Corporate Presentation March 6, 2024 Wave Life Sciences Exhibit 99.2

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 otherwise.

Building a leading RNA medicines company Proof-of-mechanism data from RestorAATion clinical program of WVE-006 for AATD in 2024 Initiate clinical trial of INHBE candidate for obesity in 1Q 2025 Data from FORWARD-53 clinical trial of WVE-N531 for DMD in 3Q 2024 Data from SELECT-HD clinical trial of WVE-003 for HD in 2Q 2024 Anticipated Upcoming Milestones *Cash runway does not include potential future milestones or opt-in payments under GSK and Takeda collaborations AATD (RNA editing), DMD (splicing), and HD (antisense) clinical programs advancing INHBE program for obesity (siRNA) designed for fat loss, muscle sparing, improved metabolic profile Multi-modal drug discovery and development platform; therapeutic candidates that optimally address disease biology Leader in RNA editing with best-in-class oligonucleotide chemistry Strategic collaborations to expand and advance pipeline In-house GMP manufacturing; Strong and broad IP portfolio Well-capitalized with cash runway into 4Q 2025*

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

Claussnitzer, et al. Nature (2020) 577, 179; King et al. PLoS Genet (2019) 15, e1008489 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

SPLICING WVE-N531 Exon 53 (DMD) 100% global 2.3K Other exons (DMD) 100% global Up to 18K SILENCING: ANTISENSE WVE-003 mHTT (HD) Takeda 50:50 Option 25K Manifest (SNP3) 60K Pre-Manifest (SNP3) Robust RNA medicines pipeline including first-in-class RNA editing programs AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington’s disease Program Discovery / Preclinical IND / CTA Enabling Studies Clinical Rights Patient population (US & Europe) RNA EDITING WVE-006 SERPINA1 (AATD) GSK exclusive global license 200K Multiple undisclosed Correction 100% global >20K (multiple) Multiple undisclosed Upregulation 100% global >3M (multiple) SILENCING: siRNA INHBE lead clinical candidate (Obesity and other metabolic disorders) 100% global 47M Editing for correction Editing for upregulation FORWARD-53 Trial (Phase 2) SELECT-HD Trial (Phase 1b/2a) RestorAATion Clinical Program

Strategic collaboration with GSK to develop transformative RNA medicines 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 Maximize global potential for WVE-006 for AATD  Advance up to eight GSK collaboration programs Up to $505 million in additional milestones and tiered royalties on net sales Up to $2.8 billion in total milestones and tiered royalties on net sales Wave to advance up to three wholly owned collaboration programs (or more with GSK’s consent)3 Expand Wave’s pipeline Recent Highlights ü $20 million milestone achieved with first individual dosing in 4Q 2023 Collaboration Highlights $170 million upfront1 Additional research funding Potential for up to $3.3 billion in milestones2 Leverage GSK’s expertise in genetics and genomics ü Advancing work on multiple targets spanning multiple modalities beyond RNA editing, including siRNA ü INHBE is Wave’s first wholly owned program emerging from GSK collaboration

WVE-006 (RNA editing) AATD

WVE-006: Designed to correct mutant SERPINA1 transcript to address both liver and lung manifestations of AATD 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. 3) Retain M-AAT physiological regulation 2) Reduce Z-AAT protein aggregation in liver WVE-006 ADAR editing approach to address key goals of AATD treatment: 1) Restore circulating, functional wild-type M-AAT I(G) A SERPINA1 Z allele mRNA encodes Z-AAT protein with E342K mutation Edited SERPINA1 mRNA enables wild-type M-AAT protein production WVE-006 (GalNAc-conjugated AIMer) WVE-006 for AATD 200,000 Pi*ZZ patients in US and Europe M-AAT reaches lungs to protect from proteases M-AAT secretion into bloodstream RNA correction replaces mutant Z-AAT protein with wild-type M-AAT protein Z-AAT

WVE-006 treatment results in serum AAT protein levels of up to 30 uM in NSG-PiZ mice Overall percentages of serum AAT protein isoforms in NSG-PiZ mice (Week 13) Serum neutrophil elastase inhibition activity in NSG-PiZ mice 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) ≥50% editing supports restoration of MZ phenotype 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 in NSG-PiZ mice ✓ Confirmed restored wild-type M-AAT protein ✓ Demonstrated functionality of M-AAT protein ✓

