Wave Life Sciences Corporate Presentation

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Emerging leader in RNA medicines Multi-modal drug Differentiated,

clinical- Strategic collaborations to discovery and stage RNA medicines expand and advance development platform to pipeline with first-in- pipeline (GSK and Takeda) address new areas of class RNA editing disease biology programs RNA editing,

splicing and silencing Multiple pipeline and Well-capitalized with GMP manufacturing platform catalysts expected cash runway Strong and broad IP expected in 2023 and into 2025 beyond position Wave Life Sciences is an RNA medicines company committed

to delivering life-changing treatments for people battling devastating diseases 3 3 3

RNA medicines allow matching disease target to therapeutic modality RNA

Base Editing Splicing Silencing Efficient editing of RNA bases Restore RNA transcripts and Degradation of RNA transcripts to restore or modulate turn on protein production to turn off protein production protein production

Endogenous Skip RNase H Restored Reading Frame Endogenous AGO2 Endogenous RISC ADAR enzyme Functional Protein 4

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

First in vivo study of unconjugated siRNAs Unprecedented Ago2 loading following demonstrated 70-90% APP silencing across administration of single subcutaneous dose six brain regions in mouse CNS at 8 weeks Ago2 Ago2 l l ooa adindi g

ng HSD17B13 mRNA (liver, transgenic mice) (liver, transgenic mice) 25 (liver, transgenic mice) 125 Wk 2 Wk 7 Wk 14 20 100 15 75 50 10 **** * 25 * 5 0 0 2 4 6 8 10 12 14 16 0 Time (weeks) PBS Reference Wave siRNA Reference Wave siRNA RNAi is one of

multiple Wave modalities being advanced in strategic research collaboration with GSK Left, Middle: Mice expressing human HSD17B13 transgene treated (3 mg/kg)siRNA 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; Right: ICV: Intracerebroventricular; APP: Amyloid precursor protein ; CNS: 5 central nervous system; B6 mice were administered

PBS or 100 g of APP siRNA by ICV injection on day 0 (n=7). Mice euthanized 8 weeks after administration. Taqman qPCR assays used for RNA PD, relative fold changes of App to Sfrs9 mRNA normalized to percentage of PBS group. All treated group

show P 0.0001 compared to PBS group in 2way ANOVA. % mRNA remaining (HSD17B13/Hprt) Fold change relative to Reference 2

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 6 linear model equivalent of the Ct 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 - SPLICING WVE-N531 100% global 2.3K Phase 1/2 Exon 53

(DMD) Other exons (DMD) 100% global Up to 18K SILENCING: ANTISENSE 25K Manifest (SNP3) Takeda 50:50 WVE-003 Phase 1/2 60K Pre-Manifest mHTT (HD) Option (SNP3) Takeda 50:50 SCA3 (ATXN3) 8K Option SILENCING: RNAi Undisclosed 100% global - Through GSK

collaboration, Wave can advance up to three collaboration programs and GSK can advance up to eight collaboration programs 7 AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington's disease; SCA3: Spinocerebellar

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

In multidose portion of study, patients received three biweekly 10

mg/kg doses Single ascending intra-patient doses Multidosing at 10 mg/kg every other week Weeks 0 2 4 6 Muscle 10 mg/kg 10 mg/kg 10 mg/kg 10 mg/kg Biopsy Initial cohort Period before initiating 6 mg/kg multidosing (~1 - 2 months) Boys

with DMD 3 mg/kg amenable to exon 53 skipping 1 mg/kg Data include: WVE-N531 muscle Exon skipping concentrations Dystrophin protein WVE-N531 localization Dose WVE-N531 12

WVE-N531 in DMD: Delivered positive proof-of-concept data in 4Q 2022

Tissue % Exon Dystrophin High exon skipping and Tissue Patient concentration skipping by Western blot muscle concentrations Source ( g/g) by RT-PCR (% of normal) after three biweekly 10 mg/kg doses 1 Deltoid 85.5 61.5 0.24

Similar exon skipping 2 Deltoid 33.5 49.8 0.23 regardless of mutation - Patient 1: del48-52 3 Bicep 8.3 47.9 0.34 - Patient 2: del45-52 - Patient 3: del51-52 Mean Mean muscle Mean exon dystrophin: PK analysis indicated

concentration: s k ipping: 0.27% of 42 g/g 53% 25-day half-life in normal (BLQ) plasma WVE-N531 appeared safe and well-tolerated Data presented March 22, 2023 at Muscular Dystrophy Association Clinical and Scientific Conference

Biopsies collected ~2 weeks post-last dose (3 biweekly doses of 10 mg/kg) 42 g/g = 6.1 M BLQ: Below level of quantification (1%) Data cut-off: December 6, 2022 13

Initiating Part B, a potentially registrational Phase 2 clinical trial

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

Design of Part B: 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 Part B expected in 2024 14 IV: intravenous; NSAA: North star ambulatory assessment

GSK Collaboration and WVE-006 for Alpha-1 antitrypsin deficiency

Strategic collaboration with GSK to develop transformative RNA

medicines for genetically defined diseases Multiple value drivers to Wave $170 million upfront to 1 Milestone / royalties Milestone / royalties Genetic targets Wave (cash and equity ) Wave to leverage GSK granted exclusive global GSK to

advance up to eight Additional research support GSK's genetic license to WVE-006 for AATD collaboration programs insights funding Up to $1.2 billion in aggregate in Potential for up to $3.3 Up to $225 million in development

initiation, development and launch 2 and launch milestones billion in milestones milestones Expands Wave's pipeline 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 programs (or more Double-digit tiered royalties as a pending agreement Tiered royalties as a percentage of Extends cash runway percentage of net sales up to high- 3 with GSK) net sales up to low-teens

teens into 2025 Development and commercialization Development and commercialization responsibilities transfer to GSK after responsibilities transfer to GSK at 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 16 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-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 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 17 et al., 2021 Curr Opin Pharmacol 59:149-56.

WVE-006 in AATD: First-in-class RNA editing candidate approaching the

clinic 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 >11 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 CTA submitted for first-in-human study 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 18 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 19 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 20 Coverage Coverage

WVE-003 Huntington's Disease

mHTT toxic effects lead to neurodegeneration; loss of wtHTT functions

may also contribute to HD Huntington's disease (HD) Healthy individual Wild-type HTT (wtHTT) is critical for normal neuronal function Expanded CAG triplet repeat in HTT gene results in production of mutant huntingtin protein

(mHTT) wtHTT Stresses HD is a monogenic autosomal dominant genetic disease; fully Huntington's disease penetrant and affects entire brain Fatal disease characterized by cognitive decline, psychiatric illness, and chorea ~50%

decrease wtHTT Stresses mHTT + 30,000 people with HD in the US in wtHTT and more than 200,000 at risk of Loss of wtHTT functions developing HD Synaptic dysfunction | Healthy CNS function Cell death | Neurodegeneration 22

WVE-003: First-in-class allele-selective candidate for HD Reductions in

mean CSF mHTT and preservation of wtHTT mHTT protein reductions observed in pooled analysis of single dose cohorts in observed in single dose cohorts SELECT-HD clinical study (Sep. 2022) wtHTT protein levels mHTT protein levels wtHTT

protein levels appear consistent with allele-selectivity Generally safe and Reduction in mHTT protein: well-tolerated Placebo 22% from baseline 35% vs. placebo WVE-003 Additional single-dose and (30 and 60 mg pooled*) available