Wave Life Sciences Corporate Presentation

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

Wave today is well positioned for significant and sustained growth DMD,

HD, and AATD clinical programs advancing Collaborations & access to genetic insights DMD, HD, and AATD clinical programs advancing Clinical proof-of- Leader in RNA editing therapeutics, emerging concept leader in RNAi Opened new Multi-modal drug

discovery biology and development platform Platform Pipeline of novel medicines for rare and learnings prevalent diseases Data Science Strategic collaborations to Foundation expand and advance pipeline Chemistry innovation GMP manufacturing

Stereochemistry Strong and broad IP Building a leading RNA medicines company 3

RNA medicines allow matching disease target to therapeutic modality Most

versatile RNA medicines Restored platform (PRISM ) in the Reading Frame industry Endogenous ADAR enzyme Functional Best-in-class nucleic acid Protein chemistry applicable editing splicing across modalities Ability to access novel / untapped

areas of disease biology Platform learnings and clinical validation continue RISC to increase probability Endogenous Endogenous of success AGO2 RNase H silencing silencing 4

Proprietary PN chemistry enhances potency across modalities RNA Editing

Splicing Silencing % Editing % Skipping Target knockdown (% remaining) 100 80 60 40 20 0 -8 -6 -4 -2 0 2 10 10 10 10 10 10 Concentration ( M) Concentration ( M) Ranked by potency of reference PS/PO compound Ranked by potency of reference

PS/PO compound PS/PO/PN PS/PO (Stereopure) PS/PO (Stereorandom) PS/PO reference compound PS/PN modified compound Left: Experiment was performed in iPSC-derived neurons in vitro; target mRNA levels were monitored using qPCR against a control gene

(HPRT1) using a 5 linear model equivalent of the DDCt method; Middle: DMD patient-derived myoblasts treated with PS/PO or PS/PO/PN stereopure oligonucleotide under free-uptake conditions. Exon-skipping efficiency evaluated by qPCR. Right: Data from

independent experiments % Editing Improved editing Improved skipping Improved knockdown

Robust RNA medicines pipeline including first-in-class RNA editing

programs Patient population Program Discovery Preclinical Clinical Rights (US & Europe) RNA EDITING WVE-006 GSK exclusive 200K SERPINA1 (AATD) global license Multiple undisclosed 100% global >20K (multiple) Correction Multiple undisclosed

100% global >3M (multiple) Upregulation SPLICING WVE-N531 Phase 1/2 100% global 2.3K Exon 53 (DMD) Other exons (DMD) 100% global Up to 18K SILENCING: ANTISENSE Takeda 50:50 25K Manifest (SNP3) WVE-003 Phase 1/2 mHTT (HD) Option 60K Pre-Manifest

(SNP3) SILENCING: RNAi INHBE* (Metabolic disorders, including 100% global 47M obesity) *Through GSK collaboration, Wave can advance up to three collaboration programs (the first of which is INHBE) and GSK can advance up to eight collaboration

programs. 6 AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington's disease Editing for correction Editing for upregulation

Strategic collaboration with GSK to develop transformative RNA medicines

for genetically defined diseases Multiple value drivers to Wave Milestone / royalties Milestone / royalties Genetic targets $170 million upfront to Wave to leverage GSK granted exclusive global GSK to advance up to eight 1 GSK's

genetic Wave (cash and equity ) license to WVE-006 for AATD collaboration programs insights Additional research support Up to $1.2 billion in aggregate in funding Up to $225 million in development initiation, development and launch and

launch milestones milestones Potential for up to $3.3 2 billion in milestones Up to $300 million in sales-related Up to $1.6 billion in aggregate in Wave to advance up milestones sales-related milestones to three wholly owned collaboration

Expands Wave's pipeline programs (or more Double-digit tiered royalties as a pending agreement Tiered royalties as a percentage of percentage of net sales up to high- 3 with GSK) net sales up to low-teens INHBE is