WVE-006 decreases lobular inflammation and PAS-D globule size, prevents increase in hepatocyte turnover 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 Mitoses (NSG PiZ mice, week 13) Fibrosis à Cirrhosis à Hepatocellular Carcinoma Correction of gain-of-function liver phenotypes Lobular inflammation (NSG PiZ mice, week 13) Week 0 Week 13 PAS-D-positive globule size (NSG PiZ mice, week 13)

RNA editing only detected at PiZ mutation site in SERPINA1 transcript RNA editing across transcriptome 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 No bystander editing observed on SERPINA1 transcript AIMer-directed editing is highly specific in mice SERPINA1 (PiZ mutation site) Coverage PBS AATD AIMer C 48.2% T 51.8% C 0% T 100% Editing site (PiZ mutation) Coverage % Editing

Proof-of-mechanism data from RestorAATion-2 expected in 2024 HV: healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending dose RestorAATion-2: AATD Patients  Informs dose & dose frequency RestorAATion-1: Healthy Volunteers SAD à MAD cohorts Dose escalation Study key objectives Safety and tolerability Pharmacokinetics Serum M-AAT levels Dosing Underway Multiple assessments of serum AAT throughout cohort Dose A Low dose Up to 7 doses Dose B Dose C Dose D Dose E Medium dose High dose RestorAATion-1: Healthy Volunteers

AIMers RNA editing capability

The AIMer-targetable ‘Edit-Verse’ is substantial The Edit-verse is the editable gene-disease universe, including upregulation >13,000 genes with a high-probability1 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 Gene-Disease Network 1(score >95th p-tile)

Innovating on applications of ADAR beyond restoring protein function mRNA mRNA Decay Cascade Unique RNA motifs Edited mRNA A single edited base permanently disrupts the motif Stable mRNA yields increased protein production Restore or correct protein function Upregulate expression to increase endogenous protein activity Correct G-to-A driver mutations with AIMers WVE-006 (GalNAc-AIMer) AATD “Dialed up” Gene Expression Attenuated gene expression

Multiple RNA editing opportunities to build high-value pipeline beyond WVE-006 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 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 Europe) ~90M ~3M ~170K ~17K ~85K ~5K Potential to advance any combination of targets into preclinical development

INHBE program (siRNA silencing) Obesity and other metabolic disorders

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;  siRNA silencing is one of multiple Wave modalities being advanced in strategic research collaboration with GSK Potential for best-in-class siRNA enabled by Wave’s PRISM platform Wk 2 Wk 14 Wk 7 Reference Wave first gen siRNA * * Ago2 loading (liver, transgenic mice) Wave first gen siRNA Reference PBS 1 Wk 2 Wk 14 Wk 7 1 PBS HSD-1933 HSD-1930 NTC PBS HSD-1933 HSD-1930 PBS HSD-1933 HSD-1930 Unprecedented Ago2 loading increases potency and durability of silencing following administration of single subcutaneous dose

Lead to weight loss at the expense of muscle mass1 Associated with poor tolerability profile4 with 68% drop-off after 1 year3 Discontinuation of therapy leads to rapid weight regain Suppress general reward system4 GLP-1 receptor agonists have several reported limitations siRNA to silence INHBE gene is expected to recapitulate the healthy metabolic profile of INHBE loss of function (LoF) heterozygous human carriers, including:1,2,3 INHBE expressed primarily in liver and gene product (activin E) acts on its receptor in adipose tissue4 Lowering of INHBE mRNA or blocking of its receptor promotes fat burning (lipolysis) and decreases fat accumulation (adiposity)5,6 INHBE silencing expected to induce fat loss, while maintaining muscle mass ≥50% reduction of INHBE in patients expected to restore and maintain a healthy metabolic profile 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 to emerge from GSK collaboration 1. Nat Commun 2022. https://doi.org/10.1038/s41467-022-32398-7;  2. Nat Commun 2022. 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 https://pubmed.ncbi.nlm.nih.gov/36626233/ 1. Sargeant, et al. 2019 Endocrinol Metab (Seoul) 34(3):247-262; 2. Prime Therapeutics Claims Analysis, July 2023; 3. Müller, et al. 2019 Molecular Metabolism 30: 72-130. Wave’s INHBE siRNA program may address these limitations and / or work synergistically with GLP-1s Reduced waist-to-hip ratio Reduced odds ratio of type 2 diabetes and coronary artery disease by >25% Reduced serum triglycerides Elevated HDL-c

