Slide 1: Rewriting the story of disease
Rewriting the story of disease Third Quarter 2026
Slide 2: Disclaimers
Disclaimers Any statemen ts made in this presentation that are not statemen ts of historical fact, including statemen ts about ou r beliefs and expectations, are forward-looking statemen ts and should be evalu ated as such. Forward- looking statemen ts include infor mation con cerning the timing and
Slide 3: Discipline Enabled by Expertise
Team Discipline Enabled by Expertise Built with Nobel Prize-winning science Our founder-led focus on developing highly Benjamin Oakes, PhD Jennifer Doudna, PhD Dave Savage, PhD Brett Staahl, PhD engineered genetic medicines for all drives Co-founder, CEO Co-founder, SAB Co-founder, SAB Co-founder, V
Slide 4: A Unique Mission
A Unique Mission Founded to purpose-build in vivo CRISPR medicines to enable the treatment of us all Starting with: preventing leading cause of death: ASCVD Rewriting the story of disease. 4
Slide 5: Proprietary Approach
Proprietary Approach Enhancing CRISPR to evolve the opportunity: from restoring health to preventing disease with Editing & Silencing TECHNOLOGIES: Improving health PROPRIETARY ELXR: Epigenetic Silencing APPROACH: ENGINEERING ENGINES Transferring CONTINUOUS SYSTEMATIC protective genetic ITERATIONS e
Slide 6: Fully committed to delivering cardioprotective genetics
Pipeline Fully committed to delivering cardioprotective genetics for the prevention and treatment of disease: LDL-C, Lp(a) & TGs LEAD IND- DISCOVERY PHASE I PHASE 2 PHASE 3 ANTICIPATED MILESTONES OPTIMIZATION ENABLING Clinical trial initiated: ELXR: Epi STX-1150 Mid 2026 Silencing LDL-C LOWERING Fir
Slide 7: Expanding our impact through strategic collaborations
Strategic Collaborations In vivo Sickle Cell Disease & Expanding our impact Other Therapies through strategic collaborations $65m 2 $1.2b+ UPFRONT ANNOUNCED FUTURE A portfolio of partnership PAYMENTS PROGRESS MILESTONES MILESTONES programs aimed at TO DATE + CO-PROMOTE OPTION accelerating CRISPR med
Slide 8: Cardiometabolic Programs: LDL-C
Cardiometabolic Programs: LDL-C Broadly delivering cardioprotective genetics: Silencing PCSK9 for LDL-C lowering, ASCVD prevention, and treatment STX-1150 Epigenetic Silencing of PCSK9 for LDL-C Lowering ELXR: Epigenetic Silencing Improving health STX-1200 STX-1400 Rewriting the story of disease. 8
Slide 9: Current modalities to treat and prevent ASCVD fall short
Cardiometabolic Programs: LDL-C The Current Paradigm Current modalities to treat and prevent ASCVD may appear clinically effective but fall short in real-world situations Current approaches Fundamental limitations to LDL-C Lowering Study: Max. LDL-C Lowering in clinical setting Discontinuation rate
Slide 10: The solution: natural genetic cardioprotection via PCSK9 modifications
Cardiometabolic Programs: LDL-C The Solution The solution: 1-3% of the population are born “lucky” with natural genetic cardioprotection via PCSK9 modifications STX-1150: Ultra-long-acting PCSK9 Silencing to recapitulate genetic cardioprotection Engineered to deliver the potency, persistence, and sa
Slide 11: ELXR Silencing: lowers mRNA levels similar to RNAi
STX-1150: Epigenetic LDL-C Lowering ELXR Silencing: lowers mRNA levels similar to RNAi with the potential for substantial advantages in durability and efficacy Lipid nanoparticle ELXR mRNA & gRNA LDLR:LDL binding Hepatocyte LDLR:LDL Open chromatin Closed chromatin PCSK9 ELXR acts at mRNA PCSK9 TSS m
Slide 12: NHP Efficacy: single dose reduces LDL-C by 52-68%
STX-1150: Epigenetic LDL-C Lowering Non-Clinical Data NHP Efficacy: A single dose of a STX-1150 prototype reduces LDL- C by 52-68% for at least two years in non-human primates ELXR mRNA ELXR gRNA Robust, durable, LDL-C reduction observed at all doses Lowest dose coh ort extended for durability analy
Slide 13: Tolerability: target specific knockdown and primate tolerability
STX-1150: Epigenetic LDL-C Lowering Non-Clinical Data Tolerability: Orthogonal assessments demonstrate target specific knockdown in vitro and strong in vivo primate tolerability No off-target gene expression changes ALT and TBIL elevation at 0.75mg/kg are observed at 3X EC90* in human hepatocytes in
Slide 14: Dose translation: potency testing on the human genome
STX-1150: Epigenetic LDL-C Lowering Non-Clinical Data Dose translation: Manufacturing and potency testing on the human genome demonstrates the potential for silencing at lower doses STX-1150 achieves saturating reduction of serum STX-1150 demonstrates at least 5x hPCSK9 in at 0.6 mg/kg dose greater
Slide 15: STX-1150 aims to improve adherence and persistence
STX-1150: LDL-C Standard Of Care STX-1150 aims to substantially improve on adherence and persistence by mimicking cardioprotective genetics, without genetic changes Atorvastatin Evolucumab Inclisiran and other orals STX-1150 Small molecule Monoclonal antibody siRNA Epigenetic silencer LDL-C lowering
Slide 16: Study Design
