On July 30, 2026, the Company updated its corporate presentation, which is available on the “Investors” section of the Company’s website at http://ir.wavelifesciences.com/. This presentation is also furnished as Exhibit 99.2 to this Current Report on Form 8-K

The information in these Items 2.02 and 7.01 are being furnished and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that Section, nor shall they be deemed incorporated by reference into any registration statement or other filing under the Securities Act of 1933, as amended, or the Exchange Act, except as shall be expressly set forth by specific reference in such filing.

Item 9.01

Financial Statements and Exhibits.

(d)

Exhibits

The following exhibits relating to Items 2.02 and 7.01 are furnished and not filed:

Exhibit No.

Description

99.1

Press Release issued by Wave Life Sciences Ltd. dated July 30, 2026

99.2

Corporate Presentation of Wave Life Sciences Ltd. dated July 30, 2026

104

Cover Page Interactive Data File (embedded within the Inline XBRL document)

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

WAVE LIFE SCIENCES LTD.

By:

/s/ Kyle Moran, CFA

Kyle Moran, CFA

Chief Financial Officer

Date: July 30, 2026

EX-99.1

Filename: d177737dex991.htm · Sequence: 2

EX-99.1

Exhibit 99.1

Wave Life Sciences Reports Second Quarter 2026 Financial Results and Provides Business Update

Dosing underway in Phase 2a multidose portion of the INLIGHTTM trial of

WVE-007 (INHBE GalNAc-siRNA) in individuals with obesity (BMI: 35-50 kg/m2) and comorbidities; trial will also

inform WVE-007’s potential in MASH, type 2 diabetes, and other cardiometabolic diseases

Phase 2

combination with incretin and post-incretin maintenance trials of WVE-007 on track to initiate in 2H 2026

FDA meeting scheduled for end of summer 2026 on potential accelerated approval pathway for WVE-006 (GalNAc-RNA

editing); data from RestorAATion-2 trial support differentiated therapeutic approach for both lung and liver manifestations of AATD

CTA submission for WVE-008 for PNPLA3 liver disease (GalNAc-RNA editing) on

track for 2H 2026

Well capitalized with cash, cash equivalents, and marketable securities of $490.6 million as of June 30, 2026 and expected cash

runway into 3Q 2028

Investor conference call and webcast at 8:30 a.m. ET today

CAMBRIDGE, Mass., July 30, 2026 – Wave Life Sciences Ltd. (Nasdaq: WVE), a clinical-stage biotechnology company focused on unlocking the broad

potential of RNA medicines to transform human health, today announced financial results for the second quarter ended June 30, 2026, and provided a business update.

“Our second quarter performance reflects disciplined execution across the pipeline,” said Paul Bolno, MD, MBA, President and Chief Executive

Officer at Wave Life Sciences. “We recently initiated dosing in the Phase 2a portion of our INLIGHT trial in obesity. Our Phase 1 clinical data have already demonstrated substantial reductions of fat – particularly harmful visceral fat

– without muscle loss, and with the potential for once or twice-yearly dosing. We expect the Phase 2a portion of the INLIGHT trial, in individuals with higher BMI and higher body fat, to demonstrate

WVE-007’s broad potential to deliver even greater fat loss and improvements in body composition, as well as benefits across additional cardiometabolic biomarkers such as liver fat. In tandem with this

progress, we are working expeditiously to initiate Phase 2 trials evaluating WVE-007 in combination with incretins and as post-incretin maintenance; we believe WVE-007

has the potential to transform the current obesity treatment landscape.”

Dr. Bolno added, “In RNA editing, our RestorAATion-2 clinical data support WVE-006’s potential to offer a new standard of care for individuals living with AATD by treating both lung and liver manifestations

of the disease, and restoring dynamic response of AAT protein, with convenient, infrequent subcutaneous dosing, and without the risks associated with DNA editing. We look forward to meeting with the FDA to discuss a pathway for accelerated approval

for WVE-006. Building on our clinical success in RNA editing, WVE-008, our PNPLA3 RNA editing program, has the potential to address the nine million individuals living

with this genetic liver disease. It’s exciting to see the clinical translation of our RNAi and RNA editing programs, enabled by our unique and proprietary chemistry, and supported by human genetics. We expect to provide further updates on our

pipeline and platform innovations at our annual investor day this fall.”

Recent Business Highlights and Expected Milestones

Obesity

•

WVE-007 is an investigational GalNAc-siRNA (SpiNA) designed to

induce fat loss without muscle loss. With strong evidence from human genetics, silencing INHBE mRNA is a promising therapeutic strategy to treat obesity, distinct from incretin-based approaches. WVE-007 is

being evaluated in the ongoing placebo-controlled INLIGHT clinical trial.

•

Phase 1 INLIGHT trial: The ongoing, single dose portion is evaluating otherwise healthy individuals with

less fat and lower BMI (average ~32 kg/m2) than Phase 2 and 3 obesity trials. Data from the INLIGHT trial have demonstrated total body fat reduction, with muscle preservation, as well as

clinically meaningful reductions in visceral fat1 and waist circumference. WVE-007 continued to be generally safe and well tolerated and data support

potential for once or twice-yearly dosing. Additional data from the INLIGHT trial, including data from the 600 mg Phase 1 SAD cohort, are expected in the second half of 2026.

•

Phase 2a INLIGHT trial: Dosing is underway in the Phase 2a multidose portion of the INLIGHT trial of

WVE-007 in individuals with higher BMI (35-50 kg/m2), with and without type 2 diabetes. This portion of the INLIGHT trial is evaluating participants with

greater adiposity, consistent with Phase 2 and 3 obesity trials. This portion of the trial is enrolling participants across the U.S. and Europe and includes multiple assessments over a 12-month period,

including body weight, waist circumference, body composition (MRI and DEXA), liver fat (MRI-PDFF), HbA1c, and lipid levels. These data will inform further development of

WVE-007 in obesity, as well as in MASH, type 2 diabetes, and other cardiometabolic diseases.

•

Combination with incretin and post-incretin maintenance: Wave expects to initiate Phase 2 trials of WVE-007 in the combination and maintenance settings in the second half of 2026.

Alpha-1 antitrypsin deficiency (AATD)

•

WVE-006 is an investigational GalNAc-conjugated, subcutaneously

delivered, RNA editing oligonucleotide (AIMer) for AATD. WVE-006 is being evaluated in the ongoing Phase 1b/2a RestorAATion-2 open-label clinical trial in individuals

with AATD who have the homozygous Pi*ZZ mutation.

•

RestorAATion-2 trial: The 200 mg, 400 mg, and 600 mg cohorts are

fully enrolled and dosing is complete.

•

In May 2026, the company shared clinical data from the 200 mg (single and biweekly), 400 mg (single and

monthly), and 600 mg (single dose) cohorts of the ongoing RestorAATion-2 clinical trial that demonstrated WVE-006 achieved key AATD treatment goals by recapitulating an MZ-like phenotype, including robust, dose-dependent reductions of circulating, mutant Z-AAT protein, with corresponding increases in wild-type

M-AAT protein, and restoration of dynamic AAT response. Wave expects to share data from the 600 mg (monthly) multidose cohort in the second half of 2026.

•

Wave’s 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

•

WVE-008: Wave is building on its clinical success in RNA editing

by advancing WVE-008, a GalNAc-conjugated AIMer for homozygous PNPLA3 I148M liver disease. There is a growing body of clinical evidence supporting RNA editing as a preferred therapeutic strategy over

silencing.