Right: Reduction in fat mass at Week 5 Results of in vivo preclinical study are consistent with UK Biobank human data on loss-of-function carriers First generation INHBE GalNAc-siRNA led to lower body weight and significant decrease in visceral fat in DIO mouse model Chow PBS HFD PBS HFD First generation INHBE siRNA ~56% reduction Visceral fat (mesenteric) *** Chow PBS HFD PBS HFD First generation INHBE siRNA Lower body weight as compared to control ✓ Reduction in fat mass across multiple types of white adipose tissue, with preferential effect on visceral fat reduction ✓ ~38% reduction Subcutaneous fat (inguinal) ***

Next generation siRNA results in more potent and durable target knockdown Highly potent silencing (ED50 < 1mg/kg) Durable silencing following one, low-single-digit dose, supporting every-six-month or annual dosing Weight loss with no loss of muscle mass Reduction in fat mass, with preferential effect to the visceral fat INHBE program: Data from DIO mouse model supports best-in-class profile 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 Expect to initiate clinical trial for INHBE candidate in 1Q 2025 INHBE lead clinical candidate has Wave’s next generation siRNA format and best-in-class profile Next generation siRNA * * * *

Chemical impact Introduction of neutral backbone Unique structural feature of PN, specifically guanidine Increased lipophilicity Stereochemistry  Extra-hepatic delivery 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 Wave’s platform chemistry enables siRNA extra-hepatic delivery PN

Sustained APP knockdown of at least 75% throughout the 16-week study in vivo in mice Single dose of next generation siRNA delivers broad, potent and durable CNS target engagement APP silencing PBS Next gen siRNA Robust target engagement translates to substantial App protein reduction across brain regions 8-weeks post single dose PBS (dotted line) or 100 μg of App siRNA administered ICV (n=7). PCR assays for RNA PD, relative fold changes of App to Hprt mRNA normalized to % of PBS; Stats: Three-way ANOVA followed by Bonferroni-adjusted post hoc test comparing condition to PBS (data not shown), Next gen siRNA significantly lower than PBS at both time points for all tissues at P < 0.0001 level; Immunohistochemical analysis of FFPE Mouse Brain tissue labeling App protein (Color Brown) with CS#19389 followed by a ready to use Polymer-HRP 2nd Detection antibody. Nuclei were counterstained with Hematoxylin (Color Blue). Single 100 ug ICV injection

PBS (dotted line) or 100 μg of App siRNA administered ICV (n=7). PCR assays for RNA PD, relative fold changes of App to Hprt mRNA normalized to % of PBS; Stats: Three-way ANOVA followed by Bonferroni-adjusted post hoc test comparing condition to PBS (data not shown), Next gen siRNA significantly lower than PBS at both time points for all tissues at P < 0.0001 level. Source: Brown, K.M., Nair, J.K., Janas, M.M. et al. Expanding RNAi therapeutics to extrahepatic tissues with lipophilic conjugates. Nat Biotechnol 40, 1500–1508 (2022). Wave siRNA demonstrates more potent and durable silencing as compared to published state-of-the-art Knockdown < 90 days post-dose Single dose 100 μg by ICV Single dose 120 μg by ICV Alnylam (APP – Cortex) Wave (APP – Cortex) Nat Biotechnol 40, 1500–1508 (2022) Knockdown > 112 days post-dose %mRNA remaining (SEM) (App/Hprt) % message remaining (relative to aCSF) Wave next generation siRNA Week 8 (Day 56) Wave next generation siRNA Week 16 (Day 112)

WVE-N531 (splicing) Duchenne muscular dystrophy

1Vyondys: www.fda.gov; viltepso; www.fda.gov; Exondys; www.fda.gov; Amondys: www.fda.gov Duchenne muscular dystrophy Genetic mutation in dystrophin gene prevents the production of dystrophin protein, a critical component of healthy muscle function Impacts approx. 1 in every 5,000 newborn boys each year; approx. 20,000 new cases annually worldwide  Approx. 8-10% are amenable to exon 53 skipping Dystrophin protein established by FDA as surrogate endpoint reasonably likely to predict benefit in boys1 for accelerated approval in DMD Increasing amount of functional dystrophin expression over minimal amount shown with approved therapies is expected to result in greater benefit for boys with DMD Dysfunctional Splicing Exon Skipping Functional dystrophin produced Translation halted Translation continues Mutant pre-mRNA Disease State Restored State mRNA with disrupted reading frame Restored mRNA Mutant pre-mRNA Skip Oligo 53 53 50 51 54 55 50 51 54 55 53 50 51 54 55 50 51 54 55 No dystrophin protein produced

