Kodiak Sciences Inc · NASDAQ:KOD

Kodiak Sciences — Jefferies Global Healthcare Conference 2026

78 slides from Kodiak Sciences's conference presentation, June 2026

  1. Slide 1: Jefferies Global Healthcare Conference

    THE OPHTHALMOLOGY MEDICINES COMPANY Jefferies Global Healthcare Conference June 2026

  2. Slide 2: Forward-Looking Statements

    Forward-Looking Statements This presentation may contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 and other federal securities laws, including statements regarding Kodiak’s plans, commitments, aspirations and goals related to Kodiak’s drug

  3. Slide 3: Kodiak is emerging into a fully integrated Vision Sciences company

    Kodiak is emerging into a fully integrated Vision Sciences company VETi: Visual Engagement Technology and imager 3

  4. Slide 4: Late-stage clinical portfolio and emerging pipeline across retina mechanisms

    We have both a late-stage clinical portfolio and an emerging pipeline that span multiple retina mechanisms of action, indications and drug types Estimated prevalence across leading causes of vision loss (U.S.) ABC: antibody biopolymer conjugate; MESI: macular edema secondary to inflammation; AMD: ag

  5. Slide 5: Three late-stage clinical assets target leading causes of vision loss

    Our three late-stage clinical assets target leading causes of vision loss KSI-101 Zenkuda KSI-501 ~146M9 Phase 3 Phase 3 Phase 3 Anti-IL-6, VEGF Trap Anti-VEGF Anti-IL-6, VEGF Trap Intravitreal Protein Intravitreal ABC® Intravitreal ABC® MESI wAMD, DR, RVO wAMD, DME ~32M6,7 ~9.6M U.S.8 ~28M4 Estimat

  6. Slide 6: All three clinical programs in Phase 3; Zenkuda is BLA ready

    We are gathering speed: all three clinical programs are in Phase 3 with topline data expected in 2026 and Zenkuda is BLA ready KSI-101 Zenkuda KSI-501 Anti-IL-6, VEGF trap Anti-IL-6, VEGF trap Anti-VEGF ABC® biologic bispecific ABC® biologic bispecific protein Differentiated efficacy, Strong immedia

  7. Slide 7: Four Phase 3 readouts in 2026 position Kodiak for three BLAs

    Four Phase 3 readouts in 2026, if successful, position Kodiak to file 3 licensing applications (BLA) in 2026 and 2027 4 successful pivotal 3 additional topline data Licensing applications (BLA) studies completed readouts expected in 2026 3 expected in 2026 and 2027 ZENKUDA 3Q ‘26 4Q ‘26 1Q ‘27 2Q ‘2

  8. Slide 8: Investment in commercial manufacturing positions Kodiak for launch

    Significant investment in commercial manufacturing has positioned Kodiak well for potential launch of multiple ABC® products into large and growing markets Ursus, a premium commercial manufacturing facility dedicated to the manufacture of Kodiak’s ABC® medicines • Custom designed for large scale pre

  9. Slide 9: Therapeutics

    lr THERAPEUTICS KADIAK

  10. Slide 10: Kodiak's ABC Platform Science for Retina

    ZENKUDA + KSI-501 Kodiak’s ABC® Platform Science for Retina 10

  11. Slide 11: The ABC Platform supports science of immediacy and durability

    The ABC Platform supports Kodiak’s science of immediacy and durability Designed-in High Extended Extended Powerful Immediacy Extended Extended Tissue In-Vitro Ocular Half- Ocular Half- via Unconjugated Clinical Durability via Residence Time Potency Life in Animals Life in Humans Antibody Conjugated

  12. Slide 12: Durability: ABC Platform-based medicines designed for longer ocular durability

    Durability: ABC® Platform-based medicines are designed for longer ocular durability ABC® Platform-based medicines have a high molecular weight which increases their ocular half-life compared to today’s intravitreal biologics 950 kDa 1000 kDa Immediacy Durability KSI-501 Zenkuda Achieved with lower I

  13. Slide 13: Zenkuda mean ocular half-life in humans of 20 days

    Durability: Zenkuda has a mean ocular half-life in humans of 20 days, which is 3-fold longer than faricimab 19.8 days (Mean) ~3x longer than faricimab 10-90th percentiles Zenkuda 8.3 31.8 (10th percentile) (90th percentile) Faricimab 10-90th percentiles 5.2 11.2 (10th percentile) (90th percentile) H

