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 November 9, 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 Multiple clinical proof-of-concept datasets expected in 2024 DMD (splicing), HD (silencing), and AATD (RNA editing) clinical programs advancing Leader in RNA editing therapeutics, emerging leader in RNAi Multi-modal drug discovery and

development platform Pipeline of novel medicines for rare and prevalent diseases Strategic collaborations to expand and advance pipeline GMP manufacturing Strong and broad IP DMD, HD, and AATD clinical programs advancing 2024 expected milestones:

Proof-of-mechanism data from RestorAATion clinical program of WVE-006 for AATD Data from FORWARD-53 clinical trial of WVE-N531 for DMD Data from SELECT-HD clinical trial of WVE-003 for HD Selection of INHBE clinical candidate for metabolic

disorders, including obesity

Combining novel biology with

validated, best-in-class chemistry to open opportunities for first-in-class medicines Accessing new endogenous enzymes for novel modalities (RNA editing) Opening up new targets, including prevalent diseases

editing splicing siRNA silencing

antisense silencing Wave has the most versatile RNA medicines platform in the industry Endogenous RNase H Endogenous AGO2 Endogenous ADAR enzyme RISC Restored Reading Frame Functional Protein Best-in-class nucleic acid chemistry applicable across

modalities Ability to access novel / untapped areas of disease biology Genetic insights for rare and common diseases are unlocking new target opportunities Platform learnings and clinical validation continue to increase probability of success

Increasing genetic insights for rare

and common diseases is unlocking 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

Silencing Proprietary PN chemistry

enhances potency across modalities Improved knockdown Splicing Improved skipping Ranked by potency of reference PS/PO compound Ranked by potency of reference PS/PO compound PS/PO reference compound PS/PN modified compound % Skipping Target knockdown

(% remaining) Left: Experiment was performed in iPSC-derived neurons in vitro; target mRNA levels were monitored using qPCR against a control gene (HPRT1) using a linear model equivalent of the DDCt 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 RNA Editing Improved editing PS/PO/PN PS/PO (Stereopure)

PS/PO (Stereorandom) Concentration ( M) % Editing

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) 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) SILENCING: siRNA INHBE* (Metabolic disorders, including obesity)

100% global 47M 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)

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) ~50% editing supports restoration of MZ phenotype

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%

Proof of mechanism data in patients

with AATD expected in 2024 Dose escalation Study key objectives Safety and tolerability Pharmacokinetics Serum M-AAT levels Expect to initiate dosing in 4Q 2023 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

First-generation AIMer designs

published in Nature Biotechnology Monian et al., 2022 published online Mar 7, 2022; doi: 10.1038.s41587-022-01225-1 SAR structure-activity relationship Specificity in vitro & in vivo (NHPs) In vitro-in vivo translation (NHPs) GalNAc conjugation

Foundational AIMer SAR AIMers detected in liver of NHP at Day 50 (PK) ADAR editing with ACTB AIMer is highly specific ACTB Confidence (LOD score) % Editing RNA editing within full transcriptome (primary human hepatocytes) Substantial and durable

editing in NHP liver in vivo (PD) Day 50 RNA editing in NHP RNA editing only detected at editing site in ACTB transcript GalNAc AIMers GalNAc AIMers

Innovating on applications of ADAR

editing Modulate protein-protein interaction Upregulate expression Modify function Post-translational modification Alter folding or processing Restore or correct protein function Achieved POC WVE-006 (GalNAc AIMer) AATD POC: proof of concept Correct

G-to-A driver mutations with AIMers Modulate protein interactions with AIMers AIMers provide dexterity, with applications beyond precise correction of genetic mutations, including upregulation of expression, modification of protein function, or

alter protein stability

Proprietary base modifications

increase editing across edit region sequences N3 U: example of proprietary base modifications N3 U consistently improves RNA editing levels, including across sequences Presented at RNA Editing 2023 - Gordon Research Conference Seq 1 (UAU) Seq 2

(GAU) Seq 3 (AAU) Seq 4 (CAC) Seq 5 (GAG) Seq 6 (GAA) Seq 7 (GAA) Seq 8 (AAA) Seq 9 (CAC) Seq 10 (GAA) Seq 11 (CAG) Seq 12 (GAG) % Editing (mean sem) Proprietary base modification (N3 U) increases UGP2 RNA editing across sequences in vitro

Cytosine N3 U ** ** ns ** * *** ** ** ** ** ns ** 5' 3' AIMer N3 U Edit Site

Upregulation: AIMers can edit RNA

motifs to restore or upregulate gene expression RNA binding proteins recognize sequence motifs to regulate mRNA stability mRNA A I(G) Edited mRNA mRNA Decay Cascade "Dialed up" Gene Expression Attenuated Gene Expression Unique RNA motifs

A single edited base permanently disrupts the motif Stable mRNA yields increased protein production RNA-binding protein Catalytically Efficient AIMer Decreased protein production AIMer edits and durably stabilizes mRNA

Edit-verse subnetwork reveals

"Target A": Metabolic syndrome target uniquely suited for AIMer upregulation Target A Liver target for upregulation, non-incretin therapy Strongly implicated in metabolic disease, with indirect causation in familial disorders Few

therapies today provide weight loss in this specific patient population Estimate 90 million potential patients in the US and Europe with metabolic syndrome and obesity Serum protein levels and biomarkers available to assess target engagement PoC:

proof-of-concept Analysis of terminal endpoints (day 31) is shown. Each variable was analyzed using Welch's two-sided t-test. Significance was evaluated a p<0.05.

Substantial upregulation

of protein induces weight loss and improves insulin sensitivity ~3-fold upregulation of Target A protein with GalNAc-AIMer led to weight reduction and improved insulin sensitivity in DIO mice Body weight data were analyzed using a linear

mixed effects model to assess the fix effects of diet, time and treatment, controlling for the initial day 0 body weight (continuous covariate) and subject (random effect). Fasted glucose and insulin data (from study termination, day 31) was

analyzed using Welch's two-sided t-test. Significance was evaluated at p<0.05. Significant Weight Loss AIMer Target A Improved Insulin Sensitivity p<0.05* p<0.001** Fasting glucose (mg/dl) Fasting insulin (ng/ml) AIMer Target

Target B upregulation offers a

first-in-class therapeutic approach for hyperlipidemia >70% editing achieves ~2-fold upregulation with corresponding increase in protein Target B Liver target for upregulation Hyperlipidemia; first-in-class therapeutic approach Estimate ~3

million target patients in US and Europe Serum biomarkers available to assess target engagement and efficacy Potential clinically meaningful benefit of >2 fold upregulation of target mRNA

Upregulation of liver Target X

stops decline in kidney function Target X Liver target for upregulation Target X produces a secreted protein to treat kidney disease Estimate ~170K target patients in US and Europe Therapeutic rationale supported by genetic insights,

PheWAS, and observational data Plasma biomarkers available to assess target engagement ~2-fold upregulation in secreted protein expected to be clinically meaningful Target X Renal Insufficiency Network

Building on success of AATD: Target

E correction restores normal metabolism in rare genetic disease Target E Liver target for correction Rare genetic disease High unmet need population not addressed with current therapeutic options ~17,000 patients addressable with correction