STX-1150: Clinical Steps First-in-human focuses on patients with hypercholesterolemia & elevated CV risk; interim data readout projected for 1H 2027 2027 Study population: Adult pts with elevated LDL-C 2026 2025 Study Design & elevated CV risk Primary objective: Safety and tolerability Initial data
Slide 17: STX-1150: Commercial Case
STX-1150: Commercial Case STX-1150 has the unique potential to return value to stakeholders across the full ecosystem of ASCVD care LLT treatment landscape today1 Is there an 1.5m ASCVD is the number 1 killer, and 2% 1 < % unmet need? Heart attacks and strokes despite available treatments it’s not e
Slide 18: Restoring genetic health associated with ASCVD risk
Pipeline & Technology Restoring genetic health associated with ASCVD risk: Solving for the genetics of severely elevated Lp(a) & Triglycerides STX-1150 XE: Gene Editing Restoring health Genetic solutions for genetic disease STX-1200 LPA GENE EDITING STX-1400 APOC3 GENE EDITING Rewriting the story of
Slide 19: XE Engineering: Proof in Execution
XE Engineering: Proof in Execution Engineering XE for safer and broader use: Achieving saturating editing in NHP liver with greater safety than Cas9 and other previous systems XE is the first non-Cas9 XE is >125 changes XE has no observed off-targets at 10x supersaturating doses CRISPR demonstrated
Slide 20: Cardiometabolic Programs: Lp(a)
>80m Cardiometabolic Programs: Lp(a) Lp(a) is genetically Lp(a) is a strong risk factor for controlled: lifestyle various Cardiovascular Diseases PATIENTS LIVING WITH changes do not ELEVATED Lp(a) impact Lp(a) levels driven by genetic changes in the IN THE US & EU LPA gene This lifetime risk of 2x L
Slide 21: STX-1200 prototype potently edits and reduces serum Apo(a)
STX-1200: XE Lp(a) Lowering A STX-1200 prototype has been shown to potently edit and reduce serum Apo(a) protein in a transgenic mouse model at 0.2-0.4mpk Saturating hepatocyte editing achieved by STX-1200 prototype substantially reduces Apo(a) protein secretion by >90% in vivo Est. max hepatocytes
Slide 22: No observable off-target editing in primary human hepatocytes
STX-1200: XE Lp(a) Lowering No observable off-target editing at >125 candidate off-target sites in primary human hepatocytes treated with STX-1200 prototype No candidate off-target sites showed significant editing at a 10X supersaturating dose 1200 on target site Net indel rate (STX-1200 – control)
Slide 23: STX-1200 surrogate reduces plasma Apo(a) in non-human primates
STX-1200: XE Lp(a) Lowering A STX-1200 prototype surrogate potently reduces plasma Apo(a) levels in the liver of non-human primates Editing at LPA locus Reduction of plasma Apo(a) levels ~97% (from baseline) Rewriting the story of disease. 23
Slide 24: Cardiometabolic Programs: Triglycerides
Cardiometabolic Programs: Triglycerides High TG levels are Epidemiological studies Severely elevated TGs are a controlled by genetics in show an association the severe FCS and MCS between higher TRLs and significant risk factor for acute populations risk of ASCVD pancreatitis in FCS & SHTG and ELEVA
Slide 25: STX-1400 prototype reduces APOC3 protein and triglycerides
STX-1400: XE Triglyceride Lowering STX-1400 prototype readily reduces APOC3 protein and triglycerides by >90% and total cholesterol by >80% in mouse model of disease STX-1400 prototype reduces APOC3 protein, triglyceride, and total cholesterol in hypertriglyceridemic mice Mouse serum Control ~96% ~9
Slide 26: No observable off-target editing for STX-1400 prototype
STX-1400: XE Triglyceride Lowering No observable off-target editing at >200 candidate off-target sites in primary human hepatocytes treated with STX-1400 prototype No candidate off-target sites showed significant editing at a 10X supersaturating dose 1400 on target site Off-target site Net indel rat
Slide 27: STX-1400 surrogate edits APOC3 locus in primates
STX-1400: XE Triglyceride Lowering In non-human primates, STX-1400 prototype surrogate potently edited APOC3 locus in the liver, without significant LFT elevations STX-1400 surrogate prototype saturates ALT and total bilirubin levels at therapeutically relevant doses editing at 1.0 mg/kg are indisti
Slide 28: Scribe's Vision
Scribe’s Vision Rewrite the story of disease: from late symptom intervention No intervention HEALTHSPAN Medicine today LIFESPAN Rewriting the story of disease. 28
Slide 29: Scribe's Vision: To Genetic Prevention
Scribe’s Vision Rewrite the story of disease: To Genetic Prevention with genetic medicines safe and effective enough to be preventative for all Genetic Tx No intervention HEALTHSPAN Potential Extensions in Healthspan Medicine today And Lifespan LIFESPAN Rewriting the story of disease. 29
Slide 30: Anticipated Key Milestones
Catalysts Anticipated Key Milestones STX-1150 First patient for elevated LDL-C in mid-2026 LDL-C Initial clinical data in 1H2027 STX-1200 Lp(a) Clinical entry as early as 2027 STX-1400 Initial data 2028 TG Partnerships Sanofi and Eli Lilly partnership updates Technology Continued engineering and evo
Slide 31: Thank you
Thank you Lipid nanoparticle technology provided by