  14. Slide 14: Zenkuda and KSI-501 combine unconjugated and conjugated protein

    Zenkuda and KSI-501 combine unconjugated and conjugated protein, enabling high immediacy and high durability in a single biologic Zenkuda – 5 mg KSI-501 – 5 mg I M M ED I A CY I M M ED I A CY 1.0 mg 1.5 mg Unconjugated Unconjugated + + D U R A B I LI T Y D U R A B I LI T Y 4.0 mg 3.5 mg ABC (conjuga

  15. Slide 15: Retinal Vascular Diseases and the Anti-VEGF Market

    ZENKUDA + KSI-501 Retinal Vascular Diseases and the Anti-VEGF Market 15

  16. Slide 16: Open space in the ~$15B retinal vascular diseases market

    There remains valuable open space in the ~$15B retinal vascular diseases market, despite the availability of approved biologics and clinical trials of new exploratory technologies Approved mainstay biologics provide: The poised opportunity is a biologic with: Gen 1.0 Gen 1.5 High Immediacy/Efficacy

  17. Slide 17: Gen 1.0 and Gen 1.5 biologics are meaningful for patients and physicians

    The Gen 1.0 biologics that provide immediacy and the Gen 1.5 biologics that provide immediacy and incremental durability are meaningful for patients and physicians Dosing regimen per label for approved intravitreal biologics and estimated worldwide sales in 2025 Wet AMD DME ~718M in 20251,2 DR RVO G

  18. Slide 18: Real-world wAMD data show patients falling short of durability promise

    Despite their commercial success, real-world data in wAMD show that most patients are falling short of the durability promise of the Gen 1.5 labels Faricimab injections observed after the first 6 months of treatment through Year 2 in the FARENTINA study1 Treatment-Naïve Eyes (n=389a) Year 2: In Year

  19. Slide 19: Implants and gene therapies engineer durability but lack immediacy

    Technologies being explored in clinical trials, including implants and gene therapies, are engineering for high durability but are lacking immediacy Implants Gene Therapies • Engineering for durability • Engineering for durability • Long-term safety unknown • Onerous monitoring and inflammation cont

  20. Slide 20: ABC Enabled Mainstay Biologics Target Product Profiles

    ABC® Enabled Mainstay Biologics Target Product Profiles Zenkuda and KSI-501: Differentiated ABC platform mainstay biologics Target product profiles ZENKUDA Anti-VEGF ABC® biologic KSI-501 Anti-IL-6, VEGF trap bispecific ABC® biologic 21

  21. Slide 21: Complementary and differentiated product profiles support a broad retinal franchise

    Zenkuda and KSI-501’s complementary and differentiated product profiles support a broad retinal franchise Primary 6-Month Phase 3 Study Endpoint Durability Across 4 pivotal studies, Zenkuda demonstrated: ZENKUDA • Non-inferior efficacy with 6-month predominant durability RVO • Favorable and well-tol

  22. Slide 22: Zenkuda in RVO: capture share in a large >$3B market

    Zenkuda in Retinal Vein Occlusion: Well-positioned to capture meaningful share in a large and growing >$3B RVO market • RVO is a meaningful and growing market Zenkuda is designed to address • ~3B estimated RVO market1 key unmet needs in RVO4 ‒ ~20% of Eylea net sales derived from RVO in 20252 • ~1M

  23. Slide 23: Zenkuda in RVO: high efficacy and durability in BEACON

    Zenkuda in Retinal Vein Occlusion: Demonstrated high efficacy and industry-leading durability in the Phase 3 BEACON study Phase 3 Zenkuda: Number of doses Number of injections through Year 1 in the second 6 months of Year 1 BEACON 50% Primary 4-6 doses: 2% Endpoint 3 doses: 5% 78% 40% 93% received r

  24. Slide 24: Comparable outcomes in all RVO patients irrespective of treatment paradigm

    Zenkuda achieved comparable visual and anatomical outcomes in all RVO patients, irrespective of the treatment paradigm used Fixed Dosing (0-24) Head-to-head Individualized Dosing (24-48) Doubling of treatment interval Zenkuda vs aflibercept With two fewer doses (4 vs 6), 75% achieved 6-month durabil