Wave's first teens wholly-owned program Development and commercialization Development and commercialization emerging from GSK responsibilities transfer to GSK after responsibilities transfer to GSK at collaboration completion of

first-in-patient study development candidate First-in-class RNA Collaboration leverages Wave's unique stereopure, TM editing program PN-chemistry containing PRISM platform, including editing, splicing, silencing (RNAi and antisense) 1 2 $120

million in cash and $50 million equity investment received in January 2023, Initiation, development, launch, and commercialization milestones for WVE-006 7 3 and programs progressed during initial 4-year research term (8 GSK collaboration programs),

GSK eligible to receive tiered royalty payments and commercial milestones from Wave

WVE-N531 Duchenne muscular dystrophy

Duchenne muscular dystrophy Genetic mutation in dystrophin gene

Disease State Restored State prevents the production of dystrophin Dysfunctional Splicing Exon Skipping Oligo protein, a critical component of healthy Mutant pre-mRNA Mutant pre-mRNA muscle function 50 51 53 54 55 50 51 53 54 55 Impacts

approx. 1 in every 5,000 Skip newborn boys each year; approx. 20,000 new cases annually worldwide 50 51 53 54 55 50 51 54 55 - Approx. 8-10% are amenable to exon 53 skipping mRNA with disrupted reading frame Restored mRNA Dystrophin

protein established by FDA as Translation halted Translation continues surrogate endpoint reasonably likely to 1 predict benefit in boys for accelerated approval in DMD Increasing amount of functional dystrophin expression over minimal

amount shown with approved therapies is expected to result No dystrophin Functional in greater benefit for boys with DMD protein produced dystrophin produced 1 9 Vyondys: www.fda.gov; viltepso; www.fda.gov; Exondys; www.fda.gov; Amondys:

Extended survival in dKO preclinical model supports potential of

exon-skipping therapeutics for DMD PN chemistry improved function and survival in dKO mice dKO survival studies in literature Restored muscle and respiratory 100% survival at time of study termination function to wild-type levels 300 200 100 0 20 40

60 80 100 120 Stimulation Frequency (Hz) Wild-type dKO: PBS dKO: PS/PO/PN Tidal volume Time (weeks) PS/PO/PN 150 mg/kg weekly PS/PO/PN 75 mg/kg bi-weekly PS/PO 150 mg/kg weekly PBS Age (days) Wild-type dKO: PBS dKO (PS/PO/PN Note: Untreated,

age-matched mdx mice had 100% survival at oligonucleotide) study termination [not shown] 10 Left: Kandasamy et al., 2022; doi: 10.1093/nar/gkac018; Right: Forand et al., 2020; doi: https://doi.org/10.1016/j.omtm.2020.03.011. Survival probability (%)

2 TVb (ml) Specific Force (Nm )

Preclinical data supported advancing WVE-N531 to clinical development

WVE-N531 reached high concentrations in heart and WVE-N531: Dystrophin diaphragm in NHP restoration of up to 71% in vitro Western Blot normalized to primary healthy human myoblast lysate Conc (uM) % Dystrophin Dystrophin Vinculin 11 th 26 Annual

ASGCT meeting, May 16-20, 2023

WVE-N531 Part A clinical data: High exon-skipping & muscle

concentrations after three bi-weekly doses WVE-N531 uptake in WVE-N531 uptake in myocyte stem cells myocyte stem cells suvodirsen WVE-N531 Mean muscle 0.7 g/g 42 g/g concentration Mean exon Not detectable 53% skipping WVE-N531 uptake in

Half-life in myogenic stem 18 hours 25 days cells plasma 22 weekly doses of 5 3 biweekly doses of 10 Dose mg/kg mg/kg Important for potential muscle regeneration WVE-N531 data presented March 22, 2023 at Muscular Dystrophy Association Clinical and

Scientific Conference; WVE-N531 biopsies collected ~2 weeks post-last dose (3 biweekly 12 doses of 10 mg/kg) 42 g/g = 6.1 M; Suvodirsen biopsies collected post-last dose (weekly doses of 5 mg/kg) on week 22; Half-life as indicated by PK

analysis; suvodirsen: discontinued first-generation non-PN chemistry compound; Right: Dual staining utilizing in-situ hybridization for WVE-N531 and PAX7 immunohistochemistry for stem cells

