Wave Life Sciences Corporate Presentation

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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,

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"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

Building a leading RNA medicines company Novel RNA medicines platform

(PRISM ) Multi-modal: RNA editing, RNAi, splicing, allele-selective silencing Best-in-class, clinically-validated oligonucleotide chemistry (PN, stereochemistry) Differentiated RNA medicines pipeline WVE-N531 in DMD WVE-006 in

AATD WVE-007 in Obesity WVE-003 in HD Well-capitalized with cash In-house GMP manufacturing Strong and broad IP runway into 2027* 3 AATD: Alpha-1 antitrypsin deficiency DMD: Duchenne muscular dystrophy HD: Huntington's disease *Cash runway

does not include potential future milestones or opt-in payments under GSK collaboration

Wave's best-in-class multi-modal platform Clinically-validated

oligonucleotide chemistry (including PN, stereochemistry) Editing Silencing Splicing Efficient editing of RNA bases to Degradation of RNA transcripts to Restore RNA transcripts and turn on restore or modulate protein turn off protein production

protein production production Antisense siRNA RISC Spliceosome Machinery (>300 proteins) Endogenous RNase H Restored Reading Frame Endogenous for Functional Protein ADAR enzyme Endogenous AGO2 WVE-006 (AATD) WVE-003 (HD) WVE-007 (obesity)

WVE-N531 (DMD) PNPLA3 (Liver disease), LDLR, APOB (HeFH) 4

Wave has driven foundational advances in nucleic acid chemistry to

expand platform technologies and develop next generation of RNA therapeutics Further information can be found in recent platform publications Silencing (RNase H and Ago2) Splicing Editing 5 Full list of Wave publications:

Three clinical updates in 2024 demonstrate continued platform

translation Clinical Clinical Therapeutic Preclinical translation trial results modalities publication 53% exon skipping, 9.0% mean muscle-adjusted Splicing 42 g/g muscle tissue dystrophin; safe and tolerable

(WVE-N531 for DMD) concentrations in 6 weeks (interim analysis) Proprietary PRISM platform 46% allele-selective mHTT Stereopure oligonucleotides 35% allele-selective Allele-selective silencing; correlation with mHTT silencing with single silencing

slowing of caudate (WVE-003 for HD) dose atrophy Novel backbone modifications (including PN chemistry) First ever RNA editing GalNAc-RNA Multidose data expected achieved; 11 M total AAT editing in 2025

protein, >60% (6.9 M ) M- Novel base and sugar (WVE-006 for AATD) AAT with single dose chemistry modifications GalNAc-RNAi Clinical trial initiation expected 1Q 2025 (WVE-007 for obesity) 6 Full list of Wave publications:

https://ir.wavelifesciences.com/events-publications/publications *mHTT reductions compared to placebo

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 RestorAATion Clinical Program 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) INHBE (Obesity and other 100% global 47M metabolic disorders) GalNAc-siRNA 100% global --

Undisclosed S PLI C I N G WVE-N531 FORWARD-53 Trial (Phase 2) 100% global 2.3K Exon 53 (DMD) Other exons (DMD) 100% global Up to 18K A LLE LE - S E LE C T I V E S I LE N C I N G 25K Symptomatic (SNP3) WVE-003 100% global SELECT-HD Trial (Phase

1b/2a) - Trial Completed mHTT (HD) 60K Pre-Symptomatic (SNP3) Editing for correction Editing for upregulation 7 AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington's disease; HeFH: heterozygous familial

hypercholesterolemia

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

WVE-006: GalNAc-conjugated AIMer designed to correct mutant SERPINA1

transcript to address both liver and lung manifestations of AATD WVE-006 for AATD Wild-type M-AAT protein A SERPINA1 Z allele mRNA encodes Z-AAT protein with E342K mutation AAT is an acute phase protein Serum AAT protects lungs predominantly

produced against neutrophil elastase by hepatocytes I(G) Gain of Loss of Function: Function: Liver Edited SERPINA1 mRNA enables wild-type Lung Disease M-AAT protein production Disease Misfolded Z-AAT Hepatocellular Emphysema Bronchiectasis protein

with Fibrosis Cirrhosis Carcinoma E342K mutation A I Subcutaneous Infrequent Highly specific injection dosing (No bystanders) Polymerization Z protein causes AAT proteotoxic Low serum AAT (GalNAc)

stress, leading to progressive leads to lung disease liver disease 9 Strnad et al., 2020 N Engl J Med 382:1443-55; Stoller et al., 1993 Alpha-1 Antitrypsin Deficiency GeneReviews. AATD Healthy