•

In May 2026, Wave shared preclinical data supporting WVE-008 in a poster

presentation at the European Association for the Study of the Liver (EASL) Congress. These data demonstrated that Wave’s PNPLA3 AIMers delivered substantial editing of the PNPLA3 I148M transcript, exceeding the ~50% threshold expected to lower

risk for liver disease.

•

A clinical trial application (CTA) filing for WVE-008 is on track for the

second half of 2026.

Other pipeline programs (HD and DMD)

•

Wave continues partnering discussions for WVE-003 (Huntington’s

disease) and WVE-N531 (Duchenne muscular dystrophy, exon 53). With respect to WVE-N531, Wave is evaluating the evolving regulatory and commercial landscape in DMD and

exploring potential partnerships in advance of filing a New Drug Application (NDA).

Emerging pipeline

•

Investor Day 2026: Wave plans to host an investor day in the fall of 2026, where the company expects to

share updates from its clinical and preclinical pipeline of RNA medicines.

Financial Highlights

•

Cash, cash equivalents, and marketable securities were $490.6 million as of June 30, 2026, compared to

$602.1 million as of December 31, 2025. Wave expects that its current cash, cash equivalents, and marketable securities will be sufficient to fund operations into the third quarter of 2028. Potential future milestone and other payments to Wave

under its GSK collaboration are not included in its cash runway.

•

Revenue recognized was $2.3 million for the second quarter of 2026 as compared to $8.7 million in the

prior year quarter.

•

Research and development expenses were $51.3 million in the second quarter of 2026 as compared to

$43.5 million in the same period in 2025.

•

General and administrative expenses were $24.8 million in the second quarter of 2026 as compared to

$18.0 million in the same period in 2025.

•

Net loss was $69.4 million for the second quarter of 2026 as compared to a net loss of $50.5 million in

the prior year quarter.

Investor Conference Call and Webcast

Wave will host an investor conference call today at 8:30 a.m. ET to review the second quarter 2026 financial results and pipeline updates. A webcast of the

conference call can be accessed by visiting “Investor Events” on the investor relations section of the Wave Life Sciences website: https://ir.wavelifesciences.com/events-publications/events. Analysts planning to participate during

the Q&A portion of the live call can join the conference call at the audio-conferencing link here. Following the live event, an archived version of the webcast will be available on the Wave Life Sciences website.

About Wave Life Sciences

Wave Life Sciences (Nasdaq: WVE) is a biotechnology company focused on unlocking the broad potential of RNA medicines to transform human health. Wave’s

PRISM® platform combines multiple modalities, chemistry innovation, and deep insights in human genetics to deliver scientific breakthroughs that treat both rare and common disorders. Its

toolkit of RNA-targeting modalities, including RNAi (SpiNA) and RNA editing (AIMers), provides Wave with unmatched capabilities for designing and sustainably delivering candidates that optimally address

disease biology. Wave’s pipeline is focused on its obesity (WVE-007), alpha-1 antitrypsin deficiency (WVE-006) and PNPLA3 I148M liver disease (WVE-008) programs, and also includes clinical programs in Duchenne muscular dystrophy and Huntington’s disease, as well as several preclinical programs utilizing the company’s versatile RNA medicines

platform. Driven by the calling to “Reimagine Possible,” Wave is leading the charge toward a world in which human potential is no longer hindered by the burden of disease. Wave is headquartered in Cambridge, MA. For more information on

Wave’s science, pipeline and people, please visit www.wavelifesciences.com and follow Wave on X and LinkedIn.

Forward-Looking

Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as

amended, concerning our goals, beliefs, expectations, strategies, objectives and plans, and other statements that are not necessarily based on historical facts, including statements regarding the following, among others: the anticipated initiation,

timing, design, progress, data and announcements related to our clinical trials, including interactions with and feedback from regulators and any potential registrational submissions based on these data; the future performance and results of our

programs in clinical trials, including the anticipated therapeutic benefits of such programs, and our expectations with respect to how our clinical data may predict success for our future therapeutic candidates and data readouts; the potential

commercialization of our programs the potential size of the markets that our therapeutics may address; preclinical activities and programs and their potential to transition into clinical-stage programs, and the timing, progress and announcement of

such events; the progress and potential benefits, including the potential achievement of milestones, of collaborations and strategic partnerships; the expected benefits of our stereopure oligonucleotides compared with stereorandom oligonucleotides;

the breadth and versatility of our PRISM® drug discovery and development platform; the potential benefits of our RNA-targeting modalities, including

RNAi (SpiNA), and RNA editing (AIMers); the potential for certain of our programs to be best-in-class or

first-in-class, or to change the existing treatment paradigm or show substantial benefits over existing standards of care; our financial performance, including the

anticipated duration of our cash runway and our ability to fund future operations; our intended uses of capital; and our expectations regarding the impact of any potential global macro events on our business. The words “may,”

“will,” “could,” “would,” “should,” “expect,” “plan,” “anticipate,” “intend,” “believe,” “estimate,” “predict,”

“project,” “potential,” “continue,” “target” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words.

Any forward-looking statements in this press release are based on management’s current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual results to differ materially from

those indicated by these forward-looking statements as a result of these risks, uncertainties and important factors, including, without limitation, the clinical results and timing of our programs, which may not support further development of our

product candidates; actions of regulatory agencies, which may affect the initiation, timing and progress of clinical trials; our effectiveness in managing current and future clinical trials and regulatory processes; the continued development and

acceptance of nucleic acid therapeutics as a class of drugs; our ability to demonstrate the therapeutic benefits of our stereopure candidates in clinical trials, including our ability to develop candidates across multiple therapeutic modalities; our

ability to obtain, maintain and

protect intellectual property; our ability to fund our operations and to raise additional capital as needed;

competition from others developing therapies for similar uses; and any impacts on our business as a result of or related to any global economic uncertainty or market disruptions, as well as the other risks and uncertainties described in the section

entitled “Risk Factors” in our most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission (SEC), as amended, and in other filings we make with the SEC from time to

time. In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. We undertake no obligation, except to the extent required by law, to update the

information contained in this press release to reflect subsequently occurring events or circumstances.

Contact:

Kate Rausch

VP, Corporate Affairs and Investor Relations

+1 617-949-4827

Investors:

James Salierno

Director, Investor Relations

617-949-4043

InvestorRelations@wavelifesci.com

Media:

Katie Sullivan

Senior Director, Corporate Communications

+1 617-949-2936

MediaRelations@wavelifesci.com

Gabriely et al., Diabetes 2002; Campos et al., Diabetes & Vascular Disease Research 2019; Huang et al.,

Front Endocrinol 2023.; Cesaro et al., Front Cardiovasc Med 2023; Khawaja et, al., Curr Cardiol Rep 2024; Hiuge-Shimizu et al., J Atheroscler Thromb 2011.; Liao et al., PLoS ONE 2023; Jung et al., Endocrinol Metab 2020; Hanlon & Yuan, Clin Liver

Dis 2021.; Liao et al., PLoS ONE 2023; Jung et al., Endocrinol Metab 2020

WAVE LIFE SCIENCES LTD.

