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 13, 2020 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.

THERAPEUTIC AREA/MODALITY TARGET

DISCOVERY PRECLINICAL CLINICAL ESTIMATED U.S. PREVALENCE* PARTNER 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 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 USH2A and multiple 100% global Metabolic liver diseases Silencing Multiple Pfizer milestones & royalties ADAR RNA-editing Multiple 100% global OTHER CNS OPHTHALMOLOGY HEPATIC Phase 1b/2a Phase

1b/2a and OLE Pipeline spanning multiple modalities, novel targets *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. ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia; CNS: Central nervous

system; OLE: Open-label extension

WVE-120101 WVE-120102

Huntington's Disease

Huntington's disease: a

hereditary, fatal disorder Sources: Auerbach W, et al. Hum Mol Genet. 2001;10:2515-2523. Dragatsis I, et al. Nat Genet. 2000;26:300-306. Leavitt BR, et al. J Neurochem. 2006;96:1121-1129. Nasir J, et al. Cell. 1995;81:811-823. Reiner A, et al. J

Neurosci. 2001;21:7608-7619. White JK, et al. Nat Genet. 1997;17:404-410. Zeitlin S, et al. Nat Genet. 1995;11:155-163. Carroll JB, et al. Mol Ther. 2011;19:2178-2185. HDSA What is Huntington's disease?'

https://hdsa.org/what-is-hd/overview-of-huntingtons-disease/ Accessed: 11/2/18.; Becanovic, K., et al., Nat Neurosci, 2015. 18(6): p. 807-16. Van Raamsdonk, J.M., et al., Hum Mol Genet, 2005. 14(10): p. 1379-92.; Van Raamsdonk, J.M., et al., BMC

Neurosci, 2006. 7: p. 80. DNA CAG Repeat RNA wild-type (healthy) allele RNA mutant allele Normal CAG Repeat Expanded CAG Repeat Healthy protein (HTT) Mutant protein (mHTT) Neuro HD Autosomal dominant disease, characterized by cognitive decline,

psychiatric illness and chorea; fatal No approved disease-modifying therapies Expanded CAG triplet repeat in HTT gene results in production of mutant huntingtin protein (mHTT); accumulation of mHTT causes progressive loss of neurons in the brain

Wild-type (healthy) HTT protein critical for neuronal function; evidence suggests wild-type HTT loss of function plays a role in Huntington's disease 30,000 people with Huntington's disease in the US; another 200,000 at risk of

developing the condition

Evidence suggests wild-type or healthy

HTT is neuroprotective in an adult brain Transport of key neurotrophic factors such as brain-derived neurotrophic factor (BDNF) are regulated by wtHTT levels Relative proportion of wild-type to mutant protein is critical Increased amount of

wild-type protein relative to mutant HTT may result in slower disease progression (measured by age-at-onset) Patients with lack of wild-type have significantly more severe disease Importance of wild-type huntingtin (wtHTT) in HD Neuro HD

Huntington's disease (HD) may be caused by a dominant gain of function in mutant HTT and a loss of function of wtHTT protein Sources: Van Raamsdonk, J.M., et al., Hum Mol Genet, 2005; Van Raamsdonk, J.M., et al., BMC Neurosci, 2006; Becanovic,

K., et al., Nat Neurosci, 2015; Saudou, F. and S. Humbert, The Biology of Huntingtin. Neuron, 2016; Gauthier, L.R., et al., Cell, 2004; Caviston, J.P. and E.L. Holzbaur, Trends Cell Biol, 2009; Ho, L.W., et al., J Med Genet, 2001, Zuccato et al.,

Science 2001; Zuccato et al., Brain Pathol 2007; Marullo et al. Genome Biol 2010 BDNF TrkB ERK CREB transport BDNF Neuroprotection

Wild-type HTT in the cortex appears

critical for striatal health Presented by Dr. Frederic Saudou at Wave's Analyst and Investor Research Day on October 7, 2019 Virlogeux et al., Cell Reports 2018 Neuro HD Neuron Type Genetic Status Compartment Cortical Striatal Network Status

Functional Dysfunctional Post-synaptic Synaptic Presynaptic Status of the presynaptic compartment determines the integrity of the network

Utilize association between single

nucleotide polymorphisms (SNPs) and genetic mutations to specifically target errors in genetic disorders, including Huntington's disease (HD) Potential to provide treatment for up to 80% of HD population Wave approach: novel, allele-selective

silencing Source: Kay, et al. Personalized gene silencing therapeutics for Huntington disease. Clin Genet. 2014;86:29-36. Neuro HD Aims to lower mHTT transcript while leaving healthy wild-type HTT relatively intact Allele-selectivity possible

by targeting SNPs associated with expanded long CAG repeat in HTT gene RNase H and ASO:RNA RNA mutant allele

Selective reduction of mHTT mRNA &

protein Reporter Cell Line* Neuro HD Source: Meena, Zboray L, Svrzikapa N, et al. Selectivity and biodistribution of WVE-120101, a potential antisense oligonucleotide therapy for the treatment of Huntington's disease. Paper presented at: 69th

Annual Meeting of the American Academy of Neurology; April 28, 2017; Boston, MA.