RestorAATion-1 and RestorAATion-2 ongoing RestorAATion-2: AATD Patients

RestorAATion-1: Healthy Volunteers RestorAATion-1: Healthy Volunteers Single ascending dose (SAD) Multiple-ascending dose (MAD) cohorts Multidosing Dose E ongoing in Dose E Up to 7 doses Dose D Cohort 3 Dose C Cohort 2 Dose B Cohort 1 200 mg

Dose A Study key objectives Safety and tolerability Pharmacokinetics Serum M-AAT levels 10 HV: healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending dose

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

Proof-of-mechanism after a single dose in RestorAATion-2 Circulating wild-type M-AAT protein in plasma: Mean of 6.9 M at day 15; more than 60% of total AAT Increases in neutrophil elastase inhibition from baseline: Consistent

with production of functional M- AAT Mean total AAT protein: Increased from below level of quantification at baseline to 10.8 M at day 15 - Meets level that has been the basis for regulatory approval for AAT augmentation

therapies Increases in total AAT from baseline and M-AAT protein: Observed as early as day 3 and through day 57 WVE-006 well tolerated with a favorable safety profile; all AEs mild-to-moderate, no SAEs Wave expects to share multidose

data from RestorAATion-2 in 2025 11 October 16, 2024 Proof-of-mechanism disclosure on first two "ZZ" AATD patients in first dose cohort of RestorAATion-2 to reach day 57;

Strategic collaboration with GSK to develop transformative RNA

medicines Maximize global Advance up to eight Collaboration Expand Wave's potential for GSK collaboration Highlights pipeline WVE-006 for AATD programs 1 $170 million upfront Wave to advance up to Up to $525 million in Up to $2.8

billion in three wholly owned Additional research total milestones and total milestones and collaboration programs funding tiered royalties on net tiered royalties on (or more with GSK's sales net sales 3 consent) Potential for

up to $3.3 billion in 2 milestones $20 million milestone $12 million aggregate INHBE is Wave's first with first individual dosing initiation payment for wholly owned program Leverage GSK's emerging from

GSK GSK's selection of two expertise in genetics RestorAATion-2 trial collaboration programs to advance and genomics underway (AATD patients) 12 1. $120 million in cash and $50 million equity investment; 2. Initiation, development, launch, and

commercialization milestones for WVE-006 and programs progressed during initial 4- year research term (8 GSK collaboration programs); 3. GSK eligible to receive tiered royalty payments and commercial milestones from Wave Recent Highlights

Wholly owned GalNAc-AIMer programs New targets meet key criteria,

expected to improve probability of success: Correction of PNPLA3 Genetically defined liver disease Strongly supported by human genetics Leverage unique platform capabilities; Upregulation of LDLR GalNAc-AIMers building on learnings

of WVE-006 Familial hypercholesterolemia Completely novel ways of treating diseases with high unmet need Correction of APOB Readily accessible biomarkers and approaches to assess PD, defined regulatory paths Familial

hypercholesterolemia PNPLA3, LDLR, APOB clinical candidates expected in 2025 13 Editing for correction Editing for upregulation

WVE-007 (INHBE program) GalNAc-siRNA silencing Obesity and other

metabolic disorders 14

Human genetic data demonstrate that INHBE heterozygous 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 Silencing INHBE mRNA by 50%

is expected to recapitulate the healthy metabolic profile of heterozygous INHBE loss of function (LoF) carriers 15 Akbari et al. Nat Commun. 2022 Aug 23;13(1):4844; Deaton et al. Nat Commun. 2022 Jul 27