UNAUDITED CONSOLIDATED BALANCE SHEETS

(In thousands, except share amounts)

June 30, 2026

December 31, 2025

Assets

Current assets:

Cash and cash equivalents

368,008

602,068

Marketable Securities

122,594

—

Accounts receivable

888

1,276

Prepaid expenses

12,121

8,395

Other current assets

3,897

3,075

Total current assets

507,508

614,814

Long-term assets:

Property and equipment, net of accumulated depreciation of $50,819 and $49,522 as of June 30, 2026

and December 31, 2025, respectively

6,833

7,405

Operating lease

right-of-use assets

39,498

12,458

Restricted cash

3,815

3,806

Other assets

667

Total long-term assets

50,813

23,685

Total assets

558,321

638,499

Liabilities, Series A preferred shares, and shareholders’ equity

Current liabilities:

Accounts payable

20,362

15,700

Accrued expenses and other current liabilities

18,242

26,564

Current portion of deferred revenue

8,703

44,440

Current portion of operating lease liability

3,508

8,361

Total current liabilities

50,815

95,065

Long-term liabilities:

Deferred revenue, net of current portion

13,904

7,798

Operating lease liability, net of current portion

40,082

9,405

Total long-term liabilities

53,986

17,203

Total liabilities

104,801

112,268

Series A preferred shares, no par value; nil and 3,901,348 shares issued and outstanding at June

30, 2026 and December 31, 2025, respectively

—

7,874

Shareholders’ equity:

Ordinary shares, no par value; 193,277,622 and 187,660,263 shares

issued and outstanding at June 30, 2026 and December 31, 2025, respectively

1,627,209

1,616,478

Additional paid-in capital

248,161

228,365

Accumulated other comprehensive loss

(172

)

(250

)

Accumulated deficit

(1,421,678

)

(1,326,236

)

Total shareholders’ equity

453,520

518,357

Total liabilities, Series A preferred shares, and shareholders’ equity

558,321

638,499

WAVE LIFE SCIENCES LTD.

UNAUDITED CONSOLIDATED STATEMENTS OF OPERATIONS AND COMPREHENSIVE LOSS

(In thousands, except share and per share amounts)

Three Months Ended June 30,

Six Months Ended June 30,

2026

2025

2026

2025

Revenue

2,272

8,699

40,518

17,874

Operating expenses:

Research and development

51,293

43,469

98,733

84,091

General and administrative

24,781

17,989

46,884

36,346

Total operating expenses

76,074

61,458

145,617

120,437

Loss from operations

(73,802

)

(52,759

)

(105,099

)

(102,563

)

Other income, net:

Interest income

4,722

2,372

10,013

5,247

Other expense

(275

)

(82

)

(356

)

(31

)

Total other income, net

4,447

2,290

9,657

5,216

Loss before income taxes

(69,355

)

(50,469

)

(95,442

)

(97,347

)

Income tax benefit

—

Net loss

(69,355

)

(50,469

)

(95,442

)

(97,347

)

Net loss per share attributable to ordinary shareholders—basic and diluted

(0.34

)

(0.31

)

(0.47

)

(0.60

)

Weighted-average ordinary shares used in computing net loss per share attributable to ordinary

shareholders—basic and diluted

204,008,712

163,987,640

202,098,901

163,266,106

Other comprehensive loss:

Net loss

(69,355

)

(50,469

)

(95,442

)

(97,347

)

Foreign currency translation gain

123

119

101

Unrealized loss on marketable securities

(41

)

—

(41

)

—

Comprehensive loss

(69,273

)

(50,426

)

(95,364

)

(97,246

)

EX-99.2

Filename: d177737dex992.htm · Sequence: 3

EX-99.2

Exhibit 99.2 Wave Life Sciences Corporate Presentation July 30,

2026

Forward-looking statements This document contains forward-looking

statements. All statements other than statements of historical facts contained in this document, including statements regarding possible or assumed future results of operations, preclinical and clinical studies, business strategies, research and

development plans, collaborations and partnerships, regulatory activities and timing thereof, competitive position, potential growth opportunities, use of proceeds and the effects of competition are forward-looking statements. These statements

involve known and unknown risks, uncertainties and other important factors that may cause the actual results, performance or achievements of Wave Life Sciences Ltd. (the “Company”) to be materially different from any future results,

performance or achievements expressed or implied by the forward-looking statements. In some cases, you can identify forward-looking statements by terms such as “may,” “will,” “should,” “expect,”

“plan,” “aim,” “anticipate,” “could,” “intend,” “target,” “project,” “contemplate,” “believe,” “estimate,” “predict,”

“potential” or “continue” or the negative of these terms or other similar expressions. The forward- looking statements in this presentation are only predictions. The Company has based these forward-looking statements largely

on its current expectations and projections about future events and financial trends that it believes may affect the Company’s business, financial condition and results of operations. These forward-looking statements speak only as of the date

of this presentation and are subject to a number of risks, uncertainties and assumptions, including those listed under Risk Factors in the Company’s Form 10-K and other filings with the SEC, some of which cannot be predicted or quantified and

some of which are beyond the Company’s control. The events and circumstances reflected in the Company’s forward-looking statements may not be achieved or occur, and actual results could differ materially from those projected in the

forward-looking statements. Moreover, the Company operates in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties that

the Company may face. Except as required by applicable law, the Company does not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or

otherwise. 2

Our Mission To unlock the broad potential of RNA medicines to transform

human health 3

Building a leading RNA medicines company Differentiated RNA medicines

Translating genetic insights into Unlocking platform and chemistry potentially best-in-class medicines emerging pipeline RNAi WVE-007 (obesity) • Extra-hepatic capabilities: • Differentiated mechanism with RNAi and RNA editing focused on

fat loss and • Proprietary chemistry muscle preservation • Leveraging deep insights in human RNA editing WVE-006 (AATD) • Bifunctional modalities: genetics WVE-008 (liver disease) single oligonucleotide constructs for dual RNAi

• Restoration of functional • Strong and broad IP silencing or RNAi silencing + protein production RNA editing • In-house GMP manufacturing Other modalities: splicing, antisense silencing Well capitalized with expected cash runway

into 3Q 2028 4

For over a decade Wave has been extending the frontiers of RNA therapies

delivering breakthroughs in nucleic acid chemistry RNAi — SpiNA RNA editing — AIMer Protein reduction Ago2 loading 100% 80% 60% 40% 20% 0% C C N3U N3U Base 2’ deoxy 2’ OMe 2’ deoxy 2’ OMe Sugar Substantial

improvements in potency, duration of activity, and Ago2 loading Increased RNA editing efficiency achieved with Wave’s proprietary SpiNA design with proprietary chemistry Proprietary chemistry has dramatically increased potency and durability 5

SpiNA: Stereopure interfering Nucleic Acid https://wavelifesciences.com/science/publications/ % Ugp2 mRNA editing

Robust RNA medicines pipeline with first-in-class RNAi and RNA editing

programs RNAi (SpiNA) Program Discovery IND / CTA Enabling Studies Clinical Patient population TM INLIGHT trial (monotherapy) WVE-007 (GalNAc) 175M Combination with incretins INHBE (obesity) (>1 billion globally) Post-incretin maintenance GalNAc

/ extra-hepatic -- Multiple RNA editing (AIMer) Program Discovery IND / CTA Enabling Studies Clinical Patient population WVE-006 (GalNAc) RestorAATion-2 trial 200K SERPINA1 (AATD) WVE-008 (GalNAc) 9M PNPLA3 (liver disease) GalNAc / extra-hepatic --

Multiple Other pipeline programs Program Discovery IND / CTA Enabling Studies Clinical Patient population WVE-N531 2.3K Exon 53 (DMD) 25K Symptomatic (SNP3) WVE-003 mHTT (HD) 60K Pre-Symptomatic (SNP3) 6 Patient population includes US and Europe

AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington’s disease

WVE-007 GalNAc-siRNA silencing Obesity 7

WVE-007 (investigational INHBE GalNAc-siRNA) is a potentially

transformative approach for the > 1 billion people living with obesity globally Significant unmet need in obesity WVE-007 Focused on adipocyte lipolysis and Current standard of care: Focused on caloric restriction by reducing appetite and slowing

gastric emptying not caloric deficit Incretins limited by: Drives total and visceral fat loss ✓ 1 Muscle loss X 2 X Frequent dosing Preserves muscle ✓ 3 Poor tolerability X 4,5 High discontinuation rates X Potential 1–2x per year

dosing ✓ Resulting in need for therapies that can: ✓ Generally safe and well tolerated • Induce fat loss with muscle preservation • Leverage orthogonal mechanism for enhanced efficacy and maintain metabolic improvements

after incretin cessation 8 1. Sargeant, et al. 2019 Endocrinol Metab (Seoul) 34, 247; 2. Wegovy PI; 3. Ghusn and Hurtado. 2024 Obesity Pillars 12, 100127; 4. Leach, et al. 2023 Prime Therapeutics Claims Analysis; 5. Gasoyan, et al. 2024 Obesity

(Silver Spring) 32, 486.

