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

Wave Life Sciences Corporate

Presentation December 15, 2023 Exhibit 99.1

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 $20 million milestone earned under GSK collaboration and $100 million offering in December 2023 extended cash runway into 4Q 2025* DMD (splicing), HD (silencing), and AATD (RNA editing) clinical programs advancing INHBE, obesity

(siRNA), muscle sparing, fat loss, improved metabolic profile Multi-modal drug discovery and development platform Leader in RNA editing with potential best-in-class oligonucleotide chemistry Strategic collaborations to expand and

advance pipeline In-house GMP manufacturing; Strong and broad IP portfolio DMD, HD, and AATD clinical programs advancing Upcoming Milestones: Proof-of-mechanism data from RestorAATion clinical program of WVE-006 for AATD in 2024 Select INHBE

clinical candidate for metabolic disorders, including obesity, in 4Q 2024 and submit CTA in 2025 Data from FORWARD-53 clinical trial of WVE-N531 for DMD in 2024 Data from SELECT-HD clinical trial of WVE-003 for HD in 2Q 2024 *Cash runway

does not include potential future milestones or opt-in payments under GSK and Takeda collaborations

Combining potential 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

Wave's versatile RNA medicines

platform unlocks genetic insights for rare and common diseases opening up new target opportunities Claussnitzer, et al. Nature (2020) 577, 179; King et al. PLoS Genet (2019) 15, e1008489 Accessing UK Biobank and building proprietary

machine learning models to generate unique genetic insights

Program Discovery Preclinical 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* (Metabolic disorders, including obesity) 100% global 47M 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 FORWARD-53 Trial (Phase 2) SELECT-HD Trial (Phase 1b/2a) RestorAATion Clinical Program *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. AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington's disease Editing for correction Editing for

Collaboration leverages Wave's

unique stereopure, PN-chemistry containing PRISMTM platform, including editing, splicing, silencing (RNAi and antisense) Strategic collaboration with GSK to develop transformative RNA medicines for genetically defined diseases 1$120 million in cash

and $50 million equity investment received in January 2023, 2Initiation, development, launch, and commercialization milestones for WVE-006 and programs progressed during initial 4-year research term (8 GSK collaboration programs), 3GSK eligible

to receive tiered royalty payments and commercial milestones from Wave First-in-class RNA editing program GSK granted exclusive global license to WVE-006 for AATD GSK to advance up to eight collaboration programs Up to $225 million in

development and launch milestones Up to $1.2 billion in aggregate in initiation, development and launch milestones Up to $300 million in sales-related milestones Up to $1.6 billion in aggregate in sales-related milestones Double-digit tiered

royalties as a percentage of net sales up to high-teens Tiered royalties as a percentage of net sales up to low-teens Development and commercialization responsibilities transfer to GSK after completion of first-in-patient study Development and

commercialization responsibilities transfer to GSK at development candidate Wave to advance up to three wholly owned collaboration programs (or more pending agreement with GSK) 3 Wave to leverage GSK's genetic insights Multiple value drivers

to Wave Milestone / royalties Genetic targets Milestone / royalties $170 million upfront to Wave (cash and equity1) Additional research support funding Potential for up to $3.3 billion in milestones2 Expands Wave's pipeline INHBE is

Wave's first wholly-owned program emerging from GSK collaboration

WVE-006 (RNA editing) AATD

3) Retain M-AAT physiological

regulation 2) Reduce Z-AAT protein aggregation in liver WVE-006: Designed to correct mutant SERPINA1 transcript to address both liver and lung manifestations of AATD M-AAT reaches lungs to protect from proteases M-AAT secretion into bloodstream 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 ADAR editing approach to address key goals of AATD treatment:

RNA correction replaces mutant Z-AAT protein with wild-type M-AAT protein Z-AAT 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 designed to correct Z allele mRNA to enable M-AAT protein to be produced 200,000 Pi*ZZ patients in US and Europe

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 Demonstrated functionality of M-AAT protein Confirmed restored wild-type M-AAT protein 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) Potent and durable editing yields functional AAT

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 Cirrhosis Hepatocellular Carcinoma Correction of gain-of-function liver phenotypes Lobular inflammation (NSG PiZ mice, week 13) Week 0 Week 13 Week 0 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 (mouse liver) RNA editing across transcriptome (mouse liver) AIMer-directed editing is highly specific in mice SERPINA1 (PiZ mutation site) % Editing 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 Coverage Coverage Editing site (PiZ mutation) PBS AATD AIMer C 0% T 100% C 48.2% T 51.8%