  25. Slide 25: Zenkuda in Diabetic Retinopathy: large, undertreated disease

    Zenkuda in Diabetic Retinopathy: A large, undertreated disease with meaningful risk progression ~9.6M DME can occur at any stage DR can progress quickly into vision- People in the threatening PDR or DME3 U.S. have DR1,2 • DME can occur at any stage, but the risk • Damage occurring in eye increases a

  26. Slide 26: A durable anti-VEGF therapy could expand treatment in DR

    Zenkuda in Diabetic Retinopathy: A durable anti-VEGF therapy could expand treatment in DR ~9% treated with anti-VEGF therapy in 20251 Zenkuda’s 6-month dosing has the potential to expand anti-VEGF • While higher than previously estimated, use remains low adoption • DR is often asymptomatic and ~9% a

  27. Slide 27: Superiority in ≥2-step DRSS improvement in GLOW1 and GLOW2

    Zenkuda in Diabetic Retinopathy: Established superiority in ≥2-step improvement in DRSS in GLOW1 and GLOW2 Proportion of patients with ≥2-Step improvement in Diabetic Retinopathy Phase 3 Severity Score (DRSS) from Baseline to Week 48 100% of GLOW1 patients on GLOW2 6-month dosing at GLOW1 GLOW2 Year

  28. Slide 28: Reduced risk of sight-threatening complications by ≥85%

    Zenkuda in Diabetic Retinopathy: Reduced the risk of developing sight- threatening complications by ≥85% in GLOW1 and GLOW2 Proportion of patients developing sight-threatening complications Phase 3 from Baseline through Week 48 100% of GLOW1 patients on GLOW2 6-month dosing at Year 1 Superiority GLO

  29. Slide 29: Superiority in ≥3-step DRSS improvement in GLOW1 and GLOW2

    Zenkuda in Diabetic Retinopathy: Zenkuda established superiority in ≥3-step improvement in DR Severity Score (DRSS) in GLOW1 and GLOW2 Proportion of patients with ≥3-Step improvement in DRSS from Phase 3 Baseline to Week 48 100% of GLOW1 patients on GLOW2 6-month dosing at Year 1 Superiority 25% GLO

  30. Slide 30: GLOW studies show Zenkuda opens door to earlier treatment

    The GLOW studies show that Zenkuda opens the door to earlier treatment with only 2 doses a year – a transformative potential for millions of patients Baseline Week 48 U.S. Prevalence ~9,600,0001 Microhemorrhages visible on the retina even if no visual symptoms are present yet DR ~9% are currently Im

  31. Slide 31: Phase 3 DAYBREAK study in wAMD design

    Zenkuda and KSI-501 in wAMD: The ongoing Phase 3 DAYBREAK study is designed to evaluate immediacy, real-world durability and efficacy Zenkuda objective: Assess 6-month durability potential in wAMD Phase 3 DAYBREAK KSI-501 objective: Explore efficacy potential of bispecific IL-6 and VEGF inhibition i

  32. Slide 32: Potential implications and upsides for Zenkuda and KSI-501 in DAYBREAK

    What are the potential ABC® Enabledimplications and Target Mainstay Biologics upsides for Zenkuda Product Profiles and KSI-501 in DAYBREAK, if successful? ZENKUDA KSI-501 Strong and immediate disease control (closing the ‘immediacy’ gap) Better vision gains vs anti-VEGF mono- therapy (aflibercept Q8

  33. Slide 33: Gen 2.0 biologics designed for high-immediacy, high-durability quadrant

    Revisiting the core unmet need: Kodiak’s Gen 2.0 biologics are designed to occupy the high-immediacy, high-durability golden quadrant 34

  34. Slide 34: KSI-101 Macular Edema Secondary to Inflammation

    KSI-101 Macular Edema Secondary to Inflammation 35

  35. Slide 35: Macular edema spectrum: inflammation and/or VEGF driven

    Macular edema, the common clinical presentation of a wide spectrum of diseases, can be caused by inflammation and/or by VEGF over-expression Macular Edema Spectrum of Diseases Diabetic Macular Uveitis Edema Inflammation driven VEGF driven Retinal Vein Systemic or Occlusion Autoimmune Disease Myopic

  36. Slide 36: Macular edema and visual impairment shared irrespective of etiology

    Macular edema and visual impairment are shared clinical features irrespective of etiology or location of inflammation Anterior Intermediate Posterior Panuveitis Location of Inflammation Macular edema is a shared clinical feature irrespective of the anatomical location of inflammation or specific eti

  37. Slide 37: MESI caused by immune dysregulation and blood-retinal barrier breakdown

    MESI is caused by immune dysregulation, leading to blood-retinal barrier breakdown and release of inflammatory mediators Immune Trigger Blood-Retinal Barrier Breaks Down IL-6 and VEGF Amplify Leakage Causes immune cells to release IL-6 upregulates VEGF. IL-6 and VEGF cause VEGF promotes vascular lea

  38. Slide 38: Corticosteroids most used for MESI but carry safety risks

    Corticosteroids are used most often for MESI, but carry significant safety risks and efficacy can be limited Most frequently prescribed medications in patients • Steroids were the most with macular edema due to noninfectious uveitis, common medication class and across any line of therapy1 remain the

  39. Slide 39: Adverse effects from current MESI treatments

    Adverse effects from current MESI treatments can lead to complex, repeated surgeries and irreversible vision loss RETISERT® Label Visual damage from glaucoma (fluocinolone acetonide Cataract repair is complex in MESI intravitreal implant) and can be contraindicated, can be irreversible and can leadi

  40. Slide 40: Patient journey case: steroid-induced glaucoma with recurrent MESI

    Patient journey case: steroids induced glaucoma with recurrent MESI over the course of approximately 2 years 1 2 3 4 5 Trial of bromfenac IOP stable and Patient presented Developed drops with initial macular edema now Worsening in Aug. 2023 with a worsening of improvement then resolved after macular

  41. Slide 41: KSI-101 first-in-class high-strength intravitreal biologic

    KSI-101 is a first-in-class, high-strength intravitreal biologic designed to target IL-6 mediated inflammation and VEGF-mediated vascular permeability simultaneously KSI-101: high formulation strength (100 mg/mL) 42

  42. Slide 42: IL-6 and VEGF each disrupt the blood-retinal barrier

    IL-6 and VEGF each disrupt the blood-retinal barrier independently. When combined, they cause an even greater loss of barrier integrity Ocular inflammation Assessing vascular endothelial barrier integrity damages tight junctions using electrical resistance measurements between endothelial cells • Th

  43. Slide 43: KSI-101 restores barrier resistance greater than monotherapies

    Bispecific KSI-101 restores barrier resistance from pre-existing insult greater than anti-IL-6 or anti-VEGF monotherapies alone Preclinical model of endothelial cells simulating the blood-retinal barrier No Exposure to VEGF + IL-6/R: 150 150 high barrier resistance due to intact tight junctions KSI-

  44. Slide 44: KSI-101 multiple-dose results from APEX Phase 1b

    KSI-101 in MESI: Multiple-dose results from APEX Phase 1b study in the U.S. and a clinical cohort of Asian patients from tertiary uveitis centers Study Design: Open-label Phase 1b in MESI Baseline Characteristics APEX U.S. (N=41) Asia* KSI-101 Weeks 0 4 8 12 16 20 24 KSI-101 2.5 mg KSI-101 5 mg KSI-

  45. Slide 45: Vision gains of >10 letters after a single injection

    Meaningful vision gains of >10 letters were observed after a single injection with continued improvement through 24 weeks Mean Change in BCVA 20 15 Mean ETDRS letters 10 5 U.S. 2.5 mg U.S. 5 mg U.S. 10 mg Asia Pooled 0 0 4 8 12 16 20 24 Weeks 2.5 mg 13 13 13 13 13 13 13 12 U.S. 5 mg 13 13 13 13 13 1

  46. Slide 46: APEX U.S. top two doses achieve >10 letter gains by Week 4

    In APEX U.S., the top two dose levels achieve meaningful vision gains of >10 letters by Week 4 and continue to improve over time, achieving a 20/25 Snellen visual acuity by Week 20 Mean Change in BCVA over time Observed BCVA over time 20 80 Mean Change Mean ETDRS Letters Mean ETDRS Letters 15 +14.4

  47. Slide 47: More than half of patients achieved ≥15 letter gain

    More than half of patients achieved a ≥15 letter gain, with additional benefit observed in the top dose levels in the U.S. Proportion of ≥15 letter gainers 100 80 Patients, % 60 62 58 54 40 38 20 0 U.S. 2.5 mg U.S. 5 mg U.S. 10 mg Asia Pooled (n=13) (n=13) (n=13) (n=12) U.S. Asian Cohort Final resul

  48. Slide 48: KSI-101 consistently achieved dryness after a single injection

    KSI-101 consistently achieved dryness (CST 250-325 μm) after a single injection, with sustained dryness observed during follow-up Observed OCT CST 600 U.S. 2.5 mg U.S. 5 mg U.S. 10 mg Asia Pooled 500 Rapid improvement Mean CST (µm) demonstrated within 1 week 400 300 Dryness (CST 250 – 325) 200 0 1 4

  49. Slide 49: ≥90% achieved absence of both IRF and SRF

    In APEX U.S., ≥90% of patients in the top two dose levels achieved absence of both IRF and SRF. A recurrence in IRF was observed in some patients 8 to 12 weeks after the last study treatment Proportion of patients in the 5 and 10 mg Proportion of patients in the 5 and 10 mg (pooled) dose level achie

  50. Slide 50: KSI-101 has been well-tolerated

    KSI-101 has been well-tolerated Asia KSI-101 KSI-101 2.5 mg KSI-101 5 mg KSI-101 10 mg All KSI-101 pooled (n=13) (n=14) (n=14) (N=41) (N=13) Summary of AEs in the Study eye, n (%) Subjects with ≥1 AEs 2 (15.4) 3 (21.4) 2 (14.3) 7 (17.1) 3 (23.1) Treatment-related AEs 1 (7.7)a 1 (7.1)b 0 2 (4.9) 0 Se

  51. Slide 51: Single-dose KSI-101 rapid responses independent of location or etiology

    Single-dose KSI-101 demonstrates rapid, meaningful responses in MESI, independent of inflammation location or macular edema etiology Location of Inflammation Anterior Intermediate Posterior Panuveitis Day 1 Effect of Week 4 a single dose of KSI-101 Specific Macular Edema Etiology Juvenile Focal Chor

  52. Slide 52: Mean Change in OCT CST and Absolute CST

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Week 4 Week 4 450 450 OCT CST (µm) OCT CST (µm) Week 8 Week 8 400 400 Week 12 Week 12 350 350 Week 16 Week 16 300 300 Dryness (CST 250 – 325) 250 250 2.5 mg 5 mg 10 mg 0.25 mg 1 mg 2.5

  53. Slide 53: Rapid onset of action observed with KSI-101

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week Effect of a Effect of a Week11 Week 11 Week 500 single dose single dose 500 Week 4 Week 4 450 450 OCT CST (µm) OCT CST (µm) Week 8 Week 8 400 400 Week 12 Week 12 350 350 Week 16 Week 16 300 300 Dryness

  54. Slide 54: Dryness levels observed with a single dose of KSI-101

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Effect of a Effect of a Week44 Week Week 4 Week 4 single dose single dose 450 450 OCT CST (µm) OCT CST (µm) Week 8 Week 8 400 400 Week 12 Week 12 350 350 Week 16 Week 16 300 300 Drynes

  55. Slide 55: Dryness levels with a single dose: effect of 2 doses

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Effect of a Week44 Week Week 4 single dose 450 450 Effect of 2 OCT CST (µm) OCT CST (µm) Week 8 Week 8 Week 8 doses 400 400 Week 12 Week 12 350 350 Week 16 Week 16 300 300 Dryness (CST

  56. Slide 56: Dryness levels with a single dose: effect of 3 doses

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Effect of a Week44 Week Week 4 single dose 450 450 OCT CST (µm) OCT CST (µm) Week 8 Week 8 400 400 Effect of 3 Week 12 Week Week 12 12 doses 350 350 Week 16 Week 16 300 300 Dryness (CS

