Wave Life Sciences Ltd. · NASDAQ:WVE
Wave Life Sciences — Investor Presentation (February 2026)
49 slides from Wave Life Sciences's investor presentation, Feb 26, 2026
Slide 1: Wave Life Sciences Corporate Presentation
Exhibit 99.2 Wave Life Sciences Corporate Presentation February 26, 2026
Slide 2: Forward-looking statements
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, r
Slide 3: Our Mission
Our Mission To unlock the broad potential of RNA medicines to transform human health 3
Slide 4: Building a leading RNA medicines company
Building a leading RNA medicines company Differentiated RNA medicines Translating genetic insights into Unlocking platform and chemistry potentially best-in-class medicines emerging pipeline RNAi WVE-007 (obesity) • Extra-hepatic capabilities: • Differentiated mechanism with RNAi and RNA editing foc
Slide 5: For over a decade Wave has been extending the frontiers of RNA therapies
For over a decade Wave has been extending the frontiers of RNA therapies delivering breakthroughs in nucleic acid chemistry RNAi — SpiNA RNA editing — AIMer Protein reduction Ago2 loading 100% 80% 60% 40% 20% 0% C C N3U N3U Base 2’ deoxy 2’ OMe 2’ deoxy 2’ OMe Sugar Substantial improvements in poten
Slide 6: Robust RNA medicines pipeline with first-in-class RNAi and RNA editing programs
Robust RNA medicines pipeline with first-in-class RNAi and RNA editing programs Patient population Program Discovery IND / CTA Enabling Studies Clinical (US & Europe) R N A i ( S p i N A ) 175M WVE-007 (GalNAc) INHBE (obesity) (>1 billion globally) GalNAc / extra-hepatic -- Multiple R N A E D I T I
Slide 7: WVE-007 GalNAc-siRNA silencing Obesity
WVE-007 GalNAc-siRNA silencing Obesity 7
Slide 8: Obesity is a metabolic disease in need of a treatment paradigm shift
Obesity is a metabolic disease in need of a treatment paradigm shift Individuals living with obesity have higher risk for many serious health conditions, including heart disease, 1 type 2 diabetes, and some forms of cancer Current standard of care: GLP-1s WVE-007 Impact of GLP-1s is often limited by
Slide 9: Body composition improvements: reducing fat while preserving lean mass
Body composition improvements: Reducing fat, including visceral fat, while also preserving lean mass Reduce fat, including visceral fat Preserve lean mass, including muscle Increased visceral adiposity is associated Maintaining metabolic rate with many diseases including cardiometabolic disorders In
Slide 10: Human genetic data show INHBE loss-of-function carriers have healthy metabolic profile
Human genetic data demonstrate that heterozygous INHBE loss-of-function (LoF) carriers have a healthy metabolic profile Heterozygous INHBE LoF carriers have favorable traits: Heterozygous INHBE LoF carriers have lower risk of lower abdominal obesity, lower triglycerides, higher HDL-c Type 2 diabetes
Slide 11: Silencing INHBE mRNA has the potential to treat obesity
Silencing INHBE mRNA has the potential to treat obesity and associated metabolic diseases Release of dimerized Binds to and activates ACVR1C Block adipose INHBE subunits creates (ALK7) receptor in adipose tissue lipolysis hepatokine Activin E Activin E Activin E Increased abdominal adiposity leads t
Slide 12: Single dose of INHBE GalNAc-siRNA led to shrinkage of adipocytes in DIO mice
A single dose of INHBE GalNAc-siRNA led to shrinkage of adipocytes in DIO mice Mean adipocyte diameter DIO Lean PBS INHBE GalNAc-siRNA (μm) ✱✱✱ 80 60 40 20 0 Lean DIO DIO PBS INHBE GalNAc- siRNA 12 Data presented at ADA Scientific Sessions June 2025 ***p<0.001; Day 28
Slide 13: INHBE siRNA led to lower inflammatory state of visceral adipose tissues
A single dose of INHBE siRNA led to a lower inflammatory state of visceral adipose tissues in DIO mice, with strong suppression of pro-inflammatory M1 macrophages in visceral fat Macrophages (Mᶲ) (F4/80) Pro-inflammatory (M1) Mᶲ Anti-inflammatory (M2) Mᶲ (CD11c) (CD163) INHBE GalNAc siRNA INHBE GalN
Slide 14: 58% reduction of adipose fibrosis with INHBE siRNA
