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 November 12, 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.

Building a leading genetic medicines

company ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia 1stereopure oligonucleotides and novel backbone chemistry modifications Innovative platform Stereopure oligonucleotides Novel backbone modifications (PN chemistry)

Allele-selectivity Multiple modalities (silencing, splicing, ADAR editing) Strong IP position1 Foundation of NEUROLOGY programs Huntington's disease ALS / FTD Neuromuscular diseases Ataxias Parkinson's disease Alzheimer's disease

Clinical development expertise Multiple global clinical trials ongoing across eight countries Innovative trial designs Manufacturing Established internal manufacturing capabilities to produce oligonucleotides at scale Wave's drug discovery and

development platform

PRISM has unlocked novel and

proprietary advances in oligonucleotide design Backbone modifications Sugar modifications Drug approvals (FDA)2 1975 2020 2000 Mixtures of 2n molecules1 ~500,000 different molecules per dose fomivirsen pegaptanib Phosphorothioate (PS) mipomersen

nusinersen PN backbone modification chemistry Stereopure backbone 2'-4'-cEt 2'-O-methyl 2'-F 2'-4'-LNA 1n=number of chiral centers 2'-MOE Phosphorodiamidate Morpholino (PMO) eteplirsen golodirsen givosiran

patisiran inotersen viltolarsen 2oligonucleotide therapies approved by the FDA across the industry

THERAPEUTIC AREA / TARGET DISCOVERY

PRECLINICAL CLINICAL PARTNER Huntington's disease mHTT SNP1 Takeda 50:50 option Huntington's disease mHTT SNP2 Huntington's disease mHTT SNP3 ALS and FTD C9orf72 SCA3 ATXN3 CNS diseases Multiple Takeda milestones &

royalties DMD Exon 53 100% global ADAR editing Multiple AATD (ADAR editing) SERPINA1 100% global Retinal diseases USH2A and RhoP23H 100% global NEUROLOGY HEPATIC OPTHALMOLOGY WVE-003 WVE-004 WVE-120101 WVE-120102 Innovative pipeline led by neurology

programs 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; SCA3: Spinocerebellar ataxia 3; CNS: Central nervous system;

DMD: Duchenne muscular dystrophy; AATD: Alpha-1 antitrypsin deficiency Stereopure PN chemistry WVE-N531

WVE-120101 WVE-120102 WVE-003

Huntington's Disease Portfolio

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

Healthy CNS function Synaptic

dysfunction | Cell death | Neurodegeneration mHTT toxic effects lead to neurodegeneration, loss of wtHTT functions may also contribute to HD Healthy individual Stresses wtHTT Huntington's disease Stresses Toxic effects of mHTT + Loss of wtHTT

functions ~50% decrease in wtHTT CNS, central nervous system; HD, Huntington's disease; HTT, huntingtin protein; mHTT, mutant huntingtin protein; wtHTT, wild-type huntingtin protein. 1. Ross CA, Tabrizi SJ. Lancet Neurol. 2011;10(1):83-98. 2.

Saudou F, Humbert S. Neuron. 2016;89(5):910-926. 3. Cattaneo E, et al. Nat Rev Neurosci. 2005;6(12):919-930. 4. Milnerwood AJ, Raymond LA. Trends Neurosci. 2010;33(11):513-523. Neuro HD

Plays an essential role in the

transport of synaptic proteins-including neurotransmitters and receptors-to their correct location at synapses9-12 Promotes neuronal survival by protecting against stress (e.g., excitotoxicity, oxidative stress, toxic mHTT

aggregates)1-8 BRAIN CIRCUITS SYNAPSE NEURON CSF circulation Supplies BDNF to the striatum to ensure neuronal survival13-16 Regulates synaptic plasticity, which underlies learning and memory17-22 Plays a critical role in formation and function of

cilia-sensory organelles that control the flow of CSF-which are needed to clear catabolites and maintain homeostasis23 HD: Wild-type HTT is a critical protein for important functions in the central nervous system BDNF, brain-derived

neurotrophic factor; CSF, cerebrospinal fluid; mHTT, mutant huntingtin protein. 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 Neuro HD

Nature publication contributes to

weight of evidence on importance of wild-type huntingtin Source: Poplawski et al., Nature, April 2019 Htt: Huntingtin protein Conditional knock-out of Htt in 4-month old mice (post-neuronal development) Results suggest that: Htt plays a central role

in the regenerating transcriptome (potentially influencing genes such as NFKB, STAT3, BDNF) Htt is essential for regeneration Indeed, conditional gene deletion showed that Htt is required for neuronal repair. Throughout life, neuronal maintenance

and repair are essential to support adequate cellular functioning Neuro HD

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

WVE-120101: Selective reduction of

mHTT mRNA and 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 trials Single

