Zura Bio Limited · NASDAQ:ZURA

Zura Bio — Investor Presentation (August 2026)

50 slides from Zura Bio's investor presentation, Aug 11, 2026

  1. Slide 1: Corporate Overview August 2026

    Corporate Overview August 2026

  2. Slide 2: Forward-Looking Statements Disclaimer

    2 Forward-Looking Statements Disclaimer This presentation contains “forward-looking statements” within the meaning of the “safe harbor” provisions of the Private Securities Litigation Reform Act of 1995. Words such as “expect,” “estimate,” “project,” “budget,” “forecast,” “anticipate,” “intend,” “pl

  3. Slide 3: Advancing tibulizumab: a potential first- and only-in-class bispecific antibody

    3 Advancing tibulizumab: a potential first- and only-in-class bispecific antibody Tibulizumab, a potential first- and only-in-class bispecific antibody inhibiting IL-17 and BAFF in development • IL-17 and BAFF among the most clinically validated pathways in immunologic disorders1,2 • Orthogonal natu

  4. Slide 4: Addressing the distinct biology of immune-mediated diseases

    4 Addressing the distinct biology of immune-mediated diseases Immune-mediated diseases are often driven by multiple, intersecting immune pathways Targeting more than one pathway is a rational approach to address low or inadequate response rates in complex immune-mediated diseases Early clinical read

  5. Slide 5: Untapped market potential across disease areas of interest

    5 Untapped market potential across disease areas of interest ~$5B 2026 Projected Mid-2030s $15B+ TODAY: Biologic penetration in HS, SSc, and PMR remain below average because current therapies only partially address the multi-pathway biology driving these diseases 2030s: Therapies designed to address

  6. Slide 6: Three shots on goal — biologically de-risked, independent, and fully funded

    6 Three shots on goal — biologically de-risked, independent, and fully funded through topline data readouts A Phase 2 trial in adults with HS Anticipated readout: Q4 2026 A Phase 2 trial in adults with SSc Anticipated readout: 1H 2027 A Phase 2 trial in adults with PMR Anticipated initiation: YE 202

  7. Slide 7: Tibulizumab: Potential first- and only-in-class therapy

    7 Tibulizumab: Potential first- and only-in-class therapy Tibulizumab is an investigational agent. Its efficacy and safety have not been established or approved by the FDA or any other regulatory agency worldwide.

  8. Slide 8: Tibulizumab is a four-headed hammer designed to inhibit the BAFF and IL-17 pathways

    8 Tibulizumab is a four-headed hammer designed to inhibit the BAFF and IL-17 pathways ixekizumab Anti-IL-17 scFv IL-17A/A & IL-17A/Ftabalumab Anti-BAFF Ab BAFF tibulizumab Tetravalent bispecific antibody designed to block BAFF and IL-17–mediated signaling (IL-17A/A and A/F heterodimers) Tibulizumab

  9. Slide 9: Phase 1/1b data support advancement of tibulizumab into Phase 2 development

    9 Phase 1/1b data support advancement of tibulizumab into Phase 2 development • 78 participants dosed across Phase 1/1b studies • >98% median trough target engagement for both IL-17 and BAFF in peripheral blood at 300 mg Q4W • Mean terminal half-life (t½): 27 days, supporting once-monthly dosing • P

  10. Slide 10: Modulation of independent innate & adaptive immune drivers of disease

    10 Modulation of independent innate & adaptive immune drivers of disease IL-17 Amplifies inflammation, fibrosis, and tissue destruction Drives recruitment and activation of neutrophils Enhances trafficking and cross- talk of immune cells in tissues Induces pro-inflammatory protein production, creati

  11. Slide 11: Ixekizumab contributes a high-efficacy component for IL-17 pathway inhibition

    11 Ixekizumab contributes a high-efficacy component for IL-17 pathway inhibition • Consistent high efficacy: Demonstrated across multiple inflammatory diseases in large Phase 3 programs* • Validated IL-17 pathway inhibition: Neutralization of IL-17A/A and IL-17A/F produces robust clinical responses

  12. Slide 12: Tibulizumab potently inhibits IL-17A/A and IL-17A/F

    12 Tibulizumab potently inhibits IL-17A/A and IL-17A/F: the strongest drivers of IL-17 signaling Agent Target description IL-17A/A (KD) IL-17A/F (KD) IL-17F/F (KD) Tibulizumab1 Anti-BAFF & IL-17 bispecific mAb ~14 pM ~90 pM no binding Secukinumab (Cosentyx®)2 Anti-IL-17A mAb ~60–90 pM ~2400 pM no bi

  13. Slide 13: Hidradenitis Suppurativa (HS)

    13 Hidradenitis Suppurativa (HS)

  14. Slide 14: HS is a chronic, progressive inflammatory condition with high symptom burden

    14 HS is a chronic, progressive inflammatory condition with high symptom burden Patients experience pain in sensitive, high-friction areas Patients withdraw from social interactions due to visible symptoms Patients struggle with persistent drainage and odor from lesions Patients experience prolonged

  15. Slide 15: How patients are treated today — and the limitations of existing therapies

    15 How patients are treated today — and the limitations of existing therapies Current Treatment Pathway Initial Management Topicals, oral antibiotics, and in-office procedures (I&D, intralesional corticosteroids) establish control and satisfy payer requirements before advancing therapy Biologics (So

  16. Slide 16: Hidradenitis suppurativa: large, underserved market with high unmet need

    16 Hidradenitis suppurativa: large, underserved market with high unmet need Three advanced therapies (TNF, IL-17) compete for the current biologic- treated HS population Multiple advanced therapies; increased cycling expected to innovative therapies, physicians seeking durable alternatives for chron

  17. Slide 17: B cells infiltrate and chronically persist in HS lesions

    17 Unlike healthy skin, B cells infiltrate and chronically persist in HS lesions, driving a local amplified and targeted immune response Sources: 1. Gudjonsson et al., JCI Insight 2020; 2. Lowe et al., JCI Insight 2020; 3. Lowe et al., JCI Insight 2024;9:e169870; 4. Yu et al., Immunity 2024 In sever

  18. Slide 18: BAFF is elevated across HS lesