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 June 5, 2019 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.

DESIGN & OPTIMIZE SEQUENCE

STEREOCHEMISTRY CHEMISTRY Targeting genetically defined diseases with stereopure oligonucleotides Building fully integrated genetic medicines company led by neurology development programs Lead clinical program: Suvodirsen Phase 2/3 trial initiation

expected in July 2019 for DMD (exon 51); program on development path toward US and global approvals Advancing additional exon skipping candidates for DMD Commercialization activities underway Lead clinical program: Two Phase 1b/2a trials ongoing for

Huntington's disease using differentiated allele-selective approach Advancing C9orf72 candidate for ALS and FTD SNP3 (HD) and ATXN3 (SCA3) Initial candidate selection ongoing for inherited retinal diseases Stereopure oligonucleotides across

multiple therapeutic modalities Antisense | RNAi | Splicing Neuromuscular CNS Ophthalmology 100% global rights Takeda 50:50 option 100% global rights

Through iterative analysis of in vitro

and in vivo outcomes and artificial intelligence-driven predictive modeling, Wave continues to define design principles that are deployed across programs to rapidly develop and manufacture clinical candidates that meet pre-defined product profiles

DESIGN Unique ability to construct stereopure oligonucleotides with one defined and consistent profile Enables Wave to target genetically defined diseases with stereopure oligonucleotides across multiple therapeutic modalities OPTIMIZE A deep

understanding of how the interplay among oligonucleotide sequence, chemistry, and backbone stereochemistry impacts key pharmacological properties SEQUENCE STEREOCHEMISTRY CHEMISTRY

WAVE RATIONAL DESIGN Control of

stereochemistry enables the design and manufacture of oligonucleotides with one defined and consistent profile Designing the optimal, stereopure medicine STANDARD OLIGONUCLEOTIDE APPROACHES Pharmacologic properties include >500,000 permutations

in every dose Impact: Unreliable therapeutic effects Unintended off-target effects Impact: Potential for best-in-class medicines that can address difficult-to-treat diseases

Source: Iwamoto N, et al. Control of

phosphorothioate stereochemistry substantially increases the efficacy of antisense oligonucleotides. Nat Biotechnol. 2017;35:845-851. Creating a new class of oligonucleotides INDICATION, TARGET TRANSCRIPT, PRODUCT PROFILE SPLICING RNAi ANTISENSE

DEFINE MODALITY DESIGN & OPTIMIZE VALIDATE SEQUENCE STEREOCHEMISTRY CHEMISTRY Free uptake in cellular models Animal models POTENCY STABILITY SPECIFICITY IMMUNE POTENCY DURABILITY TOXICOLOGY Candidates

CNS Muscle Liver MALAT1 Transcript

Knockdown in Mice Knockdown of Serum hAPOC3 Protein Levels in Mice Two 5 mg/kg SC injections on Days 1&3 PBS Stereopure Eye MALAT1 Knockdown in Non-Human Primates Single 450 g IVT injection 10 Weeks after single 100 g ICV injection

DMD: Percent Skipped Transcript in mdx23 Mice Stereorandom Stereopure Single 150 mg/kg IV injection Data represented in this slide from in vivo studies. CNS: PBS = phosphate buffered saline; Ctx = cortex; Str = striatum; Cb = cerebellum; Hp =

hippocampus; SC = spinal cord. ICV = intracerebral; IVT = intravitreal; IV = intravenous; SC= subcutaneous. Retina Gastrocnemius MALAT1 Transcript Knockdown (% of control) Optimizing potency and durability across multiple tissues

Stereochemistry allows for Human TLR9

activation assay with 5mC modified CpG containing MOE gapmer Cytokine induction in human PBMC assay Stereochemistry affects immune activation Complement Activation Human TLR9 Activation Cytokine Induction Complement activation in non-human primate

serum assay Data represented in this slide from in vitro studies. MOE = 2 -O-methoxyethylribose; PBMC = peripheral blood mononuclear cell; TLR9 = toll-like receptor 9. Stereorandom Stereopure Stereorandom Stereopure

THERAPEUTIC AREA/MODALITY TARGET

DISCOVERY CANDIDATE CLINICAL REGISTRATION ESTIMATED U.S. PREVALENCE* PARTNER Duchenne muscular dystrophy Exon-skipping Suvodirsen Exon 51 ~2,000 WVE-N531 Exon 53 ~1,250 Exons 44, 45, 52, 54, 55 ~3,000 Neuromuscular diseases Multiple

Huntington's disease Allele - selective silencing WVE-120101 mHTT SNP1 ~10,000 / ~35,000 Takeda 50:50 option WVE-120102 mHTT SNP2 ~10,000 / ~35,000 Takeda 50:50 option mHTT SNP3 ~8,000 / ~30,000 Takeda 50:50 option ALS and FTD Allele

- selective silencing WVE-C092 C9orf72 ~1,800 (ALS) ~7,000 (FTD) Takeda 50:50 option Spinocerebellar ataxia 3 Silencing ATXN3 ~4,500 Takeda 50:50 option CNS diseases Multiple Takeda milestones & royalties Retinal diseases Multiple

Metabolic liver diseases Silencing Multiple Pfizer milestones & royalties *Estimates of U.S. prevalence and addressable population by target based on publicly available data and are approximate; for Huntington's disease, numbers

approximate manifest and pre-manifest populations, respectively. During a four-year term, Wave and Takeda may collaborate on up to six preclinical targets at any one time. A.A.: Accelerated approval; ALS: Amyotrophic lateral sclerosis; FTD:

Frontotemporal dementia; CNS: Central nervous system MUSCLE CNS OPHTHALMOLOGY HEPATIC U.S. A.A. filing planned in 2H 2020 pending dystrophin data OLE and planned Phase 2/3 Phase 1b/2a Phase 1b/2a Pipeline spanning multiple modalities, novel targets

Suvodirsen Duchenne Muscular

DMD: a progressive, fatal childhood

disorder Fatal, X-linked genetic neuromuscular disorder characterized by progressive, irreversible loss of muscle function, including heart and lung Genetic mutation in dystrophin gene prevents the production of dystrophin protein, a critical

component of healthy muscle function Symptom onset in early childhood; one of the most serious genetic diseases in children worldwide Current disease modifying treatments have demonstrated minimal dystrophin expression and clinical benefit has not

been established Impacts 1 in every 5,000 newborn boys each year; 20,000 new cases annually worldwide Neuro DMD Source: Parent Project Muscular Dystrophy. About Duchenne & Becker muscular dystrophy. Available at:

https://www.parentprojectmd.org/care/for-healthcare-providers/. Accessed: November 2, 2018.

Potential benefits of stereopure

oligonucleotide approach to treating Duchenne muscular dystrophy Exon skipping Neuro DMD Sources: Arnett ALH, et al. Mol Ther Methods Clin Dev. 2014;1:14038. doi:10.1038/mtm.2014.38. Counsell JR, et al. Sci Rep. 2017;7:79. doi:

10.1038/s41598-017-00152-5. Duan D. Mol Ther. 2018;25:2337-2356. Martinsen B, Dreyer P. Open Nurs Jrnl. 2016;10:131-138. Stitelman DH, et al. Mol Ther Methods Clin Dev. 2014;1:14040. doi:10.1038/mtm.2014.40. Scalable manufacturing Scalable

manufacturing process to meet clinical and commercial supply requirements Cost of goods consistent with conventional oligonucleotide therapies Repeat administration Repeat administration may better address muscle cell turnover and need for broad

distribution Functional dystrophin Production of meaningful levels of functional dystrophin protein Expected to result in therapeutic benefit Delivery Entry into cells (including progenitor cells) via free-uptake Enhanced nuclear uptake

