Wave Life Sciences Corporate Presentation

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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

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

Building a leading RNA medicines company Novel RNA medicines platform

(PRISM ) Multi-modal: RNA editing, RNAi, splicing, allele-selective silencing Potential best-in-class, clinically-validated oligonucleotide chemistry (PN, stereochemistry) Pioneering a novel RNA Potential best-in-class

Leadership in allele- Novel approach designed to modality with RNA editing reduce fat, preserve muscle profile selective silencing WVE-007 in Obesity WVE-006 in AATD WVE-N531 in DMD WVE-003 in HD Well-capitalized with cash In-house GMP manufacturing

Strong and broad IP runway into 2027* 4 Patient populations represent US and Europe; WVE-006 is partnered with GSK AATD: Alpha-1 antitrypsin deficiency DMD: Duchenne muscular dystrophy HD: Huntington's disease *Cash runway does not include

potential future milestones or other payments under GSK collaboration

The powerful convergence of a validated, potential best-in-class

platform with deep genetic insights Multi-modal: RNA editing, RNAi, Real-time integration of new human antisense silencing, splicing genetic insights into discovery Best positioned to engage Proprietary deep learning

models Unmatched Data-driven endogenous machinery unveiling novel targets/ toolkit to discovery target sites Unlocking new, high-impact access novel powered by therapeutic targets Accelerating time to clinic biology human genetics

Breakthroughs in intracellular delivery Step-change in potency, distribution, Foundation in durability of effect chemistry innovation No complex delivery vehicles (AAV, LNP) 5

Robust, diversified RNA medicines pipeline including first-in-class RNA

editing programs IND / CTA Enabling Patient population Program Discovery Clinical Rights Studies (US & Europe) R N A E D I T I N G GSK exclusive WVE-006 (GalNAc) 200K SERPINA1 (AATD) global license GalNAc-AIMer 100% global 9M PNPLA3 (liver

disease) GalNAc-AIMer 100% global 900K (30M expansion) LDLR (HeFH) GalNAc-AIMer 100% global 70K APOB (HeFH) R N A i WVE-007 (GalNAc) 100% global 175M INHBE (Obesity) GalNAc-siRNA 100% global -- Undisclosed S PLI C I N G WVE-N531 100% global 2.3K

Exon 53 (DMD) Other exons (DMD) 100% global Up to 18K A LLE LE - S E LE C T I VE S I LE NC I NG 25K Symptomatic (SNP3) WVE-003 100% global mHTT (HD) 60K Pre-Symptomatic (SNP3) Editing for correction Editing for upregulation 6 AATD: Alpha-1

antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington's disease; HeFH: heterozygous familial hypercholesterolemia

WVE-007 GalNAc-siRNA silencing Obesity 7

Advancing WVE-007 as a novel, long acting, muscle sparing approach for

obesity WVE-007 is a GalNAc-siRNA that targets INHBE to treat obesity Adults with obesity have higher risk for many serious health conditions, including heart disease, type 2 1 diabetes, and some forms of cancer GLP-1s are current

standard of care for weight loss, but impact is often limited by: 2 Loss of muscle mass 3 Poor tolerability 4 Frequent dosing 5,6 High discontinuation rates ~175 million adults living with obesity in US and Europe 8

1. CDC.gov; 2. Sargeant, et al. 2019 Endocrinol Metab (Seoul) 34, 247; 3. Ghusn and Hurtado. 2024 Obesity Pillars 12, 100127; 4. Wegovy PI; 5. Leach, et al. 2023 Prime Therapeutics Claims Analysis; 6. Gasoyan, et al. 2024 Obesity (Silver Spring) 32,

486.; GalNAc-siRNA: GalNAc-conjugated small interfering RNA

Human genetic data demonstrate that heterozygous INHBE LoF carriers have

a healthy metabolic profile Heterozygous INHBE LoF carriers have favorable traits: Heterozygous INHBE LoF carriers have lower risk of Type 2 lower abdominal obesity, lower triglycerides, higher HDL-c diabetes and CHD Odds Ratio Favorable association

with liver traits Standard Deviations Standard Deviations Silencing INHBE mRNA by 50% is expected to recapitulate the healthy metabolic profile of heterozygous INHBE loss of function (LoF) carriers 9 Akbari et al. Nat Commun. 2022 Aug

23;13(1):4844; Deaton et al. Nat Commun. 2022 Jul 27 Waist to hip ratio: waist to hip ratio adjusted for BMI; HDL-c: high-density lipoprotein cholesterol; ALT: alanine transaminase; ApoB: apolipoprotein B; cT1: corrected T1

INHBE GalNAc-siRNA expected to address health issues associated with

pathogenesis of obesity associated metabolic disease Reduced release of Diminished activation of Increased adipose GalNAc-siRNA ACVR1C (ALK7) receptor in lipolysis shrinks hepatokine Activin E adipose tissue adipocytes Decreased abdominal adiposity

leads to weight loss and reduced risk for CVD and T2D 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

Single doses of INHBE GalNAc-siRNA result in dose-dependent weight loss

and reduction of visceral fat, without affecting muscle mass, in DIO mice Reduction in body weight Reduction in visceral fat No muscle loss Quadricep weight (Day 28) Epididymal fat weight (Day 28) * PBS INHBE GalNAc-siRNA

(3 mg/kg) INHBE GalNAc-siRNA (10 mg/kg) -23% -40% * * * * * * Single dose INHBE GalNAc-siRNA Preclinical data support INHBE GalNAc-siRNA as a single agent for healthy weight loss 11 Data from preclinical studies conducted in DIO mice; Stats: (left,

middle, right) Linear Mixed Effects ANOVA with post hoc comparisons of marginal treatment effects vs. PBS per timepoint (left) or per tissue (middle, right) * p < 0.05

INHBE GalNAc-siRNA can be used synergistically with GLP-1s or to

curtail weight regain after the cessation of treatment with GLP-1 ~2x greater overall weight loss when added to Curtails weight regain after the cessation of GLP-1 GLP-1 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 12 Data from

preclinical studies conducted in DIO mice; Left: 10nmol/kg in mouse is equivalent to therapeutic dose of GLP-1s in human. 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 * p < 0.05 Difference in body weight (% of PBS, same time point)

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

DIO mice Mean adipocyte diameter DIO Lean PBS INHBE GalNAc-siRNA ( m) 13 Data presented at ADA Scientific Sessions June 2025 ***p<0.001

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 (M ) (F4/80) Pro-inflammatory (M1) M Anti-inflammatory (M2) M (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 14 Data presented at ADA Scientific Sessions June 2025

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

Preclinical data support potential best-in-class profile and potential

to use WVE- 007 across multiple treatment settings with potential for 1-2x per year dosing Monotherapy Add-on to GLP-1s Maintenance WVE-007 in addition to GLP-1 WVE-007 for patients who stop WVE-007 as a single agent therapy treatment with GLP-1

therapy Weight loss similar to semaglutide with a single When administered as an add- Curtailed rebound weight dose on to semaglutide: gain upon cessation of No loss of muscle mass semaglutide and A single dose of

Wave's prevention of weight Reduction in fat mass with INHBE GalNAc-siRNA cycling, which worsens the preferential effect to the doubled the weight loss outcomes of various visceral fat observed with semaglutide metabolic diseases

Without suppressing food alone intake 15

INLIGHT: Phase 1 trial of WVE-007 in adults living with overweight or

obesity, otherwise healthy Randomized, double-blind, placebo-controlled (3:1) study of ascending doses of WVE-007 SAD Cohort 5 Trial Design MAD Cohort 3 Objective: Assess dose safety, tolerability, PK and PD SAD Cohort 4 Key

measurements MAD Cohort 2 - Primary: Safety and tolerability SAD Cohort 3 - Secondary: PK, Activin E 400mg - Exploratory PD: MAD Cohort 1 Body weight SAD Cohort 2 Body composition 240 mg (n=32) Metabolic health

Biochemical markers SAD Cohort 1 75 mg (n=8) Expect to deliver SAD Cohort 1 and Cohort 2 clinical data in 4Q 2025 and SAD Cohort 3 clinical data in 1Q 2026 16 SAD: single-ascending dose; MAD: multi-ascending dose

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

Advancing WVE-006 (RNA editing) in AATD WVE-006: GalNAc-conjugated,

subcutaneously delivered, designed to address AATD-related lung disease, liver disease, or both AATD is a rare, inherited genetic disorder that is commonly caused by a G-to-A point mutation in the SERPINA1 gene Characterized by

aggregation of mutant Z-AAT protein in hepatocytes and a lack of functional AAT in lungs People with AATD typically exhibit progressive lung damage, liver damage, or both Weekly intravenous augmentation therapy is the only treatment

option for AATD in those with the lung pathology No approved therapies to address AATD liver disease ~200K people in the US and Europe are homozygous for the Z allele 18 Strnad et al., 2020 N Engl J Med 382:1443-55; Blanco et al. 2017 Int J

Chron Obstruct Pulmon Dis 12:561-69

WVE-006 to address both liver and lung manifestations of AATD WVE-006

RNA WVE-006 RNA editing approach to address editing treatment key goals of AATD treatment: Restore circulating, Reduce Z-AAT Retain M-AAT Subcutaneous 1 functional wild-type 2 protein aggregation 3 physiological injection M-AAT in liver regulation