Human genetic data demonstrate that heterozygous INHBE loss-of-function

(LoF) carriers have lower visceral fat and a healthier metabolic profile Heterozygous INHBE LoF carriers versus non-carriers: Favorable traits : Waist-to-hip ratio✓ Lower abdominal obesity Visceral adipose volume by MRI ✓ Reduced

visceral fat Serum triglycerides ✓ Lower triglycerides HDL-c ✓ Higher “good” cholesterol ApoB ✓ Lower ApoB %HbA1c✓ Improved glucose control Liver cT1 by MRI ✓ Less liver inflammation/fibrosis ALT

✓ Less liver damage Standard deviations -0.4 -0.2 0 0.2 0.4 Type 2 diabetes ✓ Lower risk of type 2 diabetes Coronary heart disease ✓ Lower risk of CHD Odds ratio 0.50 0.75 1 1.5 2.0 9 Akbari et al. Nat Commun. 2022 Aug

23;13(1):4844; Deaton et al. Nat Commun. 2022 Jul 27;13(1):4319. Waist-to-hip ratio, BMI-adjusted: Visceral adipose volume (MRI), BMI adjusted; HDL-c: high-density lipoprotein cholesterol; %HbA1c: glycated hemoglobin; ALT: alanine transaminase;

ApoB: apolipoprotein B; CHD: coronary heart disease; cT1: corrected T1

Silencing INHBE mRNA has the potential to treat obesity and associated

metabolic diseases Release of dimerized Binds to and activates ACVR1C Block adipose INHBE subunits creates (ALK7) receptor in adipose tissue lipolysis hepatokine Activin E Activin E Activin E Increased abdominal adiposity leads to obesity, I II I I

CVD and T2D Adipocyte ALK7 Decreased abdominal adiposity leads to weight loss and reduced risk for CVD and T2D Reduction of Reduced release of Diminished activation of Increased adipose INHBE mRNA with hepatokine Activin E ACVR1C (ALK7) receptor in

lipolysis and shrink GalNAc-siRNA adipose tissue adipocytes 10 1. Cell Reports (2018) 25, 1193–1203; 2. Biochemical Journal (2024) 481 547–564; 3. PNAS 2023 Vol. 120 No. 32 e2309967120; 4. Nat Commun 2022. https://doi.org/10.1038/s41467-

022-32398-7; 5. Nat Commun 2022. https://doi.org/10.1038/s41467-022-31757-8

Higher circulating Activin E levels are correlated with higher BMI,

higher abdominal fat, and higher fasting insulin in non-diabetic adults BMI Fasting Insulin Abdominal Fat Further supports INHBE suppression as a weight loss approach for individuals living with obesity 11 Dubey et al. Activin E levels correlate

with indicators of metabolic dysfunction in humans. ObesityWeek 2025.

WVE-007 is designed to improve body composition by decreasing fat and

preserving muscle Total Fat REDUCED Subcutaneous fat Visceral Fat REDUCED Visceral fat Muscle Muscle PRESERVED 12

WVE-007’s mechanism is focused on lipolysis and directly reducing

visceral and subcutaneous fat Visceral fat drives insulin resistance and Reduced visceral fat is associated with many cardiometabolic disorders multiple health benefits Visceral fat decrease • MASH ≥ 5% 1 Improved insulin sensitivity :

Lower HbA1c and better • Type 2 lipid profile diabetes ≥ 5-10% • Cardiovascular 2 Reduced cardiovascular risk : Reduced blood pressure, improved lipids, lower systemic inflammation diseases ≥ 10% • PMOS Visceral fat 3

Reduced liver fat (steatosis) : Significant reduction in hepatic triglycerides, improved liver enzymes Waist circumference is a 4 Decreased hepatic fibrosis : Resolution of steatohepatitis clinical proxy for visceral fat in up to 90%, fibrosis

regression in many cases 13 1. Gabriely et al., Diabetes 2002; Campos et al., Diabetes & Vascular Disease Research 2019; Huang et al., Front Endocrinol 2023. 2. Cesaro et al., Front Cardiovasc Med 2023; Khawaja et al., Curr Cardiol Rep 2024;

Hiuge-Shimizu et al., J Atheroscler Thromb 2011. 3. Liao et al., PLoS ONE 2023; Jung et al., Endocrinol Metab 2020; Hanlon & Yuan, Clin Liver Dis 2021. 4. Liao et al., PLoS ONE 2023; Jung et al., Endocrinol Metab 2020

WVE-007 aims to address a key limitation of current standard of care:

up to 40% of weight loss is driven by muscle loss Preservation of muscle mass is linked to many health benefits 5,6 • Higher basal metabolic rate • Reduced visceral fat 1 (BMR) 7,8 • Prevent weight regain 2,3 • Improved

insulin sensitivity • Improved glucose 2,3 • Increased caloric expenditure homeostasis 1 post-exercise • Increased bone density, • Preserve muscle strength and strength, function, and 4 9,10 function longevity 14 1. J. Clin.

Med. 2024, 13, 5862; 2. J. Diab. Res. 2017, 8314852; 3. J. Funct. Morphol. Kinesiol. 2025, 10, 244; 4. J Bone Mineral Res. 2018, 33(2): 211–220; 5. Front. Nutr. 2023, 10:1246157; 6. Nat. Med. 2026, 32: 869–882; 7. Med Sci Sports Exerc.

2022, 54(12):2031-2036; 8. The Lancet eClinical Medicine, 2024, 69: 102475; 9. Ann Geriatr Med Res 2025, 29(1):1-14; 10. Age and Ageing, 2025, 54(7): afaf189; 11. Sargeant, et al. 2019 Endocrinol Metab (Seoul) 34, 247.