Exon 51: Most frequent mutation

among DMD patients ~13% of DMD patients amenable to Exon 51 skipping One exon-skipping therapy conditionally approved by FDA Minimal increase in dystrophin expression over baseline observed after 48 weeks; Mean increase 0.28%, Median increase 0.1%1

Clinical benefit not established Not approved ex-US Demand for additional treatment options remains high Established US and EU regulatory paths Neuro DMD Sources: 1eteplirsen label; 2Decision Resources, 3US, EU5, Japan; market-based pricing of

commercially available DMD treatments Prevalent patient population represents >$1.5B global market opportunity3 Prevalent patient populations amenable to exon 51 skipping2 Suvodirsen: Wave's lead stereopure exon skipping oligonucleotide for

exon 51 amenable DMD

Exon 51: improved skipping

efficiency RNA skipping determined by quantitative RT-PCR Wave isomers demonstrated a dose-dependent increase in skipping efficiency in vitro Free uptake at 10uM concentration of each compound with no transfection agent Same foundational

stereopure chemistry for Wave isomers; individually optimized to select candidate Neuro DMD Dose Response on Skipping Efficiency (mRNA, in vitro) (4 days) Experimental conditions: Free uptake of ASO in human DMD myoblast cells. Skipping quantified

Exon 51: increased dystrophin

restoration in vitro Analogs dystrophin (400-427 kDa) vinculin (120 kDa) Marker Mock drisapersen eteplirsen* suvodirsen WV-isomer 2 WV-isomer 3 Skeletal Muscle Tissue lysates Marker 0 M Skeletal Muscle Tissue (2 fold less lysate) 0.1 M

0.3 M 1 M 3 M 10 M Skeletal Muscle Tissue dystrophin (400-427 kDa) vinculin (120 kDa) Experimental conditions: DMD protein restoration by Western Blot in patient-derived myotubes with clear dose effect. Free uptake at 10

M concentration of each compound with no transfection agent. suvodirsen Neuro DMD Oligonucleotide at 10 M concentration In vitro dystrophin restoration suvodirsen ~52% drisapersen analogue ~1% eteplirsen analogue ~1%

Exon 51: improved oligonucleotide

uptake in the nucleus where splicing occurs Stereopure oligonucleotides are designed to readily enter the nuclei of cells under free-uptake conditions, which approximates natural delivery in the body Free uptake of stereorandom and stereopure ASOs

Experimental conditions: Free uptake of ASOs in 18 hour differentiating human DMD myoblasts ( 48-50). Red Oligonucleotide Blue Nucleus Neuro DMD

Exon 51: in vivo target engagement

of suvodirsen in healthy non-human primate 5 doses @ 30 mg/kg /week for 4 weeks healthy NHP by subcutaneous dosing Nested PCR Assay Neuro DMD Experimental conditions: Muscle tissues were collected 2 days after the last dose and fresh frozen.

Total RNAs were extracted with phenol/chloroform and converted to cDNA using high capacity kit. Nested PCR assay was performed and analyzed by fragment analyzer.

Exon 51: no apparent tissue

accumulation observed Standard oligonucleotides tend to accumulate in liver and kidney Wave rationally designed oligonucleotides optimized to allow compound to clear more effectively Suvodirsen demonstrated broad tissue distribution in dose

dependent fashion No apparent accumulation observed after multiple doses Neuro DMD Experimental conditions: Mdx23 mice received a single 30-mg/kg intravenous bolus injection of suvodirsen or drisapersen analog (n=3/group), and sacrificed 24 or 48

hours post dose. Oligo quantifications in tissues were performed using hybridization ELISA assay. Single 30-mpk IV injection in mdx23 mice suvodirsen drisapersen analog g/g

Suvodirsen: Phase 1 and OLE clinical

trials 136 patients randomized in Phase 1 and four screened patients expected to enroll directly into Phase 1 OLE OLE: Open-label Extension; Full Phase 1 Results presented at MDA 2019 Scientific and Clinical Conference. Open-Label Extension Trial