100% survival at time of study termination Restored muscle and respiratory function to wild-type levels Kandasamy et al., 2022; doi: 10.1093/nar/gkac018 dKO: double knock-out PN chemistry improved function and survival in dKO mice Extended survival in dKO preclinical model supports potential of Wave’s PN-modified exon-skipping therapeutics for DMD Wild-type dKO: PBS dKO: PS/PO/PN Wild-type dKO: PBS dKO (PS/PO/PN oligonucleotide) PS/PO/PN 150 mg/kg weekly PS/PO/PN 75 mg/kg bi-weekly PS/PO 150 mg/kg weekly PBS Note: Untreated, age-matched mdx mice had 100% survival at study termination [not shown] Tidal volume Age (days) TVb (ml) Survival probability (%) Time (weeks)

PBS PS/PO/PN modified oligonucleotides for mouse exon 23 Wave’s PN chemistry yields excellent muscle exposure, exon skipping and dystrophin protein expression in dKO mouse model Kandasamy et al., 2022 Nuc Acids Res doi: 10.1093/nar/gkac018 dose dKO* mouse D37 %Dystrophin Skeletal muscle Diaphragm Heart %Exon skipping Muscle concentration (ug/g) **** *** **** ** *** ** ** ** *** PS/PO modified oligonucleotides for mouse exon 23

Preclinical data supported advancing WVE-N531 to clinical development WVE-N531 reached high concentrations in heart and diaphragm in NHP 26th Annual ASGCT meeting, May 16-20, 2023 WVE-N531: Dystrophin restoration of up to 71% in vitro in patient-derived myoblasts

1: 42 µg/g = 6.1 µM (6,100 nM), 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 doses of 10 mg/kg); 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. Suvodirsen N= 8; WVE-N531 N=3 boys Clinical data from WVE-N531 Part A: High exon-skipping & muscle concentrations after three doses every other week WVE-N531 uptake in myogenic stem cells Important for potential muscle regeneration Mean muscle concentration Mean exon skipping Half-life in plasma Dose suvodirsen WVE-N531 0.7 µg/g (700 ng/g) Not detectable 18 hours 22 weekly doses of 5 mg/kg 42 µg/g (42,000 ng/g)1 53% 25 days 3 doses of 10 mg/kg every other week WVE-N531 uptake in myocyte stem cells

Design of FORWARD-53: Phase 2, open-label, 10 mg/kg every other week Endpoints: Dystrophin (powered for >5% of normal), safety/tolerability, pharmacokinetics, digital and functional assessments (incl. NSAA and others) Muscle biopsies to assess dystrophin expression Fully enrolled (n=11) and dosing underway IV: intravenous; NSAA: North star ambulatory assessment Potentially registrational 24-week dystrophin expression data are expected in 3Q 2024 Dosing underway in FORWARD-53, a potentially registrational Phase 2 clinical trial of WVE-N531 in DMD (Exon 53) Screening Every other week IV dosing Functional assessment Biopsy after 24 weeks of treatment Functional assessment Biopsy after 48 weeks of treatment Functional assessment Safety Follow-up

Potential for Wave to address up to 40% of DMD population Left: Aartsma-Rus, et al. 2009 Hum Mutat 30, 293. Exon 45 Exon 44 Exon 52 WVE-N531 Exon 53 Exon 51 Not Amenable to Skipping 11-13% 8-10% 44% DMD Population Exon 52 Exon 51 Exon 44 Exon skipping and dystrophin restoration demonstrated in vitro Exon Skipping Protein Restoration