A single dose of INHBE GalNAc-siRNA led to shrinkage of adipocytes in

DIO mice Mean adipocyte diameter DIO Lean PBS INHBE GalNAc-siRNA (μm) ✱✱✱ 80 60 40 20 0 Lean DIO DIO PBS INHBE GalNAc- siRNA 15 Data presented at ADA Scientific Sessions June 2025 ***p<0.001; Day 28

A single dose of INHBE siRNA led to a lower inflammatory state of

visceral adipose tissues in DIO mice, with strong suppression of pro-inflammatory M1 macrophages in visceral fat Macrophages (Mᶲ) (F4/80) Pro-inflammatory (M1) Mᶲ Anti-inflammatory (M2) Mᶲ (CD11c) (CD163) INHBE GalNAc siRNA INHBE

GalNAc siRNA INHBE GalNAc siRNA PBS 3 mg/kg 10 mg/kg PBS 3 mg/kg 10 mg/kg PBS 3 mg/kg 10 mg/kg ✱ 1.0 0.8 0.6 0.4 0.2 0.0 PBS 3 mg/kg 10 mg/kg PBS 3 mg/kg 10 mg/kg PBS 3 mg/kg 10 mg/kg 16 Data presented at ADA Scientific Sessions June 2025

***p<0.001, *p<0.05, ns=non-significant %F4/80 positive area

Lowering of inflammatory state of epiWAT visceral fat induced by single

dose of INHBE siRNA resulted in 58% reduction of adipose fibrosis Reduced staining illustrates decreased tissue fibrosis Fibrosis in mouse adipose (Day 56) 10 mg/kg PBS 3 mg/kg ✱ 15 10 5 0 PBS 3 mg/kg 10 mg/kg 17 Data are means ± SEM of

6 mice. Each dot represents an individual mouse. Kruska-Wallis test with Dunn’s multiple comparisons. *P<0.05 Trichrome % Trichrome positive area

Treatment with WVE-007 (investigational INHBE GalNAc-siRNA) is expected

to drive fat reduction and improve key measures of cardiometabolic health 1 Driving fat reduction And improving clinical outcomes Leading siRNA design (SpiNA) WVE-007 Reduction of INHBE mRNA and (INHBE GalNAc-siRNA) circulating Activin E

Proprietary, Cardiometabolic clinically validated ✓ outcomes chemistry Adipocyte Adipocyte lipolysis size Risk of CVD Subcutaneous delivery Insulin ✓ (GalNAc) Risk of T2D sensitivity Proinflammatory macrophages Potential for infrequent

✓ dosing (1 – 2x year) Fibrosis 18 1. SpiNA design is derived from Liu et al., 2023 Nucleic Acids Research doi: 10.1093/nar/gkad268

Single dose of INHBE GalNAc-siRNA led to durable Activin E reductions,

and sustained improvements in body composition in DIO mice Muscle Durable Activin E Reduction in fat Reduction in body weight ✓ ✓ ✓ preservation ✓ reduction Serum Activin E Epididymal fat weight Quadricep weight Single

dose INHBE GalNAc-siRNA * 0.25 150 -23% 0.75 0.20 -40% INHBE siRNA 100 0.15 0.50 0.10 50 0.25 Semaglutide 0.05 0 0.00 0.00 PBS INHBE INHBE INHBE PBS Sema- PBS INHBE INHBE 10 mg/kg 3 mg/kg 3 mg/kg 10 mg/kg glutide 10 mg/kg 19 Left and right panels:

Semaglutide 10 nmol/kg daily SC in mouse is equivalent to therapeutic dose of 2.4mg weekly SC in human; INHBE GalNAc-siRNA 10 mg/kg dose. All data from preclinical studies were conducted in mice fed with 60% high fat diet. Linear Mixed Effects ANOVA

with post hoc comparisons of marginal treatment effects vs. PBS per tissue.* p < 0.05 Activin E (%Control) Tissue weight (g) Tissue weight (g)

WVE-007 has potential for use synergistically with GLP-1s or to curtail

weight regain after the cessation of treatment with GLP-1, based on preclinical data Combined with GLP-1: Greater weight loss After cessation of GLP-1: Curtails weight regain ✓ ✓ p<0.05 ~2x greater weight loss Not significant Day

Day Single dose INHBE GalNAc-siRNA Daily GLP-1 PBS Daily GLP-1 Semaglutide Semaglutide Control for Semaglutide INHBE GalNAc-siRNA Dose INHBE GalNAc-siRNA Semaglutide + Control for siRNA Semaglutide + INHBE GalNAc-siRNA INHBE GalNAc-siRNA 20 Data

from preclinical studies conducted in mice fed with 60% high fat diet; Left: semaglutide10 nmol/kg daily SC in mouse is equivalent to therapeutic dose of 2.4mg weekly SC in human. Left Stats: Linear Mixed Effects ANOVA with post hoc comparisons of

marginal treatment effects of Semaglutide vs. Semaglutide + INHBE GalNAc-siRNA per time point * p < 0.05; Right Stats: Linear Mixed Effects ANOVA with post hoc comparison of Day 28 vs. Day 56 marginal effects per treatment Difference in body

weight (% of PBS, same time point)

TM Phase 1 portion of INLIGHT trial is investigating WVE-007 in

individuals living with overweight or obesity, otherwise healthy Phase 1 lower BMI (SAD) Phase 2a high BMI (MAD) • Average BMI: 32 kg/m² SAD Cohort 4 MAD high BMI (35–50 kg/m²)+T2D cohorts 600 mg (n=32) • HbA1c: <5.9%

• Otherwise healthy SAD Cohort 3 MAD high BMI (35–50 kg/m²) cohorts • Assessments include: 400 mg (n=32) Safety and tolerability, PK, Activin E, body • Individuals with higher BMI with and without type 2 diabetes SAD

Cohort 2 composition (DEXA), 240 mg (n=32) • Assessments to additionally include: biomarkers, body weight – Body composition (MRI in addition to DEXA) • No diet or exercise SAD Cohort 1 – Liver fat (MRI-PDFF) modifications 75

mg (n=8) PK/PD and safety only (no DEXA) • Diet and exercise modifications included Evaluate safety, tolerability, and PK; assess metabolic and body composition Evaluate safety, tolerability, and PK improvements as well as weight loss 21 SAD:

single-ascending dose; MAD: multi-ascending dose; PK: pharmacokinetics. Average BMI of 75 mg, 240 mg, and 400 mg cohorts.

Clinically meaningful improvements in body composition at six months

following a single dose of WVE-007 Phase 1 otherwise healthy (SAD) Lower BMI of ~32 kg/m² TM Activin E change in INLIGHT trial Improved body composition six months following single 240 mg dose: * - Significant reduction in visceral fat (-14% )

- Reduction in waist circumference (-3%) - Reduction in total fat (-5%) - Stabilization of lean mass (+2%) - Reduction in body weight (-1%) • 400 mg three-month data emphasize impact of baseline body composition on therapeutic effect •

Durable and dose-dependent suppression of Single dose WVE-007 (GalNAc-siRNA) Activin E sustained through at least 7 months continues to support 1-2x yearly dosing Dose Placebo (N=26) WVE-007 75 mg (N=6) WVE-007 240 mg (N=24) • Generally safe

and well tolerated WVE-007 400 mg (N=24) WVE-007 600 mg (N=24) Durability of suppression continues to support dosing WVE-007 once or twice per year 22 INLIGHT interim Phase 1 data reported March 26, 2026; Left: figure shows sample means and SEMs.

All MMRM baseline and placebo comparisons from Day 8 onwards are p<0.003. Right: *p<0.05. All reductions are placebo-adjusted % change from baseline were estimated using an MMRM model with fixed effects for treatment group, visit,

treatment-by-visit interaction, and baseline as a covariate; estimates were based on geometric mean ratios.