FORWARD-53, a potentially registrational Phase 2 clinical trial of

WVE-N531 in DMD (Exon 53) Screening Biweekly Dosing (10 mg/kg IV) Safety Follow-up Functional Biopsy after 24 weeks of Biopsy after 48 weeks of treatment assessment treatment Functional assessment Functional

assessment Design of FORWARD-53: Phase 2, open-label, 10 mg/kg every other week, up to 10 patients Endpoints: Dystrophin (powered for >5% of normal), safety/tolerability, pharmacokinetics, functional assessments (incl. NSAA and

others) Biopsies: - After 24 weeks of treatment - After 48 weeks of treatment Data from FORWARD-53 expected in 2024 13 IV: intravenous; NSAA: North star ambulatory assessment

Potential for Wave to address up to ~40% of DMD population Exon

skipping and dystrophin restoration demonstrated in vitro Exon Skipping 1.1 M 2.5 M 2.5 M DMD Population 3.3 M 5 M 5 M 100 100 100 10 M 10 M 10 M WVE-N531 Exon 53 Not Amenable 50 50 50 to

Skipping 8-10% Exon 51 17% 0 0 0 11-13% Ex51 Ex51 mock Ex52 Ex52 mock Ex44 Ex44 mock SSO-1 SSO-2 SSO-1 SSO-2 SSO-1 SSO-2 6% Exon 44 Protein Restoration 4% 1.1 M 2.5 M 2.5 M 150 150 Exon 52 3.3 M 5 M 5 M 100 10

M 10 M 10 M 8% Exon 45 100 100 44% 50 Other Exons 50 50 0 0 0 Ex51 Ex51 mock Ex52 Ex52 mock Ex44 Ex44 mock SSO-1 SSO-2 SSO-1 SSO-2 SSO-1 SSO-2 Exon 51 Exon 52 Exon 44 14 Left: Aartsma-Rus, et al. 2009 Hum Mutat 30, 293. %

Dystrophin Relative to WT % Exon 51 Skipping Rel to Total DMD % Dystrophin Relative to WT % Exon 52 Skipping Rel to Total DMD % Dystrophin Relative to WT % Exon 44 Skipping Rel to Total DMD

WVE-006 for Alpha-1 antitrypsin deficiency (AATD)

WVE-006: Designed to correct mutant SERPINA1 transcript to address both

liver and lung manifestations of AATD WVE-006 designed to correct WVE-006 ADAR editing approach to address key goals of AATD treatment: Z allele mRNA to enable M-AAT protein to be produced 2) Reduce Z-AAT 1) Restore circulating, 3) Retain M-AAT

protein aggregation in A functional wild-type M-AAT physiological regulation liver SERPINA1 Z allele mRNA encodes Z-AAT protein with E342K mutation Z-AAT WVE-006 (GalNAc- conjugated AIMer) I(G) RNA correction replaces M-AAT reaches lungs to M-AAT

secretion into mutant Z-AAT protein protect from proteases bloodstream with wild-type M-AAT protein Edited SERPINA1 mRNA enables wild- type M-AAT protein production 200,000 Pi*ZZ patients in US and Europe AAT: Alpha-1 antitrypsin Strnad et al., 2020

N Engl J Med 382:1443-55; Blanco et al., 2017 Int J Chron Obstruct Pulmon Dis 12:561-69; Remih 16 et al., 2021 Curr Opin Pharmacol 59:149-56.

WVE-006 in AATD: First-in-class RNA editing clinical candidate

Potentially comprehensive approach to address both lung and liver manifestations of AATD Increased AAT protein Confirmed restored Demonstrated functionality in NSG-PiZ mice wild-type M-AAT protein of M-AAT protein WVE-006 treatment results in serum

AAT Overall percentages of serum AAT Serum neutrophil elastase protein levels of up to 30 uM in NSG-PiZ mice protein isoforms in NSG-PiZ mice inhibition activity in NSG-PiZ mice (Week 13) 2000 PBS 1800 WVE-006 1600 WVE-006 (NO LOADING DOSE) 1400

1200 ~7-fold 1000 increase 800 600 11 M 400 200 0 Week ~50% editing supports restoration of MZ phenotype AATD: Alpha-1 antitrypsin deficiency; M-AAT protein: wild-type AAT protein; WVE-006 administered subcutaneously (10 mg/kg bi-weekly) in