INHBE GalNAc-RNA expected to address health issues associated with

pathogenesis of obesity, associated metabolic disease Release of dimerized INHBE Binds to and activates Block adipose subunits creates hepatokine ACVR1C (ALK7) receptor in lipolysis Activin E adipose tissue Activin E Activin E Increased abdominal

adiposity leads to obesity, II II I CVD and T2D I Adipocyte ALK7 Decreased abdominal adiposity leads to weight loss and reduced risk for GalNAc-siRNA CVD and T2D Diminished activation of Reduced release of Increased adipose ACVR1C (ALK7) receptor in

hepatokine Activin E lipolysis and shrink adipose tissue adipocytes 16 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 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 INHBE GalNAc-siRNA has potential as monotherapy weight loss therapeutic 17 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

prevent weight regain after the cessation of treatment with GLP-1s ~2x greater overall weight loss when added to Prevents weight regain after the cessation of GLP-1s GLP-1s 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 18 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)

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

WVE-007 across multiple treatment settings with 1-2x a year dosing Monotherapy: as a single agent. Weight loss similar to semaglutide with no loss of muscle mass and a reduction in fat mass with preferential effect to the visceral fat, and

without suppressing food intake Add-on to GLP-1s: WVE-007 in addition to GLP-1 therapy. When administered as an add-on with semaglutide, a single dose of Wave's INHBE GalNAc-siRNA doubled the weight loss observed with semaglutide

alone Maintenance: for patients who stop treatment with GLP-1 therapy. Curtailed rebound weight gain upon cessation of semaglutide and prevention of weight cycling, which worsens the outcomes of various metabolic diseases 19

CTA expected before year-end for Phase 1 trial of WVE-007 in adults

living with overweight or obesity, otherwise healthy Randomized, double-blind, placebo-controlled study of ascending doses of WVE-007 MAD Cohort 3 Trial Design SAD Cohort 5 Objective: Assess dose safety, tolerability, PK and PD MAD Cohort 2

SAD Cohort 4 Key measurements - Primary: Safety and Tolerability MAD Cohort 1 - Secondary: PK, Activin E SAD Cohort 3 - Exploratory PD: Body Weight Body compositions SAD Cohort 2 Metabolic health Biochemical

markers SAD Cohort 1 Expect to initiate clinical trial for WVE-007 in 1Q 2025 20

WVE-N531 Splicing Duchenne muscular dystrophy 21

Urgent need for improved therapeutic options for the treatment of DMD

Duchenne is a devastating and fatal disease Genetic mutation in dystrophin gene prevents the production of dystrophin protein, a critical component of healthy muscle function Impacts ~1 / 5,000 newborn boys annually; ~20,000 new

cases annually worldwide - ~8-10% are amenable to exon 53 skipping - Potential for Wave to address up to 40% of DMD with additional exon skipping therapeutics Multiple urgent unmet needs 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 Boy living with DMD cardiac function 22 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: An ongoing potentially registrational open-label Phase 2

clinical trial of WVE-N531 in boys with DMD amenable to exon 53 skipping 10 mg/kg Q2W Screening Safety Follow-up N = 11 Baseline functional Muscle biopsy after 24 Muscle biopsy after 48 Interim weeks of treatment weeks of

treatment assessments analysis Functional assessments Functional assessments Key Assessments: Safety and tolerability Muscle biopsies after 24 and 48 weeks of treatment - PK: Drug tissue concentrations - PD:

Exon-skipping, Dystrophin level (% of normal) as assessed by Western Blot Functional outcome measures 11 participants enrolled, including two from prior Part A clinical trial - Pre-specified analyses in ambulatory patients 23 IV:

Intravenous; Q2W: Every 2 Weeks; PK: Pharmacokinetics; PD: Pharmacodynamics

Results of interim analysis: WVE-N531 has potential to be the

best-in-class therapeutic for exon 53 DMD Highly consistent dystrophin expression Muscle delivery and extended dosing across patients intervals 9.0% muscle-content adjusted dystrophin (5.5% Skeletal muscle tissue concentrations of