Lowering of inflammatory state of epiWAT visceral fat induced by single dose of INHBE siRNA resulted in 58% reduction of adipose fibrosis Reduced staining illustrates decreased tissue fibrosis Fibrosis in mouse adipose (Day 56) 10 mg/kg PBS 3 mg/kg ✱ 15 10 5 0 PBS 3 mg/kg 10 mg/kg 14 Data are means
Slide 15: Higher circulating Activin E correlated with higher BMI and abdominal fat
Higher circulating Activin E levels are correlated with higher BMI, higher abdominal fat, and higher fasting insulin in non-diabetic adults BMI Fasting Insulin Abdominal Fat Further supports INHBE suppression as a weight loss approach for individuals living with obesity 15 Ref: Dubey et al. Activin
Slide 16: WVE-007 expected to drive fat reduction and improve cardiometabolic health
Treatment with WVE-007 (investigational INHBE GalNAc-siRNA) is expected to drive fat reduction and improve key measures of cardiometabolic health 1 Driving fat reduction And improving clinical outcomes Leading siRNA design (SpiNA) WVE-007 Reduction of INHBE mRNA and (INHBE GalNAc-siRNA) circulating
Slide 17: Single dose led to durable Activin E reductions and body composition improvements in mice
Single dose of INHBE GalNAc-siRNA led to durable Activin E reductions, and sustained improvements in body composition in DIO mice Muscle Durable Activin E Reduction in fat Reduction in body weight ✓ ✓ ✓ preservation ✓ reduction Serum Activin E Epididymal fat weight Quadricep weight Single dose INHBE
Slide 18: WVE-007 potential with GLP-1s or to curtail weight regain
WVE-007 has potential for use synergistically with GLP-1s or to curtail weight regain after the cessation of treatment with GLP-1, based on preclinical data Combined with GLP-1: Greater weight loss After cessation of GLP-1: Curtails weight regain ✓ ✓ p<0.05 ~2x greater weight loss Not significant Da
Slide 19: INLIGHT: Clinical trial of WVE-007 in overweight or obesity
INLIGHT: Clinical trial of WVE-007 in individuals living with overweight or obesity Randomized, double-blind, placebo-controlled study with multiple clinical trial sites, including US Phase 1 SAD Phase 2a MAD SAD Cohort 4 Key study criteria: 600 mg (n=32) • Individuals with higher • HbA1c: <5.9 BMI
Slide 20: Body composition improvements three months after single WVE-007 dose
Improvements in body composition observed at three months after a single WVE-007 dose (lowest therapeutic dose); durability supports 1-2x yearly dosing Highly durable, dose dependent, serum Activin E Reductions in visceral and total fat mass with preservation reductions support dosing once or twice
Slide 21: Fat loss similar to GLP-1 at three months without muscle loss
Single dose of WVE-007 led to improvements in body composition with fat loss similar to GLP-1 at three months without muscle loss 1. For INLIGHT, all DEXA percentage changes and p-values are model-based, using the SAP pre-specified analysis. 2. For BELIEVE, all data points are approximate and based
Slide 22: Visceral fat is associated with insulin sensitivity, MASH, type 2 diabetes and CVD
Visceral fat is associated with insulin sensitivity and incidence of MASH, type 2 diabetes and cardiovascular disease Visceral fat reduction is associated with multiple Visceral fat increases risk of 5 health benefits cardiovascular disease Health Outcome Visceral Fat Reduction Associated Benefits I
Slide 23: Potential to address more than one billion individuals with obesity globally
Potential to address more than one billion individuals with obesity globally Monotherapy Add-on Maintenance Single agent in individuals Combination with incretin An off-ramp post-incretin living with obesity treatments treatments • To induce fat loss with muscle • To leverage an orthogonal • To prev
Slide 24: WVE-006 RNA editing (AIMer) Alpha-1 antitrypsin deficiency (AATD)
WVE-006 RNA editing (AIMer) Alpha-1 antitrypsin deficiency (AATD) 24
Slide 25: AATD impacts multiple organ systems and has limited treatment options
