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 September 18, 2017

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.

Genetic medicines company Developing

targeted therapies for patients impacted by rare diseases Rationally designed stereopure nucleic acid therapeutics Utilizing multiple modalities including antisense, exon skipping and RNAi 6 proprietary neurology development programs by the end of

2018 Expertise and core focus in neurology 2 Phase 1b/2a trials initiated in Huntington's disease DMD Exon 51 trial expected to initiate in 2017 Clinical data readouts anticipated in 2019 for first 3 programs Robust R&D platform, ability

to partner additional therapeutic areas Cash position $197MM as of June 30 2017

Paving the way to potentially safer,

more effective medicines 1 first to design and bring stereopure and allele-specific medicines to clinic 6 neurology development programs by end of 2018 3 clinical studies expected to initiate in 2017 10K+ Wave stereopure oligonucleotides created and

analyzed to date 5 nucleic acid modalities being advanced with Wave stereopure chemistry 12+ discovery programs 5 therapeutic areas under active investigation 25M+ total potentially addressable patients amenable to Wave's partnered and

proprietary programs

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 DISEASE

CLINICAL NEXT ANTICIPATED MILESTONES CANDIDATE DISCOVERY ESTIMATED U.S. ADDRESSABLE PATIENTS * TARGET BIOMARKER MECHANISM E = exon skipping. A = allele-specific silencing. A A A A CNS Huntington's disease Phase 1b/2a ~10k / ~35k mHTT SNP1 mHTT

Top line data 1H 2019 Huntington's disease Phase 1b/2a ~10k / ~35k mHTT SNP2 mHTT Top line data 1H 2019 ~1,800 C9orf72 dipeptide Amyotrophic lateral sclerosis Trial initiation Q4 2018 Frontotemporal dementia ~7,000 C9orf72 dipeptide Trial

initiation Q4 2018 E E MUSCLE Duchenne muscular dystrophy 51 ~2,000 exon 51 dystrophin Trial initiation Q4 2017 Duchenne muscular dystrophy 53 ~1,250 exon 53 dystrophin Trial initiation Q1 2019 A A A HEPATIC APOC3 undisclosed undisclosed

Current programs Neuromuscular diseases

DMD (additional exons) Spinal muscular atrophy (SMN2) Charcot-Marie-Tooth type 1A (PMP22) Neurodegenerative movement disorders Spinocerebellar ataxia (ATXN3) Discovery engine Huntington's disease (HTT SNP1) Huntington's disease (HTT

SNP2) Duchenne muscular dystrophy (exon 51) Duchenne muscular dystrophy (exon 53) Amyotrophic lateral sclerosis (C9orf72) Frontotemporal dementia (C9orf72) Neurodegenerative movement disorders Parkinson's disease Progressive supranuclear palsy

Neurodegenerative dementias Alzheimer's disease Developmental diseases Fragile X Batten disease Neurophysiology/ neuropsychiatry/pain Epilepsy Schizophrenia Neurology leadership Opportunities for expansion Neuro

CNS Muscle Broad platform relevance

across therapeutic areas

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. Nature Biotechnology. 2017. Creating a new class of oligonucleotides WAVE RATIONAL DESIGN

Chemistry may optimize medicines

across multiple dimensions Stability of stereopure molecules with reduced PS content (liver homogenate) Oligonucleotide exposure (spinal cord) Human TLR9 activation assay with 5mC modified CpG containing MOE gapmer IL-6 MIP-1 Cytokine

induction in human PBMC assay Stereochemistry enables enhanced delivery of oligonucleotides Improved Stability Controlled Immunogenicity Enhanced Delivery Gymnotic uptake of ASOs:18h differentiating myoblasts Data represented in this slide from in

vitro studies. Experimental conditions: Human TLR9 assay - Source: Ohto U, et al. Structural basis of CpG and inhibitory DNA recognition by Toll-like receptor 9, Nature 520, 702-705, 2015. Intracellular trafficking assay - Cells were

washed and fixed and oligos were detected by viewRNA assay and visualized on immunofluorescence microscope with deconvolution capabilities. Z-stacks were taken to eliminate artifacts. Uptake without transfection agent between a stereopure and

stereorandom oligonucleotide

Stereochemistry is applicable across

modalities Antisense RNAi Exon skipping Stereochemistry allows for novel approaches to previously difficult diseases and inaccessible targets *

SUPERIOR PHARMACOLOGY + SCALABLE

SYNTHESIS MULTI- MODALITY BROAD IMPACT UNLOCKING THE PLATFORM Antisense RNAi Splice Correction Exon skipping Gene editing CNS Muscle Eye Liver Skin Broad addressable patient population across multiple therapeutic areas Transforming nucleic acid

