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 3, 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.

Wave Life Sciences is a clinical-stage,

genetic medicines company unlocking the potential of a proprietary chemistry platform that enables the precise design, optimization and production of stereopure nucleic acid therapies. We are leading a new era of precision medicine in which

rationally designed nucleic acid therapies are the key to delivering safer, more effective treatments for serious, genetically-defined diseases.

Architects of transformation Wave has

reinvented the design, synthesis and manufacture of nucleic acid therapies to potentially optimize potency, durability and safety PRECISION Ability to design nucleic acid compounds that have one defined and consistent profile SCALE Platform

potential across multiple modalities and tissues Internal expertise and capacity for large-scale GMP manufacturing Wave's chemistry platform is built on a foundation of two core capabilities:

WAVE RATIONAL DESIGN Stereochemistry

enables precise control, ability to optimize critical constructs into one defined and consistent profile Building 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 safer, more effective, targeted 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

Optimizing potency and durability

across multiple tissues 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)

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

Pipeline spanning multiple modalities,

novel targets CLINICAL CANDIDATE DISCOVERY ESTIMATED U.S. PREVALENCE* TARGET MECHANISM PARTNER WAVE'S COMMERCIAL RIGHTS *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. Pfizer has nominated

four undisclosed targets in addition to APOC3. E = exon skipping. A = allele-specific silencing. S = silencing. MUSCLE E Duchenne muscular dystrophy ~2,000 Exon 51 Phase 1/OLE - 100% Global E Duchenne muscular dystrophy ~1,250 Exon 53 -

100% Global Duchenne muscular dystrophy Exons 44, 45, 52, 54, 55 - 100% Global Neuromuscular diseases Multiple - 100% Global ~1,500 E OPHTHALMOLOGY HEPATIC S Metabolic liver diseases APOC3 and Multiple (4) Pfizer Milestones &

Royalties Retinal diseases RHO, USH2A, ABCA4, CEP290 - 100% Global ~10,000 OLE = Open-label extension. CNS A Huntington's disease ~10k / ~35k mHTT SNP1 Phase 1b/2a Takeda 50% Global A Huntington's disease ~10k / ~35k mHTT SNP2

Phase 1b/2a Takeda 50% Global A Amyotrophic lateral sclerosis ~1,800 C9orf72 Takeda 50% Global A Frontotemporal dementia ~7,000 C9orf72 Takeda 50% Global S Spinocerebellar ataxia 3 ATXN3 Takeda 50% Global ~4,500 CNS diseases Multiple Takeda

Milestones & Royalties A Huntington's disease ~ 8k / ~ 30k mHTT SNP3 Takeda 50% Global

Duchenne Muscular Dystrophy (DMD)

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.

Wave approach: stereopure exon

skipping oligonucleotide Neuro DMD Potential benefits of an oligonucleotide approach to treating a lifelong disease Chronic administration may better address high muscle cell turnover and need for broad and durable distribution Entry into cells,

including progenitor cells, via free-uptake Production of functional dystrophin protein, not micro-dystrophin Scalable manufacturing Exon skipping with stereopure oligonucleotides has the potential to enable production of meaningful levels of

functional dystrophin which is expected to result in therapeutic benefit 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. Exon skipping

Exon 51: suvodirsen (WVE-210201)

clinical program Neuro DMD PHASE 2/3 Open-Label Extension (OLE) PHASE 1 OBJECTIVE Determine safety and tolerability profile and select dose(s) for OLE and Phase 2/3 STUDY DESCRIPTION Phase 1 single ascending dose clinical trial KEY MILESTONES Safety

and tolerability profile supports Phase 2/3 initiation One dose selected for Phase 2/3 trial, pending final analysis Results to be presented at upcoming scientific meetings OBJECTIVE Provide data that will be an important component of submission for

accelerated approval in US STUDY DESCRIPTION Multi-dose, open-label study open to patients from Phase 1 KEY MILESTONES Initiated in August 2018 On track to deliver interim analysis of dystrophin expression in H2 2019 OBJECTIVE Provide efficacy and

safety data as basis of regulatory submissions globally STUDY DESCRIPTION Phase 2/3 clinical trial to assess clinical efficacy and dystrophin expression KEY MILESTONES Selected for FDA pilot program for complex innovative trial designs Expect to

initiate in 2019 Dystrophin readout expected H2 2019 OPEN-LABEL EXTENSION PHASE 1 PHASE 2/3