Demonstrated delivery to brain

tissue WVE-120101 and WVE-120102 distribution in cynomolgus non-human primate brain following intrathecal bolus injection In Situ Hybridization ViewRNA stained tissue Red dots are WVE-120102 oligonucleotide Arrow points to nuclear and perinuclear

distribution of WVE-120102 in caudate nucleus Red dots are WVE-120101 oligonucleotide Arrow points to nuclear and perinuclear distribution of WVE- 120101 in cingulate cortex CIC = cingulate cortex In Situ Hybridization ViewRNA stained tissue

Neuro HD CN = caudate nucleus Source: Meena, Zboray L, Svrzikapa N, et al. Selectivity and biodistribution of WVE-120101, a potential antisense oligonucleotide therapy for the treatment of Huntington's disease. Paper presented at: 69th Annual

Meeting of the American Academy of Neurology; April 28, 2017; Boston, MA.

PRECISION-HD clinical trial design

Two parallel, multicenter, double-blind, randomized, placebo-controlled Phase 1b/2a clinical trials for WVE-120101 and WVE-120102 Single Dose (3:1) Multidose Randomization 3:1 196 1 At least 8 week washout CSF sample Dose 28 56 84 112 Study Day* 140

OLE 2 mg 4 mg 8 mg 16 mg 32 mg Multidose Cohorts N = 12 per cohort OLE: Open label extension; CSF: cerebrospinal fluid *Study day may be longer depending on patient washout period PRECISION-HD2 OLE: Initiated October 2019 PRECISION-HD1 OLE: Expected

to initiate in 2020 Neuro HD PRECISION-HD2 data from 32 mg cohort in expected in 2H 2020 PRECISION-HD1 topline data, including 32 mg cohort, in 2H 2020

PRECISION-HD2 topline results

Clinical trial ongoing Neuro HD Doses Safety Biomarker Effects Topline results announced December 30. 2019; mHTT: mutant huntingtinwtHTT: wild-type HTTtHTT: total HTT 1 Hodges-Lehmann non-parametric shift estimates of the difference between

treatment and placebo; 2 Wilcoxon-Mann-Whitney non-parametric significance test; 3 Multiple Contrast Test (MCT) mHTT wtHTT WVE-120102 2-16 mg (pooled) Generally safe and well tolerated Reduction in mHTT compared to placebo (-12.4%1,

p<0.052) Analysis across groups suggests dose response at highest doses (p=0.03)3 No change in tHTT compared to placebo Ongoing evaluation 32 mg cohort initiated Assessing dose for next cohort Safety profile supports addition of higher dose

cohorts Potential for greater mHTT reduction at higher doses Larger reductions of mHTT expected to result in discernible impact on tHTT

Advancing allele-selective HD

programs Intend to explore efficacy in early manifest and pre-manifest HD patient populations Neuro HD Potential to address ~80% of HD patient population % Huntington's Disease Patient Population with SNP SNP1 SNP2 SNP3 SNP1 SNP2 SNP1 SNP2

SNP3 ~50% ~50% ~40% ~70% ~80% +10% of HD patients vs. SNP1 + SNP2

SNP3 Preclinical Program

Huntington's Disease

Potent mutant HTT knockdown activity

Greater knockdown of mutant HTT as compared to pan-silencing compound Wave allele-selective compounds are more potent than pan-silencing RG6042 analog in preclinical study involving patient-derived neurons ~7-fold shift Pan-silencing RG6042 analog

Wave SNP3 Compound-1 Wave SNP3 Compound-2 HTT mRNA remaining in iCell neurons (homozygous for SNP) incubated with the indicated ASO under free-uptake conditions. Data show mean sem (n=4). Homozygous iCell Neurons Neuro HD

Stereopure oligonucleotides are

selective in vitro Stereopure isomers targeting a SNP variant promote RNase H-mediated degradation of mutant HTT while sparing wild-type HTT Biochemical RNase H assays RNase H experiments performed with synthetic RNA substrates corresponding to mHTT

and wtHTT variants (S:E = 100:1; n=2). Percentage of the indicated full-length RNA substrate remaining over time is plotted for the stereopure SNP3 Compound-1 (left) and stereopure SNP3 Compound-2 (right). Abbreviations: S, substrate; E, enzyme.