7-week old NSG-PiZ mice (n=5 per group); Loading dose: 3 x 10 mg/kg at Day 0. Left: Liver biopsies collected at wk 13 (1 wk after last dose) and SERPINA1 editing quantified by Sanger sequencing; Right: Total 17 serum AAT protein quantified by ELISA;

Stats: Two-Way ANOVA with adjustment for multiple comparisons (Tukey) 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Serum AAT protein (ug/ml) (Mean, s.e.m)

WVE-006 decreases lobular inflammation and PAS-D globule size, prevents

increase in hepatocyte turnover Fibrosis Cirrhosis Hepatocellular Carcinoma Correction of gain-of-function liver phenotypes Lobular inflammation Mitoses PAS-D-positive globule size (NSG PiZ mice, week 13) (NSG PiZ mice, week 13) (NSG

PiZ mice, week 13) ns ns 5 40 ns 25 4 20 30 3 15 20 2 10 10 5 1 0 0 0 Week 0 Week 13 Week 0 Week 13 Week 0 Week 13

Left (Lobular inflammation) and Middle (Mitoses): Scatter plot showing inflammation grade or mitoses score. Each circle represents an individual mouse, (Mean SEM); Right (PAS-D Globule Size): 40 largest globules in each of 5 mice were

measured. Each circle represents a single PAS-D globule, (Mean 18 SEM). Baseline: week 0 (7 weeks old); Treated week 13 (20 weeks old); Stats: Kruskal-Wallis followed by Dunn's test Baseline PBS WVE-006 Baseline PBS WVE-006 Baseline PBS

WVE-006 Score (0-4) Number of mitotic figures/10 MPF + Mean PAS-D globule diameter ( m)

AIMer-directed editing is highly specific in mice No bystander editing

observed on SERPINA1 transcript RNA editing only detected at PiZ mutation site in SERPINA1 transcript RNA editing across transcriptome (mouse liver) (mouse liver) C 0% SERPINA1 PBS (PiZ mutation site) T 100% C 48.2% AATD AIMer T 51.8% % Editing

Editing site (PiZ mutation) Dose 3x10 mg/kg (days 0, 2, 4) SC with AATD AIMer (SA1 - 4). Liver biopsies day 7. RNA-seq to quantify on-target SERPINA1 editing, to quantify off-target editing reads mapped to entire mouse genome; plotted circles

represent sites with LOD>3 (N=4), SERPINA1 edit site is indicated 19 Coverage Coverage

Proof of mechanism data in patients with AATD expected in 2024 Informs

dose & RestorAATion-2: AATD Patients RestorAATion-1: Healthy Volunteers dose frequency SAD MAD cohorts Dose E Up to 7 doses High dose Dose D Dose C Medium dose Dose B Low dose Multiple assessments of serum AAT throughout cohort Dose A

Study key objectives Expect to initiate dosing in 4Q 2023 Safety and tolerability Serum M-AAT levels Pharmacokinetics 20 HV: healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending dose

AIMers RNA base editing capability

First-generation AIMer designs published in Nature Biotechnology

Specificity in vitro & in vivo (NHPs) GalNAc conjugation In vitro-in vivo translation (NHPs) Foundational AIMer SAR AIMers detected in liver of NHP at Day 50 Substantial and durable editing in NHP ADAR editing with

ACTB AIMer is (PK) liver in vivo highly specific (PD) RNA editing within full transcriptome (primary human hepatocytes) GalNAc AIMers Day 50 RNA editing ACTB in NHP GalNAc AIMers % Editing 22 RNA editing only detected at editing Monian et al., 2022

published online Mar 7, 2022; doi: 10.1038.s41587-022-01225-1 site in ACTB transcript SAR structure-activity relationship Confidence (LOD score)

Innovating on applications of ADAR editing Correct G-to-A driver

mutations with AIMers Modulate protein interactions with AIMers Achieved POC Restore or correct Modulate protein- protein function protein interaction Upregulate expression WVE-006 Modify function (GalNAc AIMer) AATD Post-translational modification

Alter folding or processing AIMers provide dexterity, with applications beyond precise correction of genetic mutations, including upregulation of expression, modification of protein function, or alter protein stability 23 POC: proof of

Proprietary base modifications increase editing across edit region