(GalNAc) Infrequent dosing Z-AAT Highly specific A I M-AAT reaches lungs to RNA correction replaces M-AAT secretion into (no bystanders) protect from proteases mutant Z-AAT protein with bloodstream wild-type M-AAT protein 19 Strnad et al.,

2020 N Engl J Med 382:1443-55; Stoller et al., 1993 Alpha-1 Antitrypsin Deficiency GeneReviews.

RestorAATion-2 clinical trial in Pi*ZZ AATD patients ongoing

RestorAATion-2: AATD Patients RestorAATion-1: Healthy Volunteers RestorAATion-1: Healthy Volunteers SAD MAD Multi-dosing complete in RestorAATion-1 SAD MAD Dose E Up to seven doses in multi-dose portion Cohort 3 Dose D Cohort 2 400

mg Dose C Cohort 1 Dose B 200 mg Study key objectives Dose A Safety and tolerability Pharmacokinetics Serum M-AAT levels Multi-dosing complete in 200 mg cohort of RestorAATion-2; Dosing complete in second single dose cohort

(400 mg) 20 HV: healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending dose

Achieved proof-of-mechanism for Wave's RNA editing platform

Proof-of-mechanism achieved after a single dose in RestorAATion-2 Total AAT protein increased to a mean of 10.8 M at day 15 Meets level that has been the basis for regulatory approval for AAT augmentation therapies

Circulating wild-type M-AAT protein reached a mean of 6.9 M at day 15; more than 60% of total AAT Increases in total AAT from baseline and M-AAT protein were observed as early as day 3 and through day 57 Increases in

neutrophil elastase inhibition from baseline were consistent with production of functional M- AAT WVE-006 well tolerated with a favorable safety profile; all AEs mild-to-moderate, no SAEs Data from the complete 200 mg single and multidose

cohorts expected in 3Q 2025; Data from the complete 400 mg single dose cohort expected in the fall of 2025 21 October 16, 2024 Proof-of-mechanism disclosure on first two "ZZ" AATD patients in first dose cohort (200 mg) of RestorAATion-2

Wholly owned GalNAc-AIMer programs Correction of PNPLA3 Strongly

supported by human genetics Genetically defined liver disease Patient population: ~9 million Leverage unique platform capabilities; Building on learnings of WVE-006 Upregulation of LDLR HeFH Patient population: ~900,000, with Novel

ways of treating diseases with expansion to ~30 million in follow on indications high unmet need Readily accessible biomarkers and Correction of APOB ways to assess pharmacodynamics HeFH Patient population: ~70,000 Expect to

initiate clinical development of additional RNA editing programs, including PNPLA3, LDLR, and APOB programs in 2026 22 Patient populations are in US and Europe Editing for correction Editing for upregulation HeFH: heterozygous familial

hypercholesterolemia

WVE-N531 Splicing Duchenne muscular dystrophy 23

Advancing WVE-N531 in exon 53 amenable DMD WVE-N531: exon skipping

oligonucleotide designed to induce production of endogenous, functional dystrophin protein High unmet need for therapies delivering more consistent dystrophin expression, as few patients today achieve dystrophin >5% of normal

Opportunity to extend dosing intervals beyond weekly standard of care to alleviate burden for patients and caregivers Need to reach stem cells and distribute broadly to muscle tissues to potentially enable muscle regeneration and impact

respiratory and cardiac function WVE-N531 has Rare Pediatric Disease Designation and Orphan Drug Designation from FDA DMD impacts ~1 / 5,000 newborn boys annually; ~20,000 new cases annually worldwide 24 Duan, D. et al. 2021 Nat Rev Dis

Primers 7, 13; Muscular Dystrophy Association; Aartsma-Rus, et al. 2009 Hum Mutat 30, 293.

FORWARD-53 48-week clinical trial results: WVE-N531's potential

best-in- class profile for boys amenable to exon 53 skipping Statistically significant and clinically meaningful improvement (3.8s) in Time-to-Rise vs. natural history; functional benefits on other measures including NSAA Statistically

significant reductions in muscle fibrosis and CK; driven by decreases in inflammation and necrosis; transition from regenerative to mature muscle Consistent dystrophin expression averaged 7.8% between 24 and 48 weeks, with 88% of

boys above 5% dystrophin; delivery to both myofibers and muscle stem cells WVE-N531 remains safe and well-tolerated with no Serious Adverse Events NDA filing for accelerated approval with monthly dosing planned for 2026 25 Muscle

content-adjusted dystrophin