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

Analyst & Investor Research Webcast

August 25, 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.

Paul Bolno, MD, MBA President and CEO

Vision & Strategy Chandra Vargeese, PhD Chief Technology Officer PRISM Platform Update ADAR Editing Kenneth Rhodes, PhD SVP, Therapeutics Discovery Neurology Pipeline C9orf72 Program Today's speakers Conclusion and Q&A

Vision and Strategy Paul Bolno, MD, MBA

Wave Life Sciences VISION We envision a

future in which the diagnosis of a genetically-defined disease leads to effective and available treatment, providing patients and their families the ability to realize a brighter future MISSION Apply innovative nucleic acid chemistry

and deep biological insights to develop transformative medicines for millions of people living with devastating conditions Building a fully integrated genetic medicines company

Wave Life Sciences Building a fully

integrated genetic medicines company >6,000 genetically defined diseases Increases in genetic testing Greater understanding of genetic drivers of disease and definition at molecular level Evolution of PRISM Stereochemistry New ADAR editing

modality Advances in oligonucleotide design Addressing genetic mutations at RNA level Regulate dose and frequency Avoid permanent off-target effects Opportunity Unlocking the genetic medicine opportunity Leveraging PRISM to derive insights from

chemistry and apply them to biology Many diseases beyond the reach of existing treatments

PRISM platform designed to achieve four

goals Enable multiple modalities Silencing, Splicing, ADAR editing Ability to optimize pharmacology Potency, Exposure, Durability Target engagement across key tissues Scalable and cost-effective manufacturing

PRISM has unlocked novel and

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

nusinersen PN backbone chemistry Backbone stereochemistry 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

PRISM platform advancements Primary

screen hit rates in neurons far above industry standard hit rates Stereorandom Chemistry & stereochemistry optimization + Machine learning Stereopure Evolution of primary screen hit rates with 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. (2019) (2020)

Today: Building a fully integrated

genetic medicines company focused on neurology Committed cash: at least $60M in research support over 4 years Potential additional cash inflows: Category 1 programs Six programs: HD (SNP1, SNP2, SNP3) C9-ALS, C9-FTD SCA3 Milestones,

global 50:50 profit split Category 2 programs Up to six preclinical targets (Alzheimer's, Parkinson's, other CNS disorders) >$1B in precommercial milestones & royalties 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 Central nervous system <2 years exclusivity remaining in collaboration

Looking ahead: Building a fully

integrated genetic medicines company focused on neurology Employing new chemistries and modalities to expand wholly-owned neurology pipeline ADAR editing to access new target classes and new pathways PRISM enables access to larger set of potential

indications than other existing platforms Neurology pipeline expansion

Leveraging platform discovery

research to build out areas of potential new biology Hepatic diseases Ophthalmology Muscle diseases Additional therapeutic areas Opportunities outside of neurology

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 ADAR editing Multiple 100% global ADAR editing Undisclosed 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; OLE:

Open-label extension Stereopure PN chemistry

Wave Life Sciences: Redefining the

potential of RNA therapeutics in neurology Continuous learning Platform engine delivering new targets Four global clinical neurology programs expected next year, with multiple data readouts by 2022 Positioned to deliver multiple clinical trial

applications over the next three years Leveraging platform to bring new neurology targets, including editing targets in CNS, to clinic Collaborations to unlock further value Well positioned to drive near-term value from PRISM

PRISM platform update Chandra

Vargeese, PhD Chief Technology Officer

Sequence Stereochemistry Chemistry

PRISM platform enables rational drug design Chemistry R: 2' modifications OMe, MOE, F, other modifications 5' 2' 3' 5' 3' 2' R X B B X: backbone chemistry Phosphodiester (PO), phosphorothioate (PS), other

backbone modifications Sequence B: bases A, T, C, mC, G, U, other modified bases Stereochemistry Chiral control of any stereocenter 5' modifications, backbone modifications

Backbone modification (X)

Phosphodiester Phosphorothioate Stereochemistry Not chiral Chiral Charge Negative Negative Depiction PRISM backbone modifications Focused on backbone chemistry modifications amenable to all modalities Molecule structure illustrative of backbone

modification patterns Backbone linkages PS PO PO/PS Stereorandom PS backbone Rp PS backbone Sp 5' 2' 3' 5' 3' 2' R X B B R

Backbone modification (X)

Phosphodiester Phosphorothioate Phosphoramidate diester Stereochemistry Not chiral Chiral Chiral Charge Negative Negative Neutral Depiction PRISM backbone modifications Expanding repertoire of backbone modifications with novel PN backbone chemistry

Molecule structure illustrative of backbone modification patterns Backbone linkages PS PO PN PO/PS PO/PS/PN Phosphoryl guanidine x-ray structure Stereorandom PS backbone Rp PS backbone Sp PN backbone Sp PN backbone Rp PN backbone

Across many modalities, PN chemistry

enhances potency, exposure, and durability Modality Pharmacology Potency Exposure Durability Silencing Splicing Editing Efficient engagement of RNase H or Ago2 Efficient uptake in the cell nucleus Efficient engagement of ADAR Enabling infrequent

administration In the right tissues, cells and cellular compartments Target knockdown, splicing or editing