Ongoing Phase 1 Single Ascending Dose Trial 40 DMD patients amenable to exon 51 skipping1 ~20% of patients had received eteplirsen previously (following wash out) Suvodirsen had a favorable safety and tolerability profile in context of available

treatments for continued development in OLE and Phase 2/3 trial Open to all patients in Phase 1 trial 1:1 randomization to 5 mg/kg and 3.5 mg/kg doses Patients receiving weekly IV doses of suvodirsen Interim analysis of dystrophin expression

expected in 2H 2019 Neuro DMD

Suvodirsen: Path towards US and

global approvals Phase 1 Phase 1 single ascending dose clinical trial Based on in vitro and in vivo preclinical studies and Phase 1 clinical results, two suvodirsen doses selected for Phase 2/3 clinical trial Study complete Phase 2/3 Phase 2/3

clinical trial to assess clinical efficacy and dystrophin expression Efficacy and safety data to serve as basis of regulatory submissions globally Expect to initiate in July 2019 OPEN-LABEL EXTENSION PHASE 1 PHASE 2/3: DYSTANCE 51 Open-label

extension (OLE) Multi-dose, open-label study with patients from Phase 1 clinical trial currently underway Data will be an important component of submission for accelerated approval in US On track to deliver interim analysis of dystrophin expression

in 2H 2019 2H 2020: Potential FDA accelerated approval filing in exon 51 amenable DMD Neuro DMD

Phase 2/3 study selected for FDA

Complex Innovative Trial Design (CID) pilot program Designed with input from global regulatory communities and DMD patient community DMD historical control data will be leveraged to help reduce number of patients required to deliver conclusive

clinical efficacy results and potentially accelerate study completion Neuro DMD Week -6 0 1 12 22 24 36 46 48 Screening Biopsy = NSAA = Randomization Placebo once weekly (~50 patients) OLE Suvodirsen 3 mg/kg once weekly (~50 patients) Suvodirsen 4.5

mg/kg once weekly (~50 patients) Note: 4.5 mg/kg dose in DYSTANCE 51 provides approximately the same amount of active ingredient as the 5 mg/kg dose in the Phase 1 clinical trial

Building a portfolio to transform

the care of DMD Neuro DMD Sources: Aartsma-Rus A, et al. Hum Mutat. 2009;30:293-299. Bladen CL, et al. Hum Mutat. 2015;36:395-402. Suvodirsen targeting exon 51 Phase 2/3 trial expected to initiate in July 2019 for global regulatory submissions

Potential FDA accelerated approval filing in 2H 2020, pending positive clinical dystrophin expression data WVE-N531 targeting exon 53 Topline clinical data expected in 2H 2020 Advancing candidate development for exons 44, 45, 52, 54, 55 Early leads

demonstrated similar in vitro exon skipping efficiency as suvodirsen and WVE-N531 Percentage of patients with DMD amenable to exon skipping therapeutic approach ~45% Exon 51 Exon 53 Exon 44 Exon 45 Exon 52 Exon 54 Exon 55 ~17% May not be amenable to

single and double exon skipping ~38% Other exon skips Initiating commercialization activities in anticipation of first potential launch in US

Exon 53: WVE-N531 in vitro

dose-dependent dystrophin restoration Free uptake for 6 days in differentiation media with no transfection agent and no peptide conjugated to the oligonucleotide Wave stereopure exon 53 candidate demonstrated a dose-dependent increase in dystrophin

restoration in DMD patient-derived myoblasts Experimental conditions: D45-52 patient myoblasts were treated with oligonucleotide for 6d under free-uptake conditions in differentiation media. Protein harvested in RIPA buffer and dystrophin

restoration analyzed by Western Blot. Signal normalized to vinculin loading control and to primary healthy human myotube lysate (pooled from four donors) forming a standard curve in d45-52 cell lysate. Neuro DMD Topline clinical data expected in 2H