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

Dystrophin protein restoration in

vitro was quantified to be between 50-100% of normal skeletal muscle tissue lysates, as compared to about 1% by drisapersen and eteplirsen analogs Exon 51: increased dystrophin restoration *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

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 wide 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

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 H2

2020 Dystrophin protein restoration of up to 71% Western Blot normalized to primary healthy human myoblast lysate

Exon 53: targeting oligonucleotide

rapidly distributes to muscle within 24 hours after injection Bright field view 63x oil Nucleus: Hematoxylin; Light Blue Wave oligo: ViewRNA, Fast Red Nucleus: Hoechst33342; Blue Wave oligo: Fast Red/Cy3; Pink Red Fluorescence channel view Z Stack

view Data derived from in vivo preclinical research. Experimental conditions: A single dose of stereopure oligonucleotide 30 mg/kg IV was administered to mdx 23 mice. Tissues collected 24 hours post dose and ASO was detected in muscles using

Stereopure surrogate yields

substantial dystrophin protein restoration and CK reduction *Numbers indicate individual animals Note: DMD-1742 is a stereopure oligonucleotide designed to induce exon 23 skipping in the mdx23 mouse model and is a surrogate of suvodirsen, which is

designed to induce exon 51 skipping in the human dystrophin transcript Experimental conditions: Tissues collected 96 hours post final dose. Protein expression determined by Western Blot. ALT=alanine aminotransferase; AST=aspartate aminotransferase;

CK=creatine kinase; GLDH=glutamate dehydrogenase. Serum and plasma clinical chemistry were measured with an Olympus AU640 (Olympus America) and the manufacturer's reagents and procedures. Neuro DMD 80% 60% 40% 20% 10% 5% 2.5% # 1 #2 #3 #1 #2

#3 #4 #5 #5* Dystrophin Meta-vinculin Vinculin Wild Type/PBS Pool PBS DMD-1742 Gastrocnemius DMD-1742 (4 weekly 150-mg/kg IV injections) Dystrophin Protein Restoration 70-90% of dystrophin restoration Multiple Doses (in vivo mdx23

mice) Serum Enzyme Levels 87% reduction in creatine kinase (CK) levels

Single dose of surrogate results in

restoration of dystrophin in muscle fibers Neuro DMD PBS DMD-1742 Immunohistochemistry of dystrophin in gastrocnemius in mdx23 mice at 4 weeks 10X Experimental conditions: mdx23 mice received a single IV injection of PBS or DMD-1742 (150 mg/kg).

Immunohistochemistry: Blue: Nuclei, Hoechest; Yellow: Rabbit anti-Dystrophin(#ab15277) 1:400 diluent, 555/Cy3, Cy3 staining is represented by the yellow color. 10X magnification. PBS

Multiple doses of surrogate result

in further restoration of dystrophin in muscle fibers Experimental conditions: mdx23 mice received 4 weekly IV injections of PBS or DMD-1742 (150 mg/kg). Immunohistochemistry: Blue: Nuclei, Hoechest; Yellow: Rabbit anti-Dystrophin(#ab15277) 1:400

diluent, 555/Cy3, Cy3 staining is represented by the yellow color. 10X magnification. Neuro DMD PBS DMD-1742 Immunohistochemistry of dystrophin in gastrocnemius in mdx23 mice at 4 weeks 10X 0X

Expansion of stereopure exon

skipping DMD portfolio Applying learnings from ongoing DMD development efforts and platform advances to explore additional exons for candidate development, including exons 44, 45, 52, 54, 55 Early leads demonstrate similar in vitro exon skipping

efficiency as suvodirsen and WVE-N531 Aim to leverage 21st Century Cures Act to develop additional candidates Neuro DMD Committed to unlocking the promise of precision medicine to advance the treatment of DMD Percentage of DMD patients amenable to