Screen of stereopure PS/PO molecules

ranked by potency 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 (referred to as "delta-delta Ct") In vitro

knockdown of PS/PO containing compounds Silencing Splicing Editing Potency Exposure Durability PS/PO Improved potency Target knockdown in vitro in neurons

In vitro knockdown of PS/PO

containing compounds compared to PS/PN compounds Rational design using PN chemistry backbone modification increases potency on average 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 (referred to as "delta-delta Ct") Target knockdown in vitro in neurons Silencing Splicing Editing Potency Exposure Durability PS/PO PS/PN Improved potency

PN chemistry increases durability

across CNS tissues Mice received a single 100 ug ICV injection (n=3 per group). Relative fold-change in MALAT1 expression is shown for the indicated tissues 10-weeks post-dose. MALAT1 expression levels are normalized to Hprt1. PBS, phosphate

buffered saline Malat1 knockdown at 10 weeks in CNS (100 g) Hippocampus Cerebellum Spinal cord Cortex Striatum Silencing Splicing Editing Potency Exposure Durability PS/PO PS/PN

Durable Malat1 knockdown through 9

months with PN chemistry Compound or PBS (1 x 50 ug IVT) was delivered to C57BL6 mice. Relative percentage of Malat1 RNA in the posterior of the eye (retina, choroid, sclera) to PBS-treated mice is shown at 12, 20 and 36 weeks post-single injection.

PBS = phosphate buffered saline; NTC= chemistry matched non-targeting control ~50% Malat1 knockdown at 36 weeks in the posterior of the eye PBS NTC PS/PO PS/PN Silencing Splicing Editing Potency Exposure Durability % Malat1 expression Time (weeks)

Improved exon skipping with PN

chemistry DMD patient-derived myoblasts treated with PS/PO or PS/PO/PN stereopure oligonucleotide under free-uptake conditions. Exon-skipping efficiency evaluated by qPCR. Exon skipping plotted for compounds with same sequence In

vitro skipping efficiency of PS/PO containing compounds compared to PS/PO/PN compounds Exon skipping compounds have same sequence PS / PO / PN oligonucleotides have three PN backbone modifications Silencing Splicing Editing Potency Exposure

Durability % skipping Rank-order skipping (PS/PO) PS/PO PS/PO/PN PS/PO backbone PS/PO/PN backbone PS Rp PS Sp PO PN Rp

PN chemistry improves potency and

increases cellular uptake in myoblasts Left: Cultured H2K myoblasts treated with increasing concentrations of PS/PO or PS/PO/PN stereopure oligonucleotide under free-uptake conditions. Skipping efficiency evaluated by TaqMan assay. Right:

Cultured H2K cells treated with 0.5 uM oligonucleotide. Uptake quantified in cytoplasmic and nuclear extracts by hybridization ELISA. **: P 0.01, ***: P 0.001 DMD mRNA skipping (Exon 23, H2K mouse myoblasts) % skipping

Concentration ( M) Concentration (ng/ml) Concentration (ng/ml) PBS PBS Cellular uptake (H2K mouse myoblasts) PS/PO backbone PS/PO/PN backbone Cytoplasmic Nuclear Silencing Splicing Editing Potency Exposure Durability PS Rp PS Sp PO PN

DKO model to assess PN chemistry on

survival DKO model generation and in vivo studies were performed by our collaborator Professor Matthew Wood at the University of Oxford; DKO PS/PO/PN and DKO PS/PO oligonucleotides have same sequence Double knockout mouse (DKO) Protein Pathology

Utrophin Mild No decrease in survival Dystrophin Protein Pathology Utrophin None Dystrophin MDX mouse Protein Pathology Utrophin Severe muscular dystrophy Premature death Dystrophin Utrophin knockout

Silencing Splicing Editing Potency Exposure Durability

Study completion: DKO PS/PO/PN mice

sacrificed for further analyses Step-change in survival observed in DKO model using PN chemistry Mdx/utr-/- mice received weekly subQ 150 mpk dose of PS/PO or PS/PO/PN stereopure oligonucleotide beginning at postnatal day 10. Age-matched mdx/utr-/-

littermates were treated with PBS, and mdx mice were not treated. Mice with severe disease were euthanized. DKO: PS/PO/PN n=8, PS/PO n=9, PBS n=12 PBS PS/PO, QW 150 mpk weekly PS/PO/PN, QW 150 mpk weekly Silencing Splicing Editing Potency

Exposure Durability DKO Survival

Similar survival trend observed with

75% less total dose PBS PS/PO, QW 150 mpk weekly PS/PO/PN, QW 150 mpk weekly PS/PO/PN, Q2W 75 mpk bi-weekly* Silencing Splicing Editing Potency Exposure Durability *Ongoing study at (50%) reduced dose and frequency (bi-weekly vs. weekly) DKO

Survival Mdx/utr-/- mice received weekly subQ 150 mpk dose of PS/PO or PS/PO/PN stereopure oligonucleotide beginning at postnatal day 10. Age-matched mdx/utr-/- littermates were treated with PBS, and mdx mice were not treated. Mice with severe

disease were euthanized. DKO: PS/PO/PN 75 mpk n=9; PS/PO/PN 150 mpk n=8, PS/PO n=9, PBS n=12

Restoration of wild-type muscle

function using PS/PO/PN compound 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) Silencing Splicing Editing Potency Exposure Durability 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