AATD impacts multiple organ systems and has limited treatment options • AATD is a rare, inherited genetic disorder that is commonly caused by a G-to-A point mutation in the SERPINA1 gene • Pi*ZZ genotype is leading cause of severe AATD, predisposing to progressive lung damage, liver damage or both •
Slide 26: WVE-006: potential first-in-class, convenient therapy for AATD
WVE-006: Potential first-in-class, convenient therapy for AATD that addresses both liver and lung manifestations of the disease WVE-006 Restore circulating M-AAT 1 2 Reduce Z-AAT protein (RNA editing) and physiological AAT ✓ ✓ aggregation in liver protein production Proprietary ✓ chemistry Highly sp
Slide 27: RNA editing aims to increase M-AAT and restore physiological AAT production
RNA editing aims to increase M-AAT and restore physiological AAT production during acute phase response Genotype Null Pi*ZZ Pi*MZ Pi*MM No AAT protein 100% Z-AAT Z-AAT and M-AAT 100% M-AAT AAT levels increase during No No Yes Yes acute phase response Risk of lung disease Very high High Low Normal Ri
Slide 28: RNA editing aims to restore dynamic AAT levels during acute phase response
RNA editing aims to restore production of dynamic and therapeutically relevant levels of AAT protein in Pi*ZZ individuals during acute phase response Lung damage occurs during exacerbations, when AAT protein has protective functions and is produced more AAT protein is needed for protection during ac
Slide 29: First demonstration of restoring physiological serum AAT production
First-ever demonstration of ability to restore physiological serum AAT production; total AAT reached 20.6 µM during acute phase response Pi*ZZ patients have a reduced capacity to produce AAT protein during an acute phase response 1 Following WVE-006 200 mg single dose, total AAT and M-AAT increased
Slide 30: WVE-006 enables endogenous AAT production while augmentation therapy may leave patients at risk
WVE-006 enables endogenous AAT production during an acute phase response while augmentation therapy may leave patients at risk Illustrative model of impact of acute phase response Augmentation therapy WVE-006 treatment approach Lung Protected damage lungs Endogenous AAT levels increase during acute
Slide 31: WVE-006 achieved key treatment goals of restoring MZ phenotype
CRP (mg/L) WVE-006 achieved key treatment goals of restoring MZ phenotype Total AAT levels exceeded 11 µM, production of wild-type M-AAT of greater than 50%, restored physiological AAT production Plasma AAT of ~13 µM Wild-type M-AAT protein of 64% AAT reached >20 μM during an of total, reduction in
Slide 32: RestorAATion-2 clinical trial ongoing
RestorAATion-2 clinical trial ongoing; 400 mg MAD data expected in 1Q 2026 and 600 mg SAD and MAD data expected in 2026 RestorAATion-1: Healthy Volunteers RestorAATion-2: AATD Patients RestorAATion-1: Healthy Volunteers SAD → MAD Multi-dosing complete 600 mg SAD Cohort 3 MAD Cohort 3 600 mg 600 mg;
Slide 33: WVE-008 RNA editing (AIMer) PNPLA3 I148M liver disease
WVE-008 RNA editing (AIMer) PNPLA3 I148M liver disease 33
Slide 34: WVE-008 for PNPLA3 I148M liver disease
WVE-008 for PNPLA3 I148M liver disease GalNAc-RNA editing approach uniquely aims to restore PNPLA3 function to fully address disease Homozygous PNPLA3 I148M carriers Heterozygous carriers have 80% lower risk of liver-related death as have significantly higher risk of compared to homozygous carriers
Slide 35: Silencing PNPLA3 in normal liver may worsen basal physiological functions
Worsening Silencing of PNPLA3 in normal liver may worsen basal physiological functions Silencing PNPLA3 increases Silencing PNPLA3 worsens steatosis in PNPLA3 siRNA exacerbates the fibrotic 1 2 iPSC-derived human liver organoids inflammation-induced liver cell death in response in hepatic stellate c
Slide 36: RNA editing expected to restore PNPLA3 function across stages of liver disease
RNA editing is expected to restore PNPLA3 function to treat across the stages of liver diseases RNA editing approach ✓ PNPLA3 I148M aggravates steatosis Silencing PNPLA3 may only partially PNPLA3 correction expected to and fibrosis through gain-of-function address disease restore function, counter l
