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 August 17, 2022 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

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 Takeda 50:50 option ALS and FTD C9orf72 Takeda 50:50 option Huntington's disease mHTT SNP3 SCA3 ATXN3 CNS diseases Multiple 100% global DMD Exon 53 100% global HEPATIC AATD - lung and liver

disease SERPINA1 100% global 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)

WVE-004 Amyotrophic Lateral Sclerosis

(ALS) Frontotemporal Dementia (FTD)

C9orf72 repeat expansions: One of

the most common genetic causes of ALS and FTD Typically 100's-1000's of GGGGCC repeats Amyotrophic Lateral Sclerosis (ALS) Frontotemporal Dementia (FTD) Hexanucleotide (G4C2)- repeat expansions in C9orf72 gene are common autosomal

dominate cause for ALS and FTD Different manifestations across a clinical spectrum Fatal neurodegenerative disease Progressive degeneration of motor neurons in brain and spinal cord C9-specific ALS: ~2,000 patients in US Progressive neuronal

degeneration in frontal / temporal cortices Personality and behavioral changes, gradual impairment of language skills C9-specific FTD: ~10,000 patients in US Including patients with C9-associated ALS, FTD or both Sources: Balendra et al, EMBO Mol

Med, 2017; Brown et al, NEJM, 2017, DeJesus-Hernandez et al, Neuron, 2011. Renton et al, Neuron, 2011. Zhu et al, Nature Neuroscience, May 2020, Stevens et al, Neurology 1998

Reduced expression RNA variants RAN

translation C9orf72 protein RNA foci Dipeptide repeat proteins (DPRs) Sense: poly(GA), poly(GR) Antisense: poly(PR), poly(PA) Sense & Antisense: poly(GP) Toxic RNA aggregation Gain-of-function Loss-of-function Repeat-expanded allele Wild-type

C9orf72 allele Genetic mutation C9orf72 Poly(GP) biomarker selected as preferred DPR biomarker Abundant in CNS Most soluble Stable expression Only DPR derived from both sense & antisense RNAs Variant-selective oligonucleotide, lowering V1 &

V3 in preclinical studies1 Preserves C9orf72 protein expression; does not exacerbate potential loss-of-function driver of disease Reduces toxic gain-of-function drivers of disease (RNA foci, DPRs) 1Liu et al., 2022 Mol Ther Nuc Acids doi:

10.1016/j.omtn.2022.04.007 Transcription Antisense Mis-spliced RNA Stabilized intron 1 Pathological RNAs V1 V2 V3 WVE-004 is designed to affect multiple drivers of toxicity Disease drivers Sense & Antisense RNA Decrease in beneficial protein

WVE-004 addresses each biological aspect of C9orf72-associated ALS and FTD 1 2 3

* *** ** *** Spinal cord Relative

poly(GP) levels (normalized to PBS) Cortex >90% knockdown of poly(GP) DPR protein Two doses of WVE-004 Six months >80% knockdown of poly(GP) DPR protein Relative poly(GP) levels (normalized to PBS) p 0.0001 Liu et al., 2022

Molecular Therapy Nucleic Acids doi: 10.1016/j.omtn.2022.04.007; 2 x 50 ug (day 0, day 7) dosed ICV; DPRs measured by poly(GP) MSD assay. *: p 0.05 **: P 0.01, ***: P 0.001. DPR: Dipeptide repeat protein Weeks Weeks PBS

Poly(GP) DPR Oligonucleotide concentration WVE-004: WVE-004: C9orf72 protein unchanged at 6 months ns ug of oligo / g of tissue ug of oligo / g of tissue ns Relative fold change C9orf72/HPRT1 1.5 0.5 0.0 1.0 Relative fold change C9orf72/HPRT1 1.5

0.5 0.0 1.0 WVE-004 PBS WVE-004 PBS Preclinical studies with WVE-004 demonstrated durable reduction of poly(GP) in spinal cord and cortex 6 months after two doses Preclinical in vivo results: Spinal cord Cortex

WVE-004 clinical data demonstrate

successful translation of preclinical approach to clinic PK: pharmacokinetic PD: pharmacodynamic; Right: Mixed model for repeated measures used to estimate geometric mean ratio to baseline via least squares mean and to calculate p-values. P-values

represented by asterisks are for within-dose group geometric mean ratios. *p 0.05, **p 0.01, ***p 0.001. Poly(GP) assay: Wilson et al., 2022 J Neurol Neurosurg Psychiatry doi:10.1136/jnnp-2021-328710. Data presented at ENCALS

Meeting (June 1-3, 2022) PK/PD modeling using preclinical in vivo models predicted pharmacodynamically active starting dose Target engagement confirmed in patients supports advancing FOCUS-C9 clinical study Poly(GP) reduction in cortex and spinal

cord in transgenic mice with WVE-004 Sufficient concentrations of WVE-004 in cortex and spinal cord of NHP for target engagement

30 mg n=10 FOCUS-C9 clinical trial

underway 10 mg n=3 60 mg n=4 20 mg n=10 10 mg n=6 4 monthly doses Dose and frequency to be guided by DSMB Target engagement observed in single dose cohorts Single dose Multidose Open-label extension (OLE) clinical trial Initiation anticipated in 2H

2022 Additional single and multidose clinical data for WVE-004 expected in 2H 2022

WVE-003 Huntington's

Huntington's disease mHTT toxic effects lead to neurodegeneration, loss of wtHTT functions may also contribute to HD Stresses wtHTT Stresses wtHTT mHTT + ~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 function* 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

mHTT, mutant HTT; wtHTT, wild-type

HTT; PO, phosphodiester; PS, phosphorothioate; PN, phosphoryl guanidine; wtHTT literature sources: 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 mHTT RNA

wtHTT RNA WVE-003 targets mHTT "SNP3" SNP3 C A G C A G C A G C A G C A G expanded CAG repeat PO PS PN -O Negative Negative -S Neutral wtHTT supports healthy brain function, especially in the context of stress Promotes neuronal survival

Supports synaptic protein transport Regulates synaptic plasticity Supports cilia and CSF circulation Only wtHTT-sparing oligonucleotide in clinical development Contains Wave's novel PN chemistry WVE-003: Allele-selective oligonucleotide

designed to lower mHTT while sparing wtHTT

Hu97/18 mice administered 3x100 mg

intracerebroventricular doses PBS or oligonucleotide. Relative mHTT RNA in cortex (left) striatum (middle) or hippocampus (right) at 4, 8 and 12-weeks post-dosing. Data are mean SD, n=8. Stats: ns non-significant, *P<0.05, **P<0.01,

***P<0.0001, ****P<0.0001 versus PBS by 1-way ANOVA. mHTT, mutant HTT; wtHTT, wild-type HTT; Tubb, tubulin Allele-selective molecule decreases mHTT, spares wtHTT; Pan-silencer uniformly decreases both Percentage HTT RNA expression (mHTT/Tubb -

PBS) **** *** **** **** **** mHTT wtHTT Hu97/18 mouse Allele-selective activity in CNS of Hu97/18 mice **** * *** Cortex Striatum PBS Pan-silencing control Allele-selective molecule Time (weeks) Time (weeks) PBS Pan-silencing control

Allele-selective molecule

WVE-003 (SNP3) demonstrates

selective, potent, and durable reduction of mHTT in preclinical models Selectively reduces mHTT mRNA in HD iPSC neurons in vitro Results from ND50036 iPSC-derived medium spiny neurons. Total HTT knockdown quantified by qPCR and normalized to

HPRT1. Oligonucleotide or PBS [100 g 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 Similar results in cortex Pan-silencing reference compound WVE-003 PBS Weeks *** ****

**** **** **** **** Pan-silencing reference compound WVE-003 Percentage HTT mRNA Remaining Durable striatal mHTT knockdown for 12 weeks in BACHD mouse model

WVE-003 (allele-selective compound

in HD) achieves concentrations in patient CSF expected to engage target Blinded CSF WVE-003 concentrations compared to CSF WVE-120102/WVE-120101 concentrations Demonstrated allele selectivity for mHTT mHTT reduction in cortex and striatum in

transgenic mice with WVE-003 Achieved sufficient concentrations of WVE-003 in NHP brain tissues for target engagement Dose escalation continues in ongoing SELECT-HD clinical trial PK/PD modeling using preclinical in vivo models predicted

pharmacodynamically active starting dose WVE-120101 (SNP1) and WVE-120102 (SNP2): First-generation PS/PO compounds for HD

Day 1-3 15 29 57 85 Dose PK /

Biomarker Samples Clinical Evaluations SELECT-HD clinical trial: Dose level and dosing frequency guided by independent committee Dose level and dosing frequency guided by independent

committee Single ascending dose Dose Level Cohort 1 Cohort 1 Additional cohorts Proceed to MAD Monthly or less frequent dosing PK / Biomarker samples Clinical evaluations Additional cohorts Safety and tolerability UHDRS Clinical

evaluations mHTT wtHTT NfL Key biomarkers: Multi-ascending dose Adaptive cohorts Inclusion criteria: 25 to 60 years old SNP3 on mHTT allele PK: pharmacokineticmHTT: mutant HTTwtHTT: wild-type HTTNfL: neurofilament light chain Clinical

data expected in 2H 2022

WVE-N531 Duchenne muscular

Duchenne muscular dystrophy Duchenne

muscular dystrophy Genetic mutation in dystrophin gene prevents the production of dystrophin protein, a critical component of healthy muscle function. Dystrophin protein established by FDA as surrogate endpoint reasonably likely to predict benefit

in patients1 for accelerated approval in DMD Confirmatory studies ongoing Increasing amount of functional dystrophin expression over minimal amount shown with approved therapies is expected to result in greater benefit for patients Impacts 1 in

every 5,000 newborn boys each year; 20,000 new cases annually worldwide. 1Vyondys: www.fda.gov; viltepso; www.fda.gov; Exondys; www.fda.gov; Amondys: www.fda.gov

PN chemistry improved muscle

exposure and survival in preclinical mouse models Kandasamy et al., 2022; doi: 10.1093/nar/gkac018 PN boosted 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