WVE-003 (antisense silencing) Huntington’s Disease

mHTT toxic effects lead to neurodegeneration; loss of wtHTT functions may also contribute to HD 1 – Sources on wtHTT: 1. Leavitt 2006 2. Cattaneo 2005 3. Kumar 2016 4. Franco-Iborra 2020 5. Hamilton 2015 6. Ochaba 2014 7. Wong 2014 8. Rui 2015 9. Caviston 2007 10. Twelvetrees 2010 11. Strehlow 2007 12. Milnerwood 2010 13. Smith-Dijak 2019 14. Tousley 2019 15. Zhang 2018 16. McAdam 2020 17. Altar 1997 18. Zuccato 2001 19. Gauthier 2004 20. Ferrer 2000 21. Baquet 2004 22. Liu 2011 23. Karam 2015 Healthy individual Huntington’s disease Stresses wtHTT Stresses wtHTT + ~50% decrease in wtHTT Healthy CNS function Synaptic dysfunction | Cell death | Neurodegeneration Loss of wtHTT functions Huntington’s disease (HD) Wild-type HTT (wtHTT) is critical for normal neuronal function1 Expanded CAG triplet repeat in HTT gene results in production of mutant huntingtin protein (mHTT) HD is a monogenic autosomal dominant genetic disease; fully penetrant and affects entire brain Fatal disease characterized by cognitive decline, psychiatric illness, and chorea 30,000 people with HD in the US and more than 200,000 at risk of developing HD mHTT

Selectively reduces mHTT mRNA in HD iPSC neurons in vitro Durable striatal mHTT knockdown for 12 weeks in BACHD mouse model Results from ND50036 iPSC-derived medium spiny neurons. Total HTT knockdown quantified by qPCR and normalized to HPRT1. Oligonucleotide or PBS [100 μg ICV injections through cannula on days 1, 3, 5] delivered to BACHD transgenic. Mean ± SD (n=8, *P<0.0332, ***P<0.0002, ****P<0.0001 versus PBS unless otherwise noted). HPRT1, hypoxanthine-guanine phosphoribosyl transferase; iPSC, induced pluripotent stem cell; ICV, intracerebroventricular; PBS, phosphate-buffered saline NHP study demonstrating significant tissue exposure levels of WVE-003 in deep brain regions resulted in $7 million milestone payment from Takeda in 4Q 2023 WVE-003 (SNP3) demonstrates selective, potent, and durable reduction of mHTT in preclinical models Pan-silencing reference compound WVE-003 Pan-silencing reference compound WVE-003 PBS Weeks *** **** **** **** **** **** Striatum Similar results in cortex

mHTT: mutant huntingtin protein; wtHTT: wild-type huntingtin protein *Pooled considering no apparent dose response between 2 single-dose cohorts; Data cut-off: August 29, 2022 Data from 30 mg multi-dose cohort with extended follow-up, along with all single-dose data, expected 2Q 2024 WVE-003: First-in-class allele-selective candidate for HD Reductions in mean CSF mHTT and preservation of wtHTT observed in pooled analysis of single-dose cohorts in SELECT-HD clinical study mHTT protein levels Single dose of WVE-003 Reduction in mHTT protein: 22% from baseline 35% vs. placebo Reductions in mHTT Preservation of wtHTT Placebo WVE-003 (30 and 60 mg pooled*) Single dose of WVE-003 wtHTT protein levels

Anticipated upcoming milestones

Wave is poised for significant and sustained growth  Note: Bubble size illustrative of size of total addressable US market (assuming 100% share of addressable patients) AATD WVE-006 DMD WVE-N531 Exon 53 HD WVE-003 SNP3 Obesity INHBE Lead Clinical Candidate Clinical trial initiation expected 1Q 2025 Add’l AIMer Programs Clinical data in 2024 and advancement of INHBE candidate unlock potential to address > 50M patients in US and Europe

Potential for significant cash inflows in 2024 from collaboration milestones from GSK and Takeda Anticipated milestones in 2024 and beyond AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington’s disease; mHTT: Mutant huntingtin; wtHTT: Wild-type huntingtin WVE-006 (AATD) Most advanced RNA editing candidate & potential best-in-class approach for AATD 2024: Deliver proof-of-mechanism data from RestorAATion clinical program INHBE lead clinical candidate (Obesity) Driven by protective LoF variants in human genetics, potential next-gen therapeutic for obesity Selected INHBE lead clinical candidate, with clinical trial application (CTA) expected as early as year-end 2024 1Q 2025: Initiate clinical trial for INHBE candidate WVE-N531 (DMD) Potential best-in-class approach with highest exon skipping reported 3Q 2024: Deliver potentially registrational 24-week dystrophin expression data from FORWARD-53 WVE-003 (HD) First-in-class mHTT lowering, wtHTT-sparing approach 2Q 2024: Deliver data from 30 mg multi-dose cohort with extended follow up, along with all single-dose data ✓

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