Neurology CNS Muscle

Huntington's Disease

Huntington's Disease: a

hereditary, fatal disorder 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 Wildtype (healthy) HTT protein critical for neuronal function; suppression may have detrimental long-term consequences 30,000 people with

Huntington's disease in the US; another 200,000 at risk of developing the condition 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. DNA

CAG Repeat RNA wildtype (healthy) allele RNA mutant allele Normal CAG Repeat Expanded CAG Repeat Healthy protein (HTT) Mutant protein (mHTT) Neuro HD

Utilize association between single

nucleotide polymorphisms (SNPs) and genetic mutations to specifically target errors in genetic disorders, including HD. Allele-specificity possible by targeting SNPs associated with expanded long CAG repeat in mHTT gene Approach aims to lower mHTT

transcript while leaving healthy HTT relatively intact Potential to provide treatment for up to 70% of HD population (either oligo alone could address approximately 50% of HD population) Wave approach: novel, allele-specific silencing expanded CAG

repeat SNP 1 ~50% of patients SNP 2 ~50% of patients ~20% of patients may carry both SNP1 AND SNP 2 Source: Kaye, et al. Personalized gene silencing therapeutics for Huntington disease. Clin Genet 2014: 86: 29-36 Total: Due to overlap, an

estimated ~70% of the total HD patient population carry SNP 1 and/or SNP 2 Neuro HD

Selective reduction of mHTT mRNA

& protein Reporter Cell Line* Neuro HD

Demonstrated delivery to brain

tissue WVE-120101 and WVE-120102 distribution in cynomolgus non-human primate brain following intrathecal bolus injection Demonstrated delivery to brain tissue CIC = cingulate cortex. CN = caudate nucleus. 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

Novel immunoassay allows for

quantification of mutant huntingtin, the cause of HD Level of mHTT detected is associated with time to onset, increased with disease progression, and predicts diminished cognitive and motor dysfunction Assay currently being utilized in clinical

studies Mutant huntingtin: a powerful, novel biomarker Source: Wild E, et al. Quantification of mutant huntingtin protein in cerebrospinal fluid from Huntington's disease patients. J. Clin. Invest. 2015:125:1979-1986. Edward Wild, MA MB

BChir PhD MRCP Principal Investigator at UCL Institute of Neurology and Consultant Neurologist at the National Hospital for Neurology and Neurosurgery, London Novel approach enables precise measurement of target engagement and effect Neuro

placebo-controlled multi-ascending-dose trials for WVE-120101, WVE-120102 Primary objective: assess safety and tolerability of intrathecal doses in early manifest HD patients Additional objectives: exploratory pharmacokinetic, pharmacodynamic,

clinical and MRI endpoints Two simultaneous Phase 1b/2a clinical trials Blood test to determine presence of SNP 1 or SNP 2 done at pre-screening Approximately 60 patients per trial Key inclusion criteria: age 25 to 65, stage I or II HD

Top line data anticipated 1H 2019 Neuro HD

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 3,500 newborn boys each year; 20,000 new cases annually worldwide Neuro DMD

Wave approach: meaningful

restoration of dystrophin production through exon skipping Neuro DMD Meaningful restoration of dystrophin production is expected to result in therapeutic benefit Exon-skipping antisense approaches may enable production of functional dystrophin

protein Initial patient populations are those amenable to Exon 51 and Exon 53 skipping

Exon 51: improved skipping

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

stereopure chemistry for Wave isomers; individually optimized to assess ideal profile Neuro DMD

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* WVE-210201 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 10uM concentration of each compound with no transfection agent WVE-210201

Exon 51: target engagement 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 WVE-210201 demonstrated wide tissue distribution in dose dependent

fashion No apparent accumulation observed after multiple doses Single in-vivo I.V. dose at 30 mpk in MDX 23 mice Neuro DMD Experimental description: Oligo quantifications in tissues were performed using hybridization ELISA assay

Clinical trials expected to initiate

for WVE-210201 in Q4 2017 Protocol development in collaboration with DMD community Intend to explore intravenous and subcutaneous administration Trials to include ambulatory and non-ambulatory patients Objective is to allow inclusion of patients

previously treated with other exon skipping therapies Measurement of dystrophin via standardized Western Blot Exon 51: WVE-210201 clinical trial design Neuro DMD

RNA skipping determined by

quantitative RT-PCR Free uptake at 10uM and 3uM concentration of each compound with no transfection agent Current published clinical dystrophin levels achieved for Exon 53 are ~1% Early Exon 53 data suggests initial skipping efficiency around