Single dose of WVE-007 in a lower BMI population led to greater

improvement in body composition by VMR versus semaglutide Visceral Fat-to-Muscle 4 Improvement in body composition by VMR at 3 months and 6 months Ratio (VMR) • Established measure of body BELIEVE Phase 2 Trial 2 2 composition integrating

harmful BMI: ~32 kg/m BMI: ~37 kg/m visceral fat and beneficial lean WVE-007 Semaglutide Semaglutide Bimagrumab mass in a single index Single dose Weekly Weekly 2-3 doses 3 months 240 mg 1.0 mg 2.4 mg 10 mg/kg 0% • Lower VMR is associated with

0.0% decreased risk of MASH / -2.6% -5% 1,2 3 MAFLD, type 2 diabetes, and -10% -8.3% cardiometabolic disorders (e.g., -9.6% 1,3 dyslipidemia, hypertension) 6 months 0% -5% -10% -8.8% -12.2% -15% -16.5% -20% -18.8% 1. Zhang S, et al. 2023 Diabetes

Metab Res Rev. 39(2):e3597; 2. Liu C, et al. 2024 Lipids Health Dis. 23(1):104; 3. Wang Q, et al. 2019 Diabetes Metab Syndr Obes. 12:1399-1407. 4. Placebo- 23 corrected VMR calculated based on changes from baseline in visceral fat and lean mass at 3

and 6 mo. For BELIEVE, values are from Heymsfield SB, et al. 2026 Nat Med 32, 869–882. Note: The data presented above are derived from different clinical trials with differences in trial design and patient population, including with respect to

BMI. As a result, cross-trial comparisons cannot be made and no head-to-head clinical trials have been conducted. Placebo-adjusted % difference from baseline in VMR Improvement Improvement

TM Phase 2a INLIGHT trial: higher BMI population aligns with Phase 2

and 3 obesity trials, potential for continued improvements in body composition Total fat and BMI at baseline Visceral fat and BMI at baseline Phase 2 BELIEVE baseline Phase 2 BELIEVE baseline 50 1.75 (semaglutide and / or bimagrumab) (semaglutide

and / or bimagrumab) Phase 2a Phase 2a BMI (35-50 BMI (35-50 2 2 1.50 kg/m ) kg/m ) 40 240 mg WVE-007 1.25 Phase 1 (baseline) BELIEVE Phase 2 study Baseline (by cohort) 400 mg WVE-007 1.00 240 mg WVE-007 Phase 1 (baseline) 30 Week 48 (by cohort)

Phase 1 (baseline) 0.75 US population data from 400 mg WVE-007 NHANES (VAT and BMI) Phase 1 (baseline) 20 0.50 50% of population 95% of population 0.25 10 0.00 15 20 25 30 35 40 45 15 20 25 30 35 40 45 2 2 BMI (kg/m ) BMI (kg/m ) TM Expect greater

fat loss in Phase 2a INLIGHT trial in participants with more excess fat 24 NHANES population reference: Adults aged 20–59 with valid DXA-derived visceral adipose tissue measurements, pooled across 2011–2018 survey cycles (n = 11,934).

VAT mass (kg) estimated from DXA (Hologic); BMI from measured height and weight. Contours represent 2D kernel density estimates of the cross-sectional population distribution. Clinical trial data overlaid as change from baseline within the NHANES

VAT–BMI coordinate space. BELIEVE data points from Heymsfield SB, et al. 2026 Nat Med 32, 869–882. Total Body Fat Mass (kg) Visceral Adipose Tissue (kg)

Phase 2a (MAD) global, placebo-controlled study will inform further

development in obesity, as well as MASH, type 2 diabetes, and other cardiometabolic diseases High BMI • Individuals with high BMI 2 D1 D85 (35–50 kg/m ) and comorbidities Cohort 1 N=40 (3:1) 240 mg• Assessments include: •

Body weight D1 D85 • Body composition Cohort 2 N=40 (3:1) (MRI in addition to DEXA) 400 mg • Liver fat (MRI-PDFF) High BMI + T2D • HbA1c, lipid levels, CRP D1 D85 • Muscle function Cohort 1 N=40 (3:1) • Diet and

exercise modifications 240 mg included D1 D85 Cohort 2 • 12-month study duration N=40 (3:1) 400 mg • First assessment Day 85 (3 months) TM Phase 2a (MAD) portion of INLIGHT trial underway 25 SAD: single-ascending dose; MAD:

multi-ascending dose; PK: pharmacokinetics; MASH: metabolic dysfunction-associated steatohepatitis; CVD: cardiovascular disease

TM Phase 2a portion of INLIGHT monotherapy trial underway; combination

and maintenance trials of WVE-007 expected to initiate in 2H 2026 Monotherapy Combination Maintenance Single agent in individuals Add-on to incretin An off-ramp post-incretin living with obesity treatments treatments • To induce fat loss with

muscle • To leverage an orthogonal • To prevent weight regain and preservation and favorable mechanism to incretins for maintain metabolic safety and tolerability enhanced efficacy improvements upon incretin cessation Potential to

address more than one billion individuals with obesity globally 26 Phelps, NH, et al. 2024 Lancet 403, 1027

INHBE silencing provides opportunity to address additional significant

indications through lowering of visceral fat Obesity ~110M PMOS ~9M Visceral fat reductions Cardiovascular disease Type 2 diabetes ~20M ~38M MASH ~23M Therapeutic indications and US patient populations 27 PMOS: Polyendocrine Metabolic Ovarian

Syndrome 1. All prevalence are US estimates. Prevalence of obesity, type 2 diabetes, and cardiovascular disease based on CDC / NHANES figures. MASH prevalence estimated from Estes, C. et al. 2018 Hepatology 67, 123. PCOS prevalence based on WHO

estimates.

WVE-006 RNA editing (AIMer) Alpha-1 antitrypsin deficiency (AATD)

WVE-006 (investigational GalNAc-RNA editing AIMer) is a potentially

transformative approach for both lung and liver manifestations of Pi*ZZ AATD WVE-006 Significant unmet need in AATD Focused on RNA editing to restore Current standard of care: Weekly IV augmentation is the functional AAT, not augmentation only

treatment for AATD lung disease Augmentation limited by: Restores wild-type M-AAT protein ✓ X Weekly IV infusions X Does not address liver disease Reduces toxic Z-AAT protein ✓ Does not address root cause X Replaces protein, not

production X Addresses both lung and liver ✓ disease Resulting in need for therapies that can: • Address root cause of both lung and liver disease Generally safe and well tolerated ✓ • Restore dynamic production of

functional AAT with a safe, convenient subcutaneous therapy ~200,000 people living with Pi*ZZ AATD across the US and Europe 29 1. Packer, et al. 2024, Methods and Compositions for Treating Alpha-1 Antitrypsin Deficiency,

PCT/US2024/034189.

Treatment target: Heterozygous MZ genotype with M-AAT >50% AAT and a

dynamic CRP response has low risk of liver and lung disease 1 Serum AAT Protein Levels by Genotype 50 25 11 µM 0 ZZ SZ MZ MM Null Pi*ZZ Pi*SZ Pi*MZ Pi*MM Mean 64% M-AAT Serum AAT composition No AAT 100% Z-AAT S-AAT and Z-AAT 100% M-AAT 2

(range: 57%-71%) 3 Risk of lung disease Very high High Low Low Normal 3 Risk of liver disease Normal High Low Low Normal AAT levels increase with N/A No Yes Yes Yes 4 acute phase response 30 1. Range of observed serum AAT levels from Bornhorst, et

al. 2013 CHEST 143:1000-1008; 2. Percent M-AAT of total AAT from a natural history cohort of individuals with M/Z genotype using the same LC-MS/MS assay in RestorAATion-2; 3. Brode, et al. 2012 CMAJ 184:1365-1371; 4. Sanders, et al. 2018 COPD

15:10-16 Serum AAT (µM)

RNA editing expected to deliver even greater impact over time with

continued treatment and improved liver health Pi*ZZ Pi*MZ-like Liver disease Reduce Z-AAT to prevent liver damage Z-aggregate clearance over time WVE-006 High Z-AAT aggregation ~50% M-AAT Increasing hepatocyte and liver inflammation produced in

liver health Lung disease Restore M-AAT to prevent lung damage Wild-type Z-AAT M-AAT Protein Misfolded Protein 100% Z-AAT, 0% M-AAT >50% M-AAT Potential for higher levels of AAT levels responsive to CRP serum AAT 31