  57. Slide 57: Single dose of KSI-101 deeper drying than 4 doses of anti-IL-6

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Effect of a Week44 Week Week 4 single dose 450 450 OCT CST (µm) OCT CST (µm) Week 8 Week 8 400 400 Week 12 Week 12 350 Effect of 4 350 Week 16 Week Week 16 16 doses 300 300 Dryness (CS

  58. Slide 58: Continued dosing with KSI-101 deepens dryness

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Week 4 Week 4 450 450 Effect of 2 OCT CST (µm) OCT CST (µm) Week88 Week Week 8 doses 400 400 Week 12 Week 12 350 Effect of 4 350 Week 16 Week Week 16 16 doses 300 300 Dryness (CST 250

  59. Slide 59: Continued dosing with KSI-101 deepens dryness

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Week 4 Week 4 450 450 OCT CST (µm) OCT CST (µm) Week 8 Week 8 400 400 Effect of 3 Week1212 Week Week 12 doses 350 Effect of 4 350 Week 16 Week Week 16 16 doses 300 300 Dryness (CST 250

  60. Slide 60: Dual inhibition of IL-6 and VEGF provides synergistic drying

    Mean Change in OCT CST and Absolute CST APEX3 DOVETAIL1 MEERKAT2 SANDCAT2 550 Day 1 Day 1 550 Week 1 Week 1 500 500 Week 4 Week 4 450 450 OCT CST (µm) OCT CST (µm) Week 8 Week 8 400 400 Week 12 Week 12 350 Effect of 4 Effect of 4 350 Week1616 Week Week Week 16 16 doses doses 300 300 Dryness (CST 250

  61. Slide 61: Phase 3 Program in MESI – PEAK and PINNACLE study design

    Actively Enrolling The Phase 3 Program in MESI – PEAK and PINNACLE study design Fixed monthly dosing Individualized dosing Weeks D1 4 8 12 16 20 24 28 32 36 40 44 48 KSI-101 5 mg KSI-101 10 mg Sham KSI-101 5 mg injection Individualized treatment (PRN) Primary Individualized treatment criteria (Week

  62. Slide 62: PEAK and PINNACLE master protocol design

    PEAK and PINNACLE master protocol design: a single screening process that enrolls distinct and complementary MESI patient populations Master Protocol Design: a single screening process for both studies CST≥320 and BCVA 25-78 letters Moderate to severe Day 1 enroll in either study Mild macular edema

  63. Slide 63: Increased size of the KSI-101 MESI pivotal program

    We have increased the size of the KSI-101 MESI pivotal program • Patient enrollment faster than expected • No major changes to expected timelines are anticipated • Pivotal program aligned with FDA in type C meeting KSI-101 MESI Pivotal Program (PEAK and PINNACLE) n=900 First 300 patients Last 300 pa

  64. Slide 64: MESI affects ~450,000 US patients

    MESI affects ~450,000 US patients (~300,000 trial eligible) often reported by etiology (defined autoimmune, idiopathic, surgical, infectious and other) ~455K out of 5.4M ME patients in the U.S. may be classified under MESI, ~298K meet KSI-101 trial inclusion U.S. MESI EPIDEMIOLOGY Estimated by two m

  65. Slide 65: KSI-101 initial addressable population greater than 150,000 MESI patients

    KSI-101 initial addressable population is greater than 150,000 MESI patients in the US KSI-101 ADDRESSABLE POPULATION # of Patients KSI-101 initial addressable population is >150,000 Minus Acute post- 1L 2L 3L procedural and (4-6 weeks) (~3 months) (6+ months) infectious >150,000 157K 300K 455K 70K

  66. Slide 66: Most MESI patients are in care of general ophthalmologists and retinal specialists

    Most MESI patients are in the care of General Ophthalmologists and Retinal Specialists; complex cases are referred out to Uveitis Specialists OPHTHALMOLOGY PRACTICE BREAKDOWN – Method 2 % of ME patients by patient subtype across physician types • General ophthalmologists act as 8% the referral gatek

  67. Slide 67: Kodiak

    KADIAK 68

  68. Slide 68: Discovery: broadening portfolio to additional causes of severe vision loss

    Discovery: We are broadening our portfolio of investigational medicines to tackle additional high prevalence causes of severe vision loss Ocular Geographic Glaucoma ~80M4 Inflammation Atrophy Pre-IND Pre-clinical Pre-clinical Bispecific Antibodies: Bispecific Antibodies: ABC® Duet: anti-IL-6 , anti-

  69. Slide 69: Glaucoma is leading cause of irreversible blindness

    Glaucoma is the leading cause of irreversible blindness worldwide with no approved neuroprotective treatments Worldwide prevalence of glaucoma1 Neuroinflammation Glaucoma is a progressive 120 ~112M optic neuropathy driven by neuroinflammation 100 ~80M DRIVES RGC DAMAGE / DEATH 80 • Current therapies

  70. Slide 70: Glaucoma duet: single molecule targeting neuroinflammation and elevated IOP

    Glaucoma “duet”: a single molecule designed to target neuroinflammation (that causes optic neuropathy) and elevated IOP simultaneously Disease Modifying NLRP3 Inhibitor Targets the NLRP3 inflammasome complex that drives Neuroprotective neuroinflammation causing optic neuropathy + IOP Lowering Small

  71. Slide 71: Geographic atrophy is a valuable market with high unmet need

    Geographic atrophy is a valuable market with a high unmet need • Geographic atrophy (GA) is the advanced form of dry ~$1B in net sales for GA age-related macular degeneration, affecting ~1M monotherapies in 2025 people in the U.S. SYFOVRE Net Sales (in Millions) • GA is characterized by progressive

  72. Slide 72: GA is a complex interplay of complement, inflammation, and angiogenic pathways

    GA is a complex interplay of complement, inflammation, and angiogenic pathways NLRP3 inflammasome, IL- 1β, IL-6 Complement VEGF Smoking Age Advanced Diabetes AMD/GA Hypoxia, lipid Inflammation Human Genetics metabolism This interplay drives both GA and neovascular AMD, which may co-exist within the

  73. Slide 73: Multi-asset pipeline in GA addresses multifactorial disease

    Kodiak’s multi-asset pipeline in GA is designed to address the multifactorial nature of the disease NLRP3 inflammasome, IL- 1β, IL-6 Complement VEGF Smoking Age Advanced Diabetes AMD/GA Hypoxia, lipid Inflammation Human Genetics metabolism Inhibitors of NLRP3 IL-6 + complement and Complement VEGF +

  74. Slide 74: GA duet: dual inhibition of complement and NLRP3

    GA “duet”: Dual inhibition of validated complement pathways along with the inflammasome pathway (NLRP3) Peptide Inhibitor of Complement Anti-C3 and anti-C5 have been validated for GA, but current therapies do not sufficiently halt disease progression and are limited by frequent injections NLRP3 Inhi

  75. Slide 75: GA bispecific antibody combining complement regulation with VEGF or IL-6 inhibition

    GA bispecific antibody: Combining validated complement regulation with VEGF or IL-6 inhibition as a therapeutic target for GA IL-6 + Complement VEGF + Complement Reduces Prevents inflammation Anti-IL-6 wet-AMD Anti-VEGF -driven GA Fab conversion Fab progression Complement Inhibits C3 convertase Comp

  76. Slide 76: Ocular inflammatory disease: 4th leading cause of vision loss in working-age adults

    Ocular inflammatory disease: the 4th leading cause of vision loss among working-age adults with no approved biologics • ~1/3 of patients with ocular inflammation develop TNF-ɑ, IL-6 and IL-1 levels are upregulated macular edema, the leading cause of vision loss in in patients with ocular inflammatio

  77. Slide 77: KSI-102 and KSI-103 dual cytokine targeting

    KSI-102 and KSI-103: Engineered to inhibit TNF-α/IL-6 and IL-1/IL-6 through dual cytokine targeting KSI-102 KSI-103 (αTNF-α / αIL-6 bispecific) (IL-1 trap / αIL-6 bispecific) αTNF-α αTNF IL-1 Trap IL-1 trap mimics native heterodimeric receptor and can bind to IL-1α or IL-1β αIL-6 αIL-6 TNF-α IL-6 IL

  78. Slide 78: Kodiak is gathering speed

    Kodiak is gathering speed. Our position at the intersection of retinal biology, therapeutics and optics/AI is a genuine source of differentiation 15+ years experience Retinal biology, disease and therapeutics development VETi: Visual Engagement Technology and imager 79

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