Dosing underway in RestorAATion

clinical program; proof of mechanism data in patients with AATD expected in 2024 Dose escalation Study key objectives Safety and tolerability Pharmacokinetics Serum M-AAT levels Dosing Underway Multiple assessments of serum AAT throughout cohort HV:

healthy volunteer; SAD: single-ascending dose; MAD: multi-ascending dose RestorAATion-2: AATD Patients SAD MAD cohorts Dose E Dose D Dose C Dose B Dose A High dose Medium dose Low dose Informs dose & dose frequency RestorAATion-1:

Healthy Volunteers Up to 7 doses

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 1(score >95th p-tile) Gene-Disease Network

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)

Metabolic disorders, including obesity

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 **** 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; Wk 2 Wk 14 Wk 7 Reference Wave siRNA * *

Ago2 loading (liver, transgenic mice) Wave siRNA Reference PBS Unprecedented Ago2 loading increases potency and durability of silencing following administration of single subcutaneous dose 1 Wk 2 Wk 14 Wk 7 1 PBS HSD-1933 HSD-1930 NTC PBS HSD-1933

HSD-1930 PBS HSD-1933 HSD-1930

INHBE: Evolution in treatment

for obesity; muscle sparing, sustained fat loss, improved metabolic profile 1. Liang, et al. 2023 Postgraduate Medical Journal 99(1175):985; 2. Lakka, et al. 2002 JAMA 288(21):2709; 3. Sargeant, et al. 2019 Endocrinol Metab (Seoul)

34(3):247-262; 4. Liu, et al. 2022 Front. Endocrinol. 13:1043789; 5. Prime Therapeutics Claims Analysis, July 2023; 6. M ller, et al. 2019 Molecular Metabolism 30: 72-130. Metabolic syndrome* is associated with type 2 diabetes, cardiovascular

disease, hypertension, stroke, cancer, and increased mortality1,2 Estimate ~47M people in US and Europe with metabolic disorders, including obesity Therapeutic options beyond GLP-1s are needed GLP-1 receptor agonists lead to weight loss at the

expense of muscle mass3 GLP-1 receptor agonists suppress general reward system6 GLP-1 receptor agonists associated with poor tolerability profile4 with 68% drop-off after 1 year5 Preferred approach would improve metabolism and increase fat loss

while maintaining muscle mass Restoration of metabolic health via INHBE silencing expected to simultaneously address obesity and other drivers of metabolic syndrome *Patients diagnosed with metabolic syndrome based on having 3 of the following:

abdominal obesity, high bp, high blood glucose, high TG, or low HDL

Driven by clinical genetics,

GalNac-siRNA program addresses high unmet need in metabolic disorders, including obesity 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. INHBE program is Wave's first wholly owned program emerging from GSK collaboration Leverages novel genetic insights accessed

through GSK collaboration INHBE loss-of-function heterozygous carriers exhibit healthy metabolic profile1,2,3: Reduced waist-to-hip ratio Reduced odds ratio of type 2 diabetes by 28%, and coronary artery disease Reduced serum triglycerides Elevated

HDL-c Reduced HbA1c Lowered ApoB INHBE expressed primarily in liver and gene product (subunit of activin E) acts on its receptor in adipose tissue4 GalNAc-siRNA for targeted delivery to hepatocytes 50% reduction of INHBE with siRNA expected

to restore a healthy metabolic profile

INHBE knockdown of 90% demonstrated

in human hepatocytes with GalNAc-siRNA Primary hepatocytes were treated with a cross-reactive siRNA via free uptake. INHBE mRNA was quantified by RT-qPCR. This cross-reactive sequence demonstrates ~90% maximal knock-down in human hepatocytes and

~65% in mouse hepatocytes Additional human selective sequences are in development Human hepatocytes Mouse hepatocytes

~62% silencing **** Therapeutic

threshold1 INHBE knockdown demonstrated in mice at 5 weeks INHBE silencing achieved in vivo with GalNAc-siRNA exceeds therapeutic threshold and led to lower body weight 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, 120(32): e2309967120. INHBE knockdown led to 16% lower body weight as compared to control Data plotted by body weight difference as a percentage of PBS treated young DIO mice; Coskun, T. et.

al. Mol. Metab. 2018, 18, 3. Stats: Repeated Measures ANOVA; Inhbe siRNA vs. Control significantly different at P < 0.05 level weeks 2 through 5 mRNA expression (relative to PBS liver) Body weight relative to PBS (%) INHBE silencing Lower

relative body weight Control (HFD, PBS) Inhbe siRNA Weeks HFD, PBS Inhbe siRNA Similar effect seen in semaglutide preclinical studies

~56% reduction ~34% reduction ~38%