Pi*ZZ individuals have an impaired serum AAT increase during

acute-phase responses (APRs), when they need it most Lung damage occurs during exacerbations, when AAT protein has protective functions and is produced more AAT protein is needed for protection during acute phase response 30,9 10 00 0 900 30,100

Pi*MZ Pi*ZZ 30,8 00 00 0 30,8 00 00 0 700 700 CRP CRP 600 600 500 500 400 400 300 300 AAT protein AAT protein 200 200 100 100 0 0 0 7 14 21 0 7 14 21 Days Days Inflammatory stimulus Inflammatory stimulus RNA editing has potential to restore dynamic

AAT response to inflammation 32 Left: Mantovani A, Garlanda C. N Engl J Med, 2023;388:439-452; Right: Sanders et al., J COPD, 2018 Percent change in plasma concentration (%)

WVE-006 restores dynamic production of AAT protein as part of APRs to

protect lungs from damage Illustrative Models APRs require a rapid Standard of care rise in AAT levels to (augmentation prevent lung damage therapy) may leave patients at risk • Even with augmentation therapy, in ZZ individuals, •

Exogenous AAT levels exacerbations occur on risk depletion before Lung damage next scheduled IV dose IV dosing average 1–2x yearly • These exacerbations could Protected WVE-006 treatment deplete AAT levels within 1 lungs hours response

is dynamic • Endogenous AAT levels increase during acute • In healthy (including MZ) phase response individuals, AAT levels rise quickly (24–72 hours) after stimulus RNA editing dose ↑ Acute phase response 33 Right:

Illustrative model of impact of acute phase response 1. Liou & Campbell, Journal of Immunology 1996; Thulborn et al., Respiratory Research 2019; Beatty et al., Journal of Biological Chemistry 1980. AAT levels AAT levels

RestorAATion-2 trial ongoing in individuals living with Pi*ZZ AATD

RestorAATion-1: Healthy Volunteers RestorAATion-2: AATD Patients RestorAATion-1: Healthy Volunteers SAD → MAD Multi-dosing complete SAD MAD 600 mg 600 mg 600 mg x 4 doses Single dose Monthly 400 mg 400 mg 400 mg x 4 doses Single dose Monthly

200 mg 200 mg 200 mg x 7 doses 100 mg Single dose Biweekly 30 mg Study key objectives Safety and tolerability Pharmacokinetics Serum M-AAT levels 34 HV: healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending dose

Treatment with WVE-006 achieved Pi*MZ-like profile across doses:

delivering potential liver and lung benefits with a safe and convenient therapy Protecting the liver Protecting the lung Safe and convenient MZ-like Generate Total dynamic AAT • Generally safe healthy, wild- WVE-006 Reduce Z-AAT AAT and well

tolerated production type M-AAT • Subcutaneous Three acute delivery, with 200 mg 64% M-AAT of phase responses 11.9 µM 71% reduction potential for self- biweekly total AAT (up to >20 µM administration total AAT) • Potential

for CRP increases monthly dosing 400 mg 59% M-AAT of 13.6 µM 68% reduction correlated with monthly total AAT AAT increases Data from 600 mg monthly dose cohort expected in 2H 2026 35 Circulating M-AAT, Z-AAT, and total (M + Z) AAT protein in

the serum were measured by highly selective and sensitive LC-MS/MS assays (LLOQ: 0.096 µM (M), 0.029 µM (Z)) and reported as mean participant MAD maximums. In a natural history cohort of individuals with M/Z genotype using the same

LC-MS/MS assay in RestorAATion-2, M-AAT% of total AAT mean was 64% (range 57%-71%).

Up to 71% reduction in circulating, mutant Z-AAT supporting potential

improvement in liver health SAD cohorts: Dose-dependent MAD cohorts: Similar reductions with extended dosing interval Z-AAT reductions Biweekly (200 mg x 7 doses) Monthly (400 mg x 4 doses) Mean max reduction of serum Z-AAT Mean max reduction of

serum Z-AAT from baseline from baseline following single dose 0% 0% -20% -20% -40% -40% -47.3% -47.3% -49.7% -49.7% -60% -60% -59.1% -67.7% -70.5% -80% -80% SAD MAD SAD MAD 200 mg 400 mg 600 mg 36 Error bars represent the standard error of the mean

(SE).

WVE-006 generated circulating wild-type M-AAT within the MZ range (up

to 64%) with no bystander edits, supporting potential improvement in lung health SAD cohorts: Dose-dependent MAD cohorts: Similar M-AAT% with extended dosing interval M-AAT restoration Biweekly (200 mg x 7 doses) Monthly (400 mg x 4 doses) Mean max

M-AAT (% of total AAT) Mean max M-AAT (% oMean f total m AA ax T) M-AAT (% of total AAT) Mean max M-AAT (% of total AAT) following a single dose 80% 80% 64.4% 58.7% MZ 1 range 52.3% 60% 60% 48.0% 48.0% 44.4% 4 4 4 4 .4% .4% 40% 40% 20% 20% 0% 0% 0%

0% 0% Baseline SAD MAD Baseline SAD MAD Baseline 200 mg 400 mg 600 mg 37 1. In a natural history cohort of individuals with M/Z genotype using the same LC-MS/MS assay in RestorAATion-2, M-AAT% of total AAT mean was 64% (range 57%-71%). At baseline,

serum M-AAT values were below the LLOQ (0.096 µM); the LLOQ value was used for baseline calculations. Error bars represent the standard error of the mean (SE).

WVE-006 continues to demonstrate dynamic increases of AAT during acute

phase responses CRP levels are correlated with AAT Total AAT reached 20.6 µM two weeks post single 200 mg dose during acute phase response elevations across RestorAATion-2 Total AAT • Two additional acute phase responses (URI-common cold)

accompanied by Total AAT 57.8% and 59.8% increases in AAT 1 from pre-event M-AAT M-AAT • CRP increases are strongly correlated CRP with AAT increases (r=0.73, p<0.001, 0 4 8 12 2,3 n=19) SAD MAD Acute phase response due to a kidney stone

Across RestorAATion-2 even low elevations in CRP are associated with increased production of AAT 38 CRP: C-reactive protein; URI: upper respiratory infection 1 – The most recent non-missing assessment obtained prior to the first observation

where CRP exceeded the upper limit of normal (ULN); 2 –Pearson correlation of log-transformed fold changes from pre-event (p < 0.001); 3 – N=19 defined as transitions from normal (≤ ULN) to elevated (> ULN) CRP M-AAT + Z-AAT

(µM) CRP levels (mg/L)

WVE-006 offers a differentiated treatment approach for AATD compared to

current standard of care and other therapies in clinical development Protecting the liver Protecting the lung Safe and convenient Enable dynamic Provide healthy, Infrequent Reduce Z-AAT Safe & well-tolerated AAT production wild-type M-AAT SC

dosing WVE-006 100% wild-type SC, Q4W ✓✓✓ (investigational) M-AAT Approved 100% wild-type IV, weekly 1 ûû✓ augmentation therapy M-AAT Recombinant 100% Fc- 2 augmentation therapy IV, Q3-4W ûû✓

dimerized AAT (investigational) 3 IV, single dose Liver enzyme elevations ; DNA base editing Less than 50% (uncertain durability, Requires LNPs; Risk of permanent 4 ✓✓ (investigational) wild-type M-AAT redosing may not be off-target

effects, including in 5 possible) cancer-associated genes 6 AAT siRNA Potential exacerbation of lung SC, Q3M 6 ✓ûû (investigational) disease due to AAT knockdown SC: subcutaneous; IV: intravenous. 1. Prolastin label; 2.

