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 Strategic collaborations Well-capitalized with cash In-house GMP manufacturing Strong and broad IP runway into 2027* (GSK and Takeda) 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 and Takeda collaborations

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

oligonucleotide chemistry (PN, stereochemistry) Splicing Editing Silencing Restore RNA transcripts and turn on Efficient editing of RNA bases to Degradation of RNA transcripts to protein production restore or modulate protein turn off 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-N531 (DMD) WVE-003 (HD) WVE-007 (obesity)

Additional wholly owned editing programs 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:

Proprietary chemistry continues to translate in clinic across

modalities, enabling first-in-class and best-in-class therapies 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 (WVE-N531 for DMD) concentrations in 6 weeks tolerable 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) GalNAc-RNA Proof-of-mechanism data RestorAATion trial editing expected 4Q 2024

completion Novel base and sugar (WVE-006 for AATD) 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 / Preclinical Clinical Rights Studies (US & Europe) R NA E D I T I NG GSK exclusive WVE-006 RestorAATion Clinical Program 200K SERPINA1 (AATD) global license Multiple

undisclosed 100% global >20K (multiple) Correction Multiple undisclosed 100% global >3M (multiple) Upregulation R N A i WVE-007 Obesity and 100% global 47M other metabolic disorders 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 Takeda 25K Symptomatic (SNP3) WVE-003 SELECT-HD Trial (Phase 1b/2a) - Trial Completed mHTT (HD) 50:50 Option 60K Pre-Symptomatic (SNP3) Editing

for correction Editing for upregulation 7 AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington's disease

WVE-006 + AIMers RNA editing 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 aims to address the large unmet need in AATD 200,000 Pi*ZZ patients in US and Europe WVE-006 for AATD Current standard of care is weekly IV augmentation therapy

No therapies address AATD liver disease A WVE-006 ADAR editing approach to address key goals of AATD treatment: SERPINA1 Z allele mRNA encodes Z-AAT protein 1) Restore circulating, 2) Reduce Z-AAT protein 3) Retain M-AAT with E342K mutation

functional wild-type M-AAT aggregation in liver physiological regulation Z-AAT I(G) Edited SERPINA1 mRNA enables wild-type M- RNA correction replaces AAT protein production M-AAT reaches lungs to M-AAT secretion into mutant Z-AAT protein with wild-

protect from proteases bloodstream type M-AAT protein 9 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 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 10 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

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 1 5 0 0 0 Week 0 Week 13 11 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 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 RNA editing only

detected at PiZ mutation RNA editing across transcriptome site in SERPINA1 transcript PBS SERPINA1 C 0% (PiZ mutation site) T 100% AATD AIMer C 48.2% T 51.8% Editing site % Editing (PiZ mutation) No bystander editing observed on SERPINA1 transcript

12 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 Coverage Coverage

RestorAATion-2 underway, proof-of-mechanism data expected in 4Q 2024

Informs dose & dose frequency RestorAATion-1: Healthy Volunteers RestorAATion-2: AATD Patients RestorAATion-1: Healthy Volunteers Single ascending dose (SAD) Multiple-ascending dose (MAD) cohorts Dose E Up to 7 doses Dose D Cohort 3 Dose

C Cohort 2 Dose B Cohort 1 Multiple assessments of serum AAT throughout cohort Dose A Study key objectives Safety and tolerability Pharmacokinetics Serum M-AAT levels 13 HV: healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending

Multiple RNA editing opportunities to build high-value, wholly owned

pipeline beyond WVE-006 Potential to advance any combination of targets into preclinical development Hepatic (GalNAc-AIMers) Extra-Hepatic (AIMers) Target A Target B Target X Target E Target F Target G Approach Upregulation Upregulation Upregulation

Correction Upregulation Correction Tissue Liver Liver Liver Liver Kidney Lung Therapeutic Area Metabolic Metabolic Renal Rare Renal Rare Estimated Patients (US and ~90M ~3M ~170K ~17K ~85K ~5K Europe) Identifying new targets using

proprietary "Edit-Verse", which is powered by genetic datasets and deep learning models Advancing work for a diverse set of undisclosed targets addressing areas of high unmet need, including both rare and prevalent diseases

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) 15 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

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

metabolic disorders 16

Potential for best-in-class siRNA enabled by Wave's PRISM

platform Unprecedented Ago2 loading increases potency and Next-generation siRNA results in durability of silencing following administration of more potent and durable silencing single subcutaneous dose Ago2 loading Next generation siRNA

enhances Ago2 loading HSD17B13 mRNA (liver, transgenic mice) knockdown of serum Ttr protein (liver, transgenic mice) 25 (liver, transgenic mice) 125 125 Wk 2 Wk 7 Wk 14 PBS 20 100 100 Benchmark First gen siRNA 15 75 75 Next gen siRNA 50 50 10 25 *

