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 Investor

Presentation January 10, 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.

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 Ophthalmology 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 DRUGGING 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

Biological machinery in our cells can

be harnessed 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 function or production Endogenous ADAR enzyme Restored Reading Frame Endogenous RNase H Endogenous AGO2 RISC

OMe, MOE, F, other modifications PO,

PS, PN 5' modifications, backbone modifications A, T, C, mC, G, U, other modified bases PRISM enables precision modulation of RNA therapeutic properties using unique chemistry toolkit 2' modifications Backbone chemistry Bases Chiral

control of any stereocenter Potency Tissue exposure Duration of activity

Innovating stereopure

backbone chemistry modifications 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

Improvements in PRISM primary screen

hit rates accelerate drug discovery Primary screen hit rates with silencing far above industry standard hit rates Stereorandom Chemistry, PN stereochemistry & machine learning optimization Stereopure Chemistry improvements and PRISM advancement

All screens used iPSC-derived neurons; Data pipeline for improved standardization. Hit rate = % of oligonucleotides with target knockdown greater than 50%. Each screen contains >100 oligonucleotides. ML: machine learning (2019) (2020 -

Silencing Potency is enhanced with

addition of PN modifications across modalities Improved knockdown Splicing Editing Improved skipping Ranked by potency of reference PS/PO compound Ranked by potency of reference PS/PO compound Improved editing PS/PO/PN PS/PO (Stereopure) PS/PO

(Stereorandom) Concentration ( M) % Editing 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

Adding PN chemistry modifications to

C9orf72-targeting oligonucleotides improved potency in vivo Exposure ( g/g) Exposure ( g/g) Cortex %C9orf72 V3 transcript remaining Target knockdown: Liu, TIDES poster 2021; Oligonucleotide concentrations quantified by hybridization ELISA.

Graphs show robust best fit lines with 95% confidence intervals (shading) for PK-PD analysis. Manuscript submitted. Spinal Cord C9orf72-targeting oligonucleotides PS/PO backbone chemistry PS/PO/PN backbone chemistry Improved knockdown Improved

tissue exposure Neuro C9orf72

PN chemistry improves distribution

to CNS NHPs administered 1x12 mg oligonucleotide or PBS by intrathecal injection/lumbar puncture (IT). CNS tissue evaluated 11 or 29 days after injection (n=6 per group). Oligonucleotide was visualized by ViewRNA (red), and nuclei are

counterstained with hematoxylin. Images from day 29. Cerebral Cortex Cerebellum Striatum Hippocampus Spinal cord PS/PO PS/PO/PN Backbone chemistry Midbrain Distribution of oligonucleotides in NHP CNS 1-month post single IT dose Oligonucleotide

Single intrathecal dose in NHP leads

to substantial and widespread target mRNA reduction throughout the CNS Target mRNA knockdown 28 days post-dose (WVE-005) Striatum Control NHPs: Non-human primates NHPs were administered 12 mg on day 1 via IT bolus injection; tissue samples were

collected from 3 NHPs at 28 days post-dose. Target mRNA knockdown 28 days post-dose (WVE-005) Potential for infrequent IT administration, widespread CNS distribution of PN modified oligonucleotides, and availability of disease biomarkers

facilitates development of differentiated CNS portfolio

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 SERPINA1 100% global

OPHTHALMOLOGY Retinal diseases USH2A and RhoP23H 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 Modality Silencing Splicing ADAR editing (AIMers) WVE-004 (FOCUS-C9) WVE-003 (SELECT-HD) WVE-N531 NEUROLOGY HEPATIC OPHTHALMOLOGY

100 75 50 25 0 Survival probability

(%) 0 4 8 12 16 20 24 28 32 36 40 Time (weeks) Dramatic increase in effect with PN-modified splicing oligonucleotide in dKO mouse model dKO; double knockout mice lack dystrophin and utrophin protein. mdx mice lack dystrophin. dKO: PS/PO/PN 150

mg/kg n= 8 (p=0.0018); PS/PO/PN 75 mg/kg n=9 (p=0.00005); PS/PO n=9 (p=0.0024), PBS n=12 Stats: Chi square analysis with pairwise comparisons to PBS using log-rank test 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] Treatment with PN-modified molecules led to 100% survival of dKO mice at time of study termination Neuro DMD