Barjaktarevic, et al. Efdoralprin Alfa vs. Plasma-derived Alpha-1 Proteinase Inhibitor (pdA1PI) Augmentation Therapy in Adults 39 With Alpha-1 Antitrypsin Deficiency (AATD) Emphysema: Results From Phase 2 ElevAATe Trial [Conference abstract] ATS

2026; 3. BEAM-302 Topline Data Update, March 25, 2026; 4. Banerjee, et al. BEAM-302 decreases hepatic aggregates of mutant AAT and increases circulating functional AAT in rodent models of Alpha-1 Antitrypsin Deficiency [Poster] 2023 ESGCT Congress;

5. Packer, et al. (2024) Methods and Compositions for Treating Alpha-1 Antitrypsin Deficiency (International Patent Application PCT/US2024/034189). https://patentimages.storage.googleapis.com/f7/f0/9a/f88f452755cb16/WO2024259364A2.pdf ; 6. Strnad,

et al. 2022 N Engl J Med 387:514-524.

WVE-006 aims to support a differentiated value proposition for Pi*ZZ

individuals, HCPs, and payers Infrequent subcutaneous Reduce Z-AAT to prevent liver dosing; potential for self- disease administration WVE-006 for AATD Provide healthy, wild-type Generally safe and well M-AAT to protect lung tolerated Enable dynamic

AAT No bystander edits or other production during acute permanent DNA phase response modifications Expect to meet with the FDA on a potential accelerated approval pathway end of summer 2026 40

WVE-008 RNA editing (AIMer) PNPLA3 I148M liver disease 41

WVE-008 for PNPLA3 I148M liver disease GalNAc-RNA editing approach

uniquely aims to restore PNPLA3 function to fully address genetic liver disease Homozygous PNPLA3 I148M carriers Heterozygous carriers have 80% lower risk of liver-related death as have significantly higher risk of compared to homozygous carriers

100 multiple liver diseases Homozygous I148 MASH Heterozygous I148M MAFLD 98 HR = 1.70 (0.78–3.71) AIMer editing to 96 restore heterozygous phenotype 94 Homozygous I148M HR = 8.61 (3.28–22.60) 92 0 0 2 4 6 8 10 12 14 16 18 20 22 24 26

Years of follow-up Over nine million homozygous PNPLA3 I148M individuals with genetic liver disease in US and Europe 42 1. Carlsson, B., et al. 2020 Aliment Pharmacol Ther.; 2. Unalp-Arida and Ruhl 2020 Hepatology; 3. Dong, XC, 2019 Front. Med. 4.

Liver International, 2025; 45:e16133 MAFLD, Metabolic dysfunction-associated fatty liver disease; MASH, Metabolic dysfunction-associated steatohepatitis; ALD, alcoholic liver disease; AH, Alcohol-associated hepatitis; HCC, hepatocellular carcinoma

Survival (%) of liver-related death

Worsening Silencing of PNPLA3 in normal liver may worsen basal

physiological functions Silencing PNPLA3 increases Silencing PNPLA3 worsens steatosis in PNPLA3 siRNA exacerbates the fibrotic 1 2 iPSC-derived human liver organoids inflammation-induced liver cell death in response in hepatic stellate cells 3 human

primary hepatocytes UC I148M KO UC I148M KO Control OA Functional PNPLA3 is imperative for liver health beyond improvements in steatosis 43 1. Rady, B, et al. 2021 PLoS ONE 2021; 2. Hendriks, D, et al. 2023 Nat Biotechnol; 3. Tilson, SG, et al. 2021

Hepatology Worsening

RNA editing is expected to restore PNPLA3 function to treat across the

stages of liver diseases RNA editing approach ✓ PNPLA3 I148M aggravates steatosis Silencing PNPLA3 may only partially PNPLA3 correction expected to and fibrosis through gain-of-function address disease restore function, counter liver disease

ATGL PNPLA3 PNPLA3 I148M CGI-58 • Creates PNPLA3 loss of function • PNPLA3 I148M accumulates on LDs, • Restores full PNPLA3 activity • ATGL partial rescue for loss PNPLA3 sequesters CGI-58, inhibits ATGL’s lipase

• Restores lipid mobilization, reverses activity and lipid mobilization from ER • Silencing will not restore retinol metabolism steatosis, fibrosis, ballooning, and • Suppresses retinol metabolism in liver and inflammation •

Fibrosis, ballooning, and inflammation worsens inflammation and fibrosis persist • Promotes liver fat accumulation and fibrosis through activation of stellate cells 44 ATGL: adipose triglyceride lipase; CGI-58: co-factor for ATGL; ER

endoplasmic reticulum; LDs: lipid droplets; CGI-58 also called ABHD5 Liver International, 2025; 45:e16117; Human Molecular Genetics, (2014) 23(15): 4077–4085

AIMers achieve efficient editing of PNPLA3, leading to reduction of

liver fat ✱✱✱✱ Significant decrease in liver fat with PNPLA3 editing in human HEPATOPAC® model with homozygous I148M ns 1500 1000 500 PBS PNPLA3 PNPLA3 siRNA AIMer 0 Decrease in liver fat with WVE-008 in monolayer

model PNPLA3 siRNA PBS PNPLA3 siRNA WVE-008 45 One-way ANOVA with Dunnett post hoc test comparisons to Mock **** P< 0.0001 Mock PNPLA3 siRNA PNPLA3 AIMer 2 Lipid Droplet Density (pixel /cell) 2 Lipid Droplet Density (pixel /cell) % Lipid Droplet

Density vs. PBS (mean + SE) (mean + SE) (mean ± SE)

Preclinical data support WVE-008 as potential first-in-class, disease

modifying therapy, for treatment of PNPLA3 I148M liver disease Tissue exposure supports excellent Potent editing with WVE-008 Highly specific editing with WVE-008 delivery 1000 100 Semi-log scale 10 0 5 10 15 20 25 Time (day) Expect to file Clinical

Trial Application (CTA) for WVE-008 in 2H 2026 46 Left: 4-parameter log-logistic dose response curve; Middle: Analysis utilized RNA-sequencing with two separate primary human hepatocyte cell lines (PH1/2). Variant calling utilized GATK best

practices for RNA variant calling using Mutect2 and display A->G evidence found when filtering for variants found in both cell lines and all doses. Liver Tissue Conc (μg/g)

Reimagining RNA medicines 47

Reimagining RNA medicines: Bifunctional modalities ✓ Engage both

endogenous Ago2 AGO2 and ADAR enzymes, as well as AGO2 dual RNAi silencing ✓ Silence multiple targets or silence Single one target while simultaneously Single Oligonucleotide Oligonucleotide editing or upregulating another Construct Construct

unique target ✓ Unlock complex indications that require engaging multiple targets ADAR AGO2 ✓ May continue to increase durability of editing 48 AIMer SpiNA SpiNA SpiNA

Poised for significant and sustained growth driven by RNAi and RNA

editing Other hepatic targets Extra-hepatic targets RNAi WVE-007 Obesity SpiNA Bifunctional single oligonucleotide constructs RNA WVE-006 AATD Editing WVE-008 Other hepatic targets AIMers PNPLA3 I148M liver disease Extra-hepatic targets

For questions contact: investorrelations@wavelifesci.com

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