Slide 37: AIMers achieve efficient editing of PNPLA3, reducing liver fat
AIMers achieve efficient editing of PNPLA3, leading to reduction of liver fat ✱✱✱✱ Significant decrease in liver fat with PNPLA3 editing in human HEPATOPAC® model with homozygous I148M ns 1500 1000 500 PBS PNPLA3 PNPLA3 siRNA AIMer 0 Decrease in liver fat with WVE-008 in monolayer model PNPLA3 siRNA
Slide 38: Preclinical data support WVE-008 as potential first-in-class therapy
Preclinical data support WVE-008 as potential first-in-class, disease modifying therapy, for treatment of PNPLA3 I148M liver disease Tissue exposure supports excellent Potent editing with WVE-008 Highly specific editing with WVE-008 delivery 1000 100 Semi-log scale 10 0 5 10 15 20 25 Time (day) Expe
Slide 39: Bifunctional modalities Single oligonucleotide constructs
Bifunctional modalities Single oligonucleotide constructs 39
Slide 40: Reimagining RNA medicines: Bifunctional modalities
Reimagining RNA medicines: Bifunctional modalities ✓ Engage both endogenous Ago2 AGO2 and ADAR enzymes, as well as AGO2 dual RNAi silencing ✓ Silence multiple targets or silence Single one target while simultaneously Single Oligonucleotide Oligonucleotide editing or upregulating another Construct Co
Slide 41: Other clinical programs Duchenne muscular dystrophy Huntington's disease
Other clinical programs Duchenne muscular dystrophy Huntington’s disease 41
Slide 42: Advancing WVE-N531 in exon amenable DMD
Advancing WVE-N531 in exon 53 amenable DMD WVE-N531: exon skipping oligonucleotide designed to induce production of endogenous, functional dystrophin protein • High unmet need for therapies delivering more consistent dystrophin expression, as few patients today achieve dystrophin >5% of normal • Opp
Slide 43: FORWARD-53 48-week clinical trial results for WVE-N531
FORWARD-53 48-week clinical trial results: WVE-N531’s potential best-in- class profile for boys amenable to exon 53 skipping Statistically significant and clinically meaningful improvement (3.8s) in Time-to-Rise vs. ✓ natural history; functional benefits on other measures including NSAA Statisticall
Slide 44: Advancing WVE-003 to address HD across all stages of disease
Advancing WVE-003 to address HD across all stages of disease WVE-003 is a first-in-class, allele-selective oligonucleotide for the treatment of HD • HD is a monogenic autosomal dominant genetic disease; fully penetrant and affects entire brain • No current disease modifying therapies for HD • Charac
Slide 45: WVE-003 leads to allele-selective mHTT reduction, correlating with slowing of caudate atrophy
WVE-003 leads to allele-selective mHTT reduction, correlating with slowing of caudate atrophy Allele-selective mHTT Slowing of Caudate Silencing with wtHTT Functional Benefit Atrophy Preservation • mHTT reduction of up to • WVE-003 trended towards • Caudate atrophy is an 46% vs. placebo less caudate
Slide 46: Reimagining RNA medicines
Reimagining RNA medicines 46
Slide 47: Poised for significant and sustained growth driven by RNAi and RNA editing
Poised for significant and sustained growth driven by RNAi and RNA editing Other hepatic targets Extra-hepatic targets RNAi WVE-007 Obesity SpiNA Bifunctional single oligonucleotide constructs RNA WVE-006 AATD Editing WVE-008 Other hepatic targets AIMers PNPLA3 I148M liver disease Extra-hepatic targ
Slide 48: Anticipated upcoming milestones
Anticipated upcoming milestones • Deliver 6-month 240 mg data and 3-month 400 mg data in 1Q 2026 WVE-007 • Initiate Phase 2a multidose portion of INLIGHT in individuals living (INHBE) with obesity with higher BMI and comorbidities in 1H 2026 Obesity • Initiate new trials evaluating WVE-007 as an inc
Slide 49: For questions contact: investorrelations@wavelifesci.com
For questions contact: investorrelations@wavelifesci.com
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