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 January 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.

UNLOCKING THE BODY'S OWN ABILITY

TO TREAT GENETIC DISEASE realizing a brighter future for patients and families

Building a leading genetic medicines

company ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia; HD: Huntington's disease; DMD: Duchenne muscular dystrophy; AATD: Alpha-1 antitrypsin deficiency 1stereopure oligonucleotides and novel backbone chemistry modifications

Diversified Pipeline CNS: ALS, FTD, HD Muscle: DMD Hepatic diseases: AATD Clinical Expertise Multiple global clinical trials Innovative trial designs Innovative Platform Stereopure oligonucleotides Novel backbone modifications (PN chemistry)

Silencing, splicing, and editing modalities Strong and broad IP position1 GMP Manufacturing Internal manufacturing capable of producing oligonucleotides at scale LEVERAGING THE ONGOING genetic revolution Targeting THE TRANSCRIPTOME TO UNLOCK THE

BODY'S OWN ABILITY TO TREAT GENETIC DISEASE >6,000 monogenic diseases; vastly more polygenic diseases Increase in genetic testing Biomarkers to assess target engagement early in clinical development Greater understanding of genetic disease

and cellular biology Innovations for precise modification of transcriptome, proteome and interactome Many diseases out of reach for traditional medicines

rationally design oligonucleotides enables access to unique disease targets Chirality None PN backbone Sp PN backbone Rp Chirality PS backbone Rp PS backbone Sp Chirality PRISM backbone linkages PO: phosphodiester PS:

phosphorothioate -O -S N (Rp) (Sp) PO PS PN Negative charge Neutral charge Negative charge Phosphoryl guanidine x-ray structure example

Harnessing the biological machinery in

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

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

Built-for-Purpose Candidates to

Optimally Address Disease Biology Silencing | Splicing | RNA Editing DESIGN Unique ability to construct stereopure oligonucleotides and control three structural features to efficiently engage biological machinery OPTIMIZE Provides the resolution to

observe this structural interplay and understand how it impacts key pharmacological properties Sequence Stereochemistry Chemistry Unlocking the body's own ability to treat genetic disease

THERAPEUTIC AREA / TARGET MODALITY

DISCOVERY PRECLINICAL CLINICAL RIGHTS NEUROLOGY ALS and FTD C9orf72 Takeda 50:50 option Huntington's disease mHTT SNP3 SCA3 ATXN3 CNS diseases Multiple 100% Global DMD Exon 53 HEPATIC AATD - lung and liver disease SERPINA1 GSK Exclusive

Global License Robust portfolio of stereopure, PN-modified oligonucleotides ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia; SCA3: Spinocerebellar ataxia 3; CNS: Central nervous system; DMD: Duchenne muscular dystrophy; AATD:

Alpha-1 antitrypsin deficiency Therapeutic modality Silencing Splicing ADAR editing (AIMers) WVE-004 (FOCUS-C9) WVE-003 (SELECT-HD) WVE-006 WVE-N531 NEUROLOGY HEPATIC (GalNAc)

GSK Collaboration and WVE-006 for

Alpha-1 antitrypsin deficiency (AATD)

Collaboration leverages Wave's

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

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

royalty payments and commercial milestones from Wave First-in-class RNA editing program GSK receives 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 genetically-validated targets 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 Extends cash runway into

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

~50% RNA editing expected to

increase PIZZ patient serum AAT levels to PIMZ levels, with low risk of disease 1. Brode, et al. 2012 CMAJ 184:1365-1371; 2. ATS/ERS. 2003 Am J Respir Crit Care Med 168:818-900. Serum AAT Protein Levels and Risk of AATD by Genotype Risk of

Emphysema Very High High Low Very Low No Risk of Liver Disease No High Possible Possible No ~50% RNA editing ~2.5-7-fold higher 100% Z-AAT protein 100% M-AAT protein

WVE-006 supports dose-dependent RNA

editing in human preclinical model systems Left: MZ-donor derived primary human hepatocytes treated with WVE-006 at indicated concentrations for 48 hours Right: Patient-iPSC derived hepatocytes (ZZ genotype) plated on day 0 and treated on day 2 with

WVE-006 at indicated concentrations. Media refreshed every 2 days (days 4, 6, 8). RNA was collected on day 10. In each experiment, RNA editing was quantified by Sanger sequencing (n=2 biological replicates) % Editing (mean, sem) iPSC-derived human

hepatocytes (ZZ genotype) 0.31 1.25 5.0 0.08 Concentration (mM) Note: Due to MZ genotype, Y-axis ranges from ~50-100% Efficient SERPINA1 editing in donor-derived primary human hepatocytes with WVE-006 (MZ genotype) 0 2 4 6 8 10 Days: Dose Collect

RNA Dose Refresh media

WVE-006 results in circulating AAT

protein levels 7-fold above PBS control, well above established 11 M threshold 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 week 13 (one week after last dose) and SERPINA1 editing was quantified by Sanger sequencing; Stats: One-way ANOVA with adjustment for multiple comparisons (Tukey); Right: Total serum AAT protein quantified by ELISA; Stats: Two-Way ANOVA

with adjustment for multiple comparisons (Tukey) SERPINA1 mRNA editing in liver of AATD mouse model (NSG-PiZ mice) (Week 13) SERPINA1 editing WVE-006 treatment results in serum AAT protein levels >11 uM in AATD mouse model (NSG-PiZ mice) Restored

WVE-006 leads to restoration of

confirmed, wild-type M-AAT protein in serum WVE-006 administered in 7-week old NSG-PiZ mice (n=5 per group). Relative proportion of M- vs. Z-AAT protein in serum collected from animals at week 13 (one week after last dose) was measured by mass

spectrometry Overall percentages of serum AAT protein isoforms in NSG-PiZ mice (Week 13) PBS WVE-006 Wild-type M-AAT protein Mass spectrometry confirms restoration of circulating healthy M-AAT protein in vivo after WVE-006 treatment Consistent

with RNA editing of mutant transcript Z-AAT

Significant increase in neutrophil

elastase inhibition activity indicates restored M-AAT protein is functional GalNAc-conjugated AIMers administered in 7-week old NSG-PiZ mice (n=5 per group). Serum collected from mice was tested for ability to inhibit fixed concentration of

neutrophil elastase in an in vitro reaction. Stats: Two-way ANOVA with adjustment for multiple comparisons (Bonferroni) >3-fold increase over PBS PBS WVE-006 Increased neutrophil elastase inhibition activity demonstrates functionality of AAT

protein Increases in neutrophil elastase, a proteolytic enzyme, may cause emphysema and damage the surrounding lung tissue Main function of AAT protein is to neutralize/control neutrophil elastase Serum neutrophil elastase inhibition activity

Early lead pre-optimization AATD

AIMer (SA1-5) administered in huADAR/SERPINA1 mice (8-10 wKs old); lower left: 20x liver images PAS-D stained, 19 weeks; Quantification of PAS-D positive staining, Stats 2-way ANOVA; Right: Quantification lobular inflammation grade (Grade

based on # of inflammatory foci in lobules: Grade 0: 0; G1 1-5; G2 6-10; G3 11-15; G4 16) and mean globular diameter (40 largest globules/ animal) with HALO. Stats Wilcox rank-sum tests Early lead (pre-optimization) AATD AIMer reduces

aggregation of Z-AAT and inflammation in mouse liver Lobular inflammation (19 weeks) * p=0.03 Inflammation grade PBS AIMer p<0.01 Mean diameter (mm) PBS AIMer **** p<0.0001 Weeks following first dose ** %PAS-D positive area (mean sem) PBS

Early lead AATD AIMer

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%

WVE-006 is a potential first- and

best-in-class candidate for AATD Correct Z-allele mRNA to replace mutant Z-AAT protein with functional wild-type M-AAT protein RNA editing levels show potential to support conversion of a patient from ZZ to MZ mRNA expression M-AAT protein can

address lung disease Reduction of Z-AAT protein enables clearance of protein aggregates in liver M-AAT protein produced with WVE-006 would remain under physiological regulation mRNA editing is highly specific Potentially applicable across AATD

patient subpopulations Convenience of subcutaneous administration

Planning for clinical development

for WVE-006 underway Phase 1/2 placebo-controlled study to establish dose and evaluate target engagement CTA submissions for WVE-006 expected in 2023 Single-ascending dose (SAD) cohorts Multiple-ascending dose (MAD) cohorts Initial cohorts healthy

volunteers Final cohort in PiZZ patients PiZZ pts Assess dose & frequency Effective dose to be selected based on PK, PD, and safety Safety, tolerability, PK, change in relevant biomarkers, including serum AAT

WVE-N531 Duchenne muscular

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 1Vyondys: www.fda.gov; viltepso; www.fda.gov; Exondys; www.fda.gov; Amondys: www.fda.gov Dysfunctional Splicing Exon Skipping No dystrophin protein produced

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

PN chemistry improved muscle

exposure and survival in preclinical mouse models Kandasamy et al., 2022; doi: 10.1093/nar/gkac018 PN increased muscle concentrations after single dose, which correlated with exon-skipping activity PN PN Treatment with PN-modified molecules led to

100% survival of dKO mice at time of study termination Better tissue exposure 100 75 50 25 0 Survival probability (%) 0 4 8 12 16 20 24 28 32 36 40 Time (weeks) PS/PO/PN, 75 mg/kg bi-weekly PBS PS/PO, 150 mg/kg weekly PS/PO/PN, 150 mg/kg weekly

Note: Untreated, age-matched mdx mice had 100% survival at study termination [not shown]

PS/PO/PN splicing compound restores

muscle and respiratory function to wild-type levels in dKO mice Left: Mdx/utr-/- mice received weekly subQ 150 mg/kg dose of PS/PO/PN stereopure oligonucleotide (postnatal day 10). Age-matched mdx/utr-/- littermates treated with PBS, wild-type

C57BL10 mice not treated. Wild-type, dKO PBS mice: 6 wks old; dKO PS/PO/PN: 28 - 41 wks old; Electrophysiology performed at Oxford University based on Goyenvalle et al., 2010 Mol Therapy; Right: Kandasamy et al., 2022; doi: 10.1093/nar/gkac018

Wild-type dKO / PBS dKO (PS/PO/PN oligonucleotide) **** **** **** **** Specific Force (EDL) Eccentric Concentration dKO: PS/PO/PN dKO: PBS Wild-type Muscle Function Respiratory Function