Dose Multidose 196 1 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) Trial results expected in 1Q 2021 OLE: Open label extension; CSF: cerebrospinal fluid; mHTT: mutant

huntingtin; wtHTT: wild-type HTT; tHTT: total HTT * Study day may vary depending on patient washout period 1Hodges-Lehmann non-parametric shift estimates of the difference between treatment and placebo, p<0.05 (Wilcoxon-Mann-Whitney

non-parametric significance test); 2Multiple Contrast Test (MCT), p=0.03; Interim data announced December 2019 Results Two Phase 1b/2a clinical trials for WVE-120101 and WVE-120102 ongoing Patients are migrated to highest dose tested Neuro HD Safety

and tolerability Biomarkers mHTT Assay development work to measure wtHTT in CSF ongoing tHTT PRECISION-HD1 and OLE PRECISION-HD2 and OLE NfL

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 a cannula on days 1, 3, and 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 *** ****

**** **** **** **** CTA submission expected in 4Q 2020 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

Three 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 WVE-120101 SNP2 WVE-120102 SNP3 WVE-003

SNP1 SNP2 SNP1 SNP2 SNP3 ~50% ~50% ~40% ~70%1 ~80%2 +10% of HD patients vs. SNP1 + SNP2 1 Percentage of patient population with SNP1 and/or SNP2 2 Percentage of patient population with SNP1, SNP2 and/or SNP3

WVE-004 Amyotrophic Lateral

Sclerosis (ALS) Frontotemporal Dementia (FTD)

C9orf72 repeat expansions: A

critical genetic driver of ALS and FTD Normal (non-expanded) Allele < 25 GGGGCC repeats Expanded Allele Sources: DeJesus-Hernandez et al, Neuron, 2011. Renton et al, Neuron, 2011. Zhu et al, Nature Neuroscience, May 2020 Typically

100's-1000's of GGGGCC repeats C9orf72 hexanucleotide repeat expansions (GGGGCC) are the strongest known risk factor for sporadic and inherited forms of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) The C9orf72

repeat expansions also lead to accumulation of repeat-containing transcripts, nuclear sequestration of RNA binding proteins and synthesis of toxic dipeptide-repeat (DPR) proteins The C9orf72 repeat expansions lead to reduced

expression of wild-type C9orf72 and to cellular changes that reduce neuronal viability Neuro C9orf72

C9-ALS and C9-FTD: Manifestations of

a clinical spectrum Disease C9 specific US population Mean disease duration Standard of care C9-ALS Fatal neurodegenerative disease Progressive degeneration of motor neurons in brain and spinal cord ~2,000 3.1 years Significant unmet need

despite two approved therapies in US C9-FTD Progressive neuronal atrophy in frontal/temporal cortices Personality and behavioral changes, gradual impairment of language skills ~10,000 6.4 years No approved disease modifying therapies Two

devastating diseases with a shared genetic basis ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia Sources: Cammack et al, Neurology, October 2019. Moore et al, Lancet Neurology, February 2020 Neuro C9orf72

C9orf72 repeat expansions:

Mechanisms of cellular toxicity C9-ALS and C9-FTD may be caused by multiple factors: Insufficient levels of C9orf72 protein Accumulation of repeat-containing RNA transcripts Accumulation of aberrantly translated DPR proteins Recent evidence suggests

lowering C9orf72 protein exacerbates DPR-dependent toxicity Sources: Gitler et al, Brain Research, September 2016. Zhu et al, Nature Neuroscience, May 2020 Targeted by Wave ASOs Variant-selective targeting could address multiple potential drivers of

toxicity Neuro C9orf72

Normal C9orf72 allele produces three

mRNA transcripts (~80% are V2, ~20% are V1 and V3) Pathological allele with expanded repeat leads to healthy V2 and pathological V1 and V3 transcript by-products C9orf72 targeting strategy spares C9orf72 protein Wave C9orf72 candidate targets only

V1 and V3 transcripts, sparing V2 transcripts and healthy C9orf72 protein pre-mRNA variants Pathological mRNA products V1 V2 Mis-spliced V1/V3 Stabilized intron1 V3 Disease-causing factors RNA foci Dipeptide repeat proteins (DPRs) GGGGCC expansion

Accessible target for variant selectivity WVE-004 reduces Repeat-containing transcripts Neuro C9orf72

PN backbone chemistry: Improved

potency among C9orf72-targeting oligonucleotides in vivo Exposure ( g/g) Exposure ( g/g) C9orf72 compounds Spinal cord Cortex PS/PO backbone PS/PO/PN backbone %C9orf72 V3 transcript remaining Mice received 2 x 50 ug ICV doses on days

0 & 7; mRNA from spinal cord and cortex quantified by PCR (Taqman assay) 8 weeks later. Oligonucleotide concentrations quantified by hybridization ELISA. Graphs show robust best fit lines with 95% confidence intervals (shading) for PK-PD