Next-gen * 25 5 siRNA 0 0 0 2 4 6 8 10 12 14 16 125 0 0 5 10 15 20 25 30 35 40 45 50 PBS Time (weeks) Benchmark 100 Day 125 PBS Reference Wave first gen PBS First gen siRNA Reference Wave first gen siRNA 75 100 Benchmark Next gen siRNA siRNA First

gen siRNA 50 75 Next gen siRNA siRNA silencing is one of multiple Wave modalities being advanced in strategic research collaboration with GSK 25 50 0 25 0 5 10 15 20 25 30 35 40 45 50 17 Day Left and Middle: Mice expressing human HSD17B13 transgene

treated with siRNA (3 mg/kg) or PBS, liver mRNA, guide strand concentration, Ago2 loading quantified. Stats: Two-way 0 ANOVA with post-hoc test * P<0.05, ****P<0.0001. Liu et al., 2023 Nuc Acids Res doi: 10.1093/nar/gkad268; Right: Benchmark:

Foster, DJ. et.al. Mol Ther. 2018, 26(3), 708. B6 mice 0 5 10 15 20 25 30 35 40 45 50 administered PBS or 0.5 mg/kg of siRNA (subcutaneous). Stats: Mixed Two-way ANOVA followed by post hoc test comparing siRNA vs. Next gen siRNA per day derived from

linear mixed Day effects model * P < 0.0001 % mRNA remaining (HSD17B13/Hprt) Fold change relative to Reference 2 Serum Ttr SEM (rel to PBS) Serum Ttr SEM (rel to PBS) Serum Ttr SEM (rel to PBS)

Supported by human genetics, WVE-007 (INHBE GalNAc-siRNA) expected to

drive healthy, sustainable weight loss INHBE silencing expected to induce fat loss, Distinct pathway as compared to GLP-1s while maintaining muscle mass 1 Weight loss with no impact on muscle mass Silencing INHBE gene by 50%

is expected to recapitulate the healthy metabolic profile of INHBE loss of function Preferential reduction of visceral fat 1,2,3 (LoF) carriers, including: 3 No suppression of general reward system Reduced waist-to-hip

ratio Reduced serum No loss of appetite Reduced odds ratio of type 2 triglycerides diabetes and coronary artery Elevated HDL-c GalNAc-siRNA enables infrequent dosing; 1 - 2x/year disease by >25%

INHBE (Inhibin E) expressed primarily in liver and gene Wave's INHBE siRNA program may address these 4 product (activin E) acts on its receptor in adipose tissue limitations and / or work complementarily with GLP-1s

Lowering of INHBE mRNA promotes fat burning (lipolysis) 5,6 and decreases fat accumulation (adiposity) Obesity is estimated to impact 174M adults in the US and Europe 18 1. Sargeant, et al. 2019 Endocrinol Metab (Seoul) 34(3):247-262; 2. Prime

Therapeutics Claims 1. Nat Commun 2022. https://doi.org/10.1038/s41467-022-32398-7; 2. Nat Commun 2022. Analysis, July 2023; 3. M ller, et al. 2019 Molecular Metabolism 30: 72-130. https://doi.org/10.1038/s41467-022-31757-8; 3. PLOS ONE 2018.

https://doi.org/10.1371/journal.pone.0194798; 4. Adam, RC. et.al. Proc Natl Acad Sci USA. 2023, 120(32): e2309967120. 5. Yogosawa et al. 2013 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3526038/ 6. Zhao et al. 2023

WVE-007 has Wave's next generation siRNA format and best-in-class

profile with infrequent dosing INHBE program: Data from DIO mouse model supports best-in-class profile and potential use of WVE-007 in multiple treatment settings Highly potent (ED50 < 1mg/kg) and durable silencing following one,

low-single-digit dose, supporting every-six-month or annual dosing Monotherapy: Weight loss similar to semaglutide with no loss of muscle mass and a reduction in fat mass, with preferential effect to the visceral fat (consistent with

profile of INHBE LoF carriers in human genetics) Add-on to GLP-1s: 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 and this effect was

sustained throughout the duration of the study Maintenance: Curtailed rebound weight gain upon cessation of semaglutide Expect to initiate clinical trial for WVE-007 in 1Q 2025 19

WVE-N531 Splicing Duchenne muscular dystrophy 20

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 21 Duan, D. et al. 2021 Nat Rev Dis Primers 7, 13; Muscular Dystrophy Association; Aartsma-Rus, et al.

2009 Hum Mutat 30, 293.