Wave SNP3 Compound-1/mHTT Wave SNP3 Compound-1/wtHTT Time (min) % RNA substrate remaining Wave SNP3 Compound-2/mHTT Wave SNP3 Compound-2/wtHTT % RNA substrate remaining Time (min) Neuro HD

Demonstration of allele-selective

silencing Stereopure compounds selectively deplete mutant HTT mRNA Neurons were derived from GM21756 patient-derived fibroblasts (heterozygous for SNP) and treated with 2.2 mM (left) or 20 mM (right) of the indicated ASO under gymnotic conditions

for 7 days. RNA was quantified and normalized to TUBB3. Data are mean sem (n=3). Percentage of remaining wtHTT and mHTT mRNA is indicated. No loss of selectivity with increasing concentrations [20 M] PBS PBS Pan-silencing RG6042 analog

Pan-silencing RG6042 analog Wave SNP3 Compound-1 Wave SNP3 Compound-2 Wave SNP3 Compound-1 Wave SNP3 Compound-2 [2 M] Neuro HD

In vivo model to assess target

engagement and durability BACHD mouse model Expressed transcript includes SNP3 variant that Wave compounds are targeting Model is homozygous for mutant HTT with SNP3 (only has one type of HTT) Over-expresses mHTT (multiple gene copies) No ability to

assess allele selectivity Oligonucleotide concentration in tissues Achieved good tissue exposure over 12-weeks in BACHD cortex and striatum Oligonucleotide or PBS (3 x 100 g ICV) was delivered to BACHD mice. Oligonucleotides were quantified by

ELISA. Tissue exposure over time CORTEX STRIATUM Pan-silencing RG6042 analog Wave SNP3 Compound-1 Wave SNP3 Compound-2 Neuro HD

Durable in vivo mutant HTT knockdown

with stereopure SNP3 compounds Knockdown persists for 12 weeks Oligonucleotide or PBS (3 x 100 mg ICV) was delivered to BACHD mice. Relative percentage of HTT/TUBB3 mRNA in cortex with respect to levels in PBS-treated mice is shown at 2-12 weeks

post-injection. Statistics: All oligo treatment groups are statistically significantly different from PBS; One-way ANOVA ****, P 0.0001. Wave SNP3 Compound-1 and Compound-2 are also significantly different from RG6042 analog at 8 and 12 weeks

***, P<0.005; **P=0.001. Relative percentage mHTT expression Relative percentage mHTT expression PBS Pan-silencing RG6042 analog Wave SNP3 Compound-1 Wave SNP3 Compound-2 PBS Pan-silencing RG6042 analog Wave SNP3 Compound-1 Wave SNP3 Compound-2

BACHD Cortex BACHD Striatum ** **** *** **** **** **** Neuro HD Clinical development expected to initiate in 2H 2020

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

Importance of controlling

stereochemistry (Rp) (Sp) Top view Side view Yellow spheres represent S' atomsPS: Phosphorothioate Number of PS linkages in oligonucleotide backbone No. diastereomers 80T 60T 40T 20T 30B 22M 12M 2M 1M 500K 0 0 10 20 30 40 50 Antisense,

exon skipping, ssRNAi ADAR oligonucleotide CRISPR guide Stereochemical diversity Exponential diversity arises from uncontrolled stereochemistry

Continuous Learning PRISM platform

enables rational drug design Source: Iwamoto N, et al. Control of phosphorothioate stereochemistry substantially increases the efficacy of antisense oligonucleotides. Nat Biotechnol. 2017;35:845-851.

Liver Knockdown of Serum APOC3

Protein Levels in Mice Two 5 mg/kg SC injections on Days 1&3 Stereorandom Stereopure 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. Optimizing potency and durability across multiple tissues CNS Malat1 Transcript Knockdown in Mice 10 Weeks after single 100 g ICV injection Malat1

Transcript Knockdown (Percentage of control) PBS Ctx Str Cb Hp SC Eye MALAT1 Knockdown in Non-Human Primates Single 450 g IVT injection PBS Stereopure Retina MALAT1 RNA Remaining MALAT1/GAPDH 1 week 8 weeks 16 weeks APOC3 Protein (Relative to