PS/PO/PN slicing compound restores

respiratory function to wild-type levels in dKO mice Manuscript in press. 10 day old dKO mice received weekly subcutaneous 150 mg/kg doses of PS/PO/PN splicing compound or PBS. Age-matched C57BI/6 wild-type mice were also included in study. Data are

presented as mean s.d. Stats from 2-way ANOVA **** P<0.0001. Neuro DMD Wild-type dKO / PBS dKO (PS/PO/PN oligonucleotide) **** **** **** ****

PS/PO/PN compound restores muscle

function to wild-type levels in dKO mice dKO / PBS (6 week old) dKO PS/PO/PN, QW 150mpk (38-41 week old) Wild-type (6 week old) Specific Force (EDL) Eccentric Contraction (EDL) Mdx/utr-/- mice received weekly subQ 150 mpk dose of PS/PO/PN

stereopure oligonucleotide beginning at postnatal day 10. Age-matched mdx/utr-/- littermates were treated with PBS, and wild-type C57BL10 mice were not treated. Electrophysiology to measure specific force and eccentric contraction performed at

Oxford University based on Goyenvalle et al., 2010 Mol Therapy 18(1), 198-205. Neuro DMD

Clinical trial of WVE-N531 underway

Unmet need in DMD remains high Open-label clinical trial of up to 15 boys with DMD amenable to exon 53 skipping Powered to evaluate change in dystrophin expression Possible cohort expansion driven by assessment of drug distribution in muscle and

biomarkers, including dystrophin DMD: Duchenne muscular dystrophy Neuro DMD Ascending doses of WVE-N531 Up to 4 dose levels (administered 4 weeks apart) evaluated to select dose level for multidose Up to 3 additional doses given

every-other-week at selected dose level Additional patients enrolled and dosed every other week at selected dose level Up to 7 total doses to be given followed by a minimum 8-week safety monitoring period Dose level and dosing frequency guided by

independent committee Initial cohort Possible cohort expansion

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 disease across phenotypes 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 Neuro C9orf72

C9orf72 protein is important for

normal regulation of neuronal function and the immune system WVE-004 targets hexanucleotide repeat containing transcript variants that lead to loss of normal C9orf72 function and production of pathological mRNA products and toxic dipeptide repeat

(DPR) proteins Poly-GP is an important DPR transcribed from sense and antisense toxic mRNA transcripts Poly-GP is a sensitive biomarker of target engagement and reductions of mRNA transcripts and other toxic proteins by WVE-004 Neurofilament

Light-Chain (NfL) measurements will provide important insight into potential for neuroprotection WVE-004 selectively targets repeat-containing transcripts to address multiple drivers of toxicity Liu et al, Nature Communications, 2021 pre-mRNA

variants Pathological mRNA products V1 V2 Mis-spliced V1/V3 Stabilized intron1 V3 Disease-contributing factors RNA foci DPRs GGGGCC expansion Accessible target for variant selectivity Reduced by WVE-004 Repeat-containing transcripts Neuro

* *** ** *** 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 Full results presented at the

31st International Symposium on ALS/ MND (December 2020); 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 Durable reduction in vivo of Poly-GP in spinal cord and cortex after 6 months Preclinical in vivo results: Neuro C9orf72

Day 1-3 15 29 57 85 Dose PK /

Biomarker Samples Clinical Evaluations FOCUS-C9 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 ALSFRS-R

CDR-FTDLD FVC HHD Clinical evaluations PolyGP DPR in CSF p75NTRECD in urine NfL in CSF Key biomarkers: PK: pharmacokinetic Multi-ascending dose Adaptive cohorts Neuro C9orf72

Target mutant mRNA HTT transcript to

reduce mutant HTT protein Preserve wild-type HTT protein reservoir in brain Allele-selective approach to treating HD Wave has only allele-selective clinical program in Huntington's disease Only an allele-selective approach is designed to

address both toxic gain of function and toxic loss of function drivers of HD Stresses wtHTT mHTT + Reduce Preserve Neuro HD

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 Neuro HD Incorporates PN backbone chemistry modifications

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: PK: pharmacokinetic Multi-ascending dose Adaptive cohorts Neuro HD