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,"

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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 Anticipated Upcoming Milestones

DMD (splicing), HD (silencing), and AATD (RNA editing) clinical programs advancing Proof-of-mechanism data from RestorAATion clinical program of INHBE program, obesity (siRNA), muscle sparing, fat loss, WVE-006 for AATD in 2024 improved

metabolic profile Select INHBE clinical Multi-modal drug discovery and development platform candidate for obesity in 3Q 2024 and submit CTA in 2025 Leader in RNA editing with best-in-class oligonucleotide chemistry Data from

FORWARD-53 clinical trial of WVE-N531 for DMD in 3Q 2024 In-house GMP manufacturing; Strong and broad IP portfolio Data from SELECT-HD clinical trial of WVE-003 for HD in 2Q Strategic collaborations to expand and advance pipeline 2024

Well-capitalized with cash runway into 4Q 2025* 3 *Cash runway does not include potential future milestones or opt-in payments under GSK and Takeda collaborations

Combining best-in-class chemistry with novel biology and genetic

insights: Opportunities for new high-impact medicines Accessing new endogenous enzymes for novel modalities Best-in-class Unlocks (RNA editing) validated new pipeline New biology chemistry programs Opening up new targets, including

prevalent diseases 4

Wave's versatile RNA medicines platform ideal for capitalizing on new

genetic insights in rare and common diseases Accessing UK Biobank and building proprietary machine learning models to generate unique genetic insights 5 Claussnitzer, et al. Nature (2020) 577, 179; King et al. PLoS Genet (2019) 15, e1008489

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 RestorAATion Clinical Program 200K SERPINA1 (AATD) global license Multiple undisclosed 100% global >20K (multiple)

Correction Multiple undisclosed 100% global >3M (multiple) Upregulation SILENCING: siRNA INHBE (Obesity and other 100% global 47M metabolic disorders) SPLICING WVE-N531 100% global 2.3K FORWARD-53 Trial (Phase 2) Exon 53 (DMD) Other exons (DMD)

100% global Up to 18K SILENCING: ANTISENSE 25K Manifest (SNP3) WVE-003 SELECT-HD Trial (Phase 1b/2a) Takeda 50:50 Option mHTT (HD) 60K Pre-Manifest (SNP3) Editing for correction Editing for upregulation 6 AATD: Alpha-1 antitrypsin deficiency; DMD:

Duchenne muscular dystrophy; HD: Huntington's disease

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 $505 million in Up to $2.8 billion in

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

$3.3 billion in 2 milestones $20 million milestone Advancing work on INHBE is Wave's first achieved with first multiple targets wholly owned program Leverage GSK's individual dosing in spanning multiple

emerging from GSK expertise in genetics 4Q 2023 modalities beyond RNA collaboration and genomics editing, including siRNA 7 1. $120 million in cash and $50 million equity investment received in January 2023, 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-006 (RNA editing) AATD 8

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

liver and lung manifestations of AATD WVE-006 for AATD WVE-006 ADAR editing approach to address key goals of AATD treatment: 1) Restore circulating, 2) Reduce Z-AAT protein 3) Retain M-AAT A functional wild-type M-AAT aggregation in liver

physiological regulation 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 with protect from

proteases bloodstream wild-type M-AAT protein Edited SERPINA1 mRNA enables wild-type M-AAT protein production 200,000 Pi*ZZ patients in US and Europe 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 5 1 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 SERPINA1 C 0% PBS (PiZ mutation site) T 100% C 48.2% AATD AIMer T 51.8% Editing site (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

Proof-of-mechanism data from RestorAATion-2 expected in 2024 Informs

dose & dose frequency R Res estto orA rAA AT Tiio on n--1: 1: H Healt ealthy hy V Volunteers olunteers RestorAATion-2: AATD Patients SAD MAD cohorts Dose E Up to 7 doses Dose D High dose Dose C Medium dose Dose B Low dose Multiple

assessments of serum AAT throughout cohort Dose A Study key objectives Dosing Safety and tolerability Underway Pharmacokinetics Serum M-AAT levels 13 HV: healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending dose

AIMers RNA editing capability 14

The AIMer-targetable Edit-Verse' is substantial

Gene-Disease Network The Edit-verse is the editable gene-disease universe, including upregulation 1 >13,000 genes with a high-probability of being amenable to transcriptional regulation with A-to-G editing Model

development ongoing to expand access to more protein-coding genes and expand the Edit-verse AIMers are expected to be able to target ~50% of the transcriptome 15 1 (score >95th p-tile)

Innovating on applications of ADAR beyond restoring protein function

Restore or correct Upregulate expression to increase endogenous protein activity protein function Attenuated gene expression mRNA mRNA Decay Cascade Unique RNA motifs "Dialed up" Gene Expression Correct G-to-A driver mutations

with AIMers WVE-006 (GalNAc-AIMer) Edited mRNA AATD A single edited base permanently disrupts the motif Stable mRNA yields increased protein production 16

Multiple RNA editing opportunities to build high-value 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) The Edit-verse is substantial and still expanding

Advancing work for a diverse set of undisclosed targets addressing areas of high unmet need, including both rare and prevalent diseases 17

INHBE program (siRNA silencing) Obesity and other metabolic disorders

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

platform Unprecedented Ago2 loading increases potency and durability of silencing following administration of single subcutaneous dose Ago2 loading Antisense strand Ago2 loading HSD17B13 mRNA (liver, transgenic mice) (Liver, transgenic mice)

25 (liver, transgenic mice) (liver, transgenic mice) 5 125 Wk 2 Wk 7 Wk 14 Wk 2 Wk 7 Wk 14 4 20 100 3 2 15 75 1 11 .0 1 50 10 25 * 0.5 * 5 0 0 2 4 6 8 10 12 14 16 0.0 0 Time (weeks) PBS Reference Wave siRNA Reference Wave siRNA siRNA silencing is

one of multiple Wave modalities being advanced in strategic research collaboration with GSK 19 Left, Middle, and right: Mice expressing human HSD17B13 transgene treated with siRNA (3 mg/kg) or PBS, liver mRNA, guide strand concentration, Ago2

loading quantified. Stats: Two-way ANOVA with post-hoc test * P<0.05, ****P<0.0001. Liu et al., 2023 Nuc Acids Res doi: 10.1093/nar/gkad268; % mRNA remaining (HSD17B13/Hprt) ug of oligo/g of tissue (mean sem) Fold change relative to

Driven by clinical genetics, Wave's first RNAi program addresses

high unmet need in obesity INHBE program (GalNAc siRNA) is Wave's first wholly owned program emerging from GSK collaboration GLP-1 receptor agonists have several INHBE silencing expected to induce fat reported limitations loss, while

maintaining muscle mass siRNA to silence INHBE gene is expected to recapitulate 1 Lead to weight loss at the expense of muscle mass the healthy metabolic profile of INHBE loss of function 1,2,3 (LoF) heterozygous human carriers,

including: 4 Suppress general reward system 4 Reduced waist-to-hip ratio Reduced serum Associated with poor tolerability profile with 68% drop- 3 Reduced odds ratio of type 2 triglycerides off after 1 year

diabetes and coronary artery Elevated HDL-c Discontinuation of therapy leads to rapid weight regain disease by >25% INHBE expressed primarily in liver and gene product 4 (activin E) acts on its receptor in adipose tissue

Wave's INHBE siRNA program may address these Lowering of INHBE mRNA or blocking of its receptor limitations and / or work synergistically with GLP-1s promotes fat burning (lipolysis) and decreases fat 5,6 accumulation (adiposity)

50% reduction of INHBE in patients expected to restore and maintain a healthy metabolic profile 20 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

INHBE silencing achieved in vivo with GalNAc-siRNA led to lower body

weight and significant decrease in visceral fat INHBE mRNA silencing INHBE silencing led to INHBE silencing leads to demonstrated at 5 weeks 16% lower body weight as significant decrease in compared to control visceral fat at 5 weeks Results of in

vivo preclinical study are consistent with UK Biobank human data on loss-of-function carriers 21 HFD: high-fat diet. Stats: two-sided Welch's T Test **** P < 0.0001 1. Adam, RC. et.al. Proc Natl Acad Sci USA. 2023. Data plotted by body

weight difference as a % of PBS treated young DIO mice; Coskun, T. et. al. Mol. Metab. 2018, 18, 3. Stats: Repeated Measures ANOVA; Inhbe siRNA vs. Control sig. different at P < 0.05 level weeks 2 - 5; Stats: white-adj. Two-way ANOVA with

Bonferroni-adj post hoc comparisons per tissue type allowing heteroscedasticity (only HFD, Inhbe siRNA vs. HFD, PBS shown) ***P < 0.001, ****P < 0.0001

INHBE candidate for obesity expected in 3Q 2024; CTA expected in 2025

Next generation siRNA results in more Applying next-generation siRNA chemistry potent and durable target knockdown to INHBE program Potent and highly specific INHBE leads 125 PBS identified 100 Benchmark First gen siRNA

GalNAc-conjugated for targeted delivery to 75 Next gen siRNA liver * 50 * Potential for infrequent administration Next generation 25 * * siRNA 0 0 5 10 15 20 25 30 35 40 45 50 Day Wave's next generation GalNAc-siRNA demonstrates

best-in-class potential 22 Foster, DJ. et.al. Mol Ther. 2018, 26(3), 708. B6 mice administered PBS or 0.5 mg/kg of siRNA (subcutaneous). Benchmark: Stats: Mixed Two-way ANOVA followed by post hoc test comparing siRNA vs. Next gen siRNA per day

derived from linear mixed effects model * P < 0.0001 Serum Ttr SEM (rel to PBS)

Wave's platform chemistry enables siRNA extra-hepatic delivery

Chemical impact - Introduction of neutral backbone - Unique structural feature of PN, specifically guanidine - Increased lipophilicity - Stereochemistry Extra-hepatic delivery PN - Titrating siRNA lipophilicity tunable PNs (PN

variants) - Maintaining high Ago2 loading and intracellular trafficking - Titrating plasma protein binding - Altered delivery, enhanced potency and durability in various tissues PN can tune extra-hepatic delivery of siRNA using rational design,

including placement, number of modifications and PN variants 23

Single dose of next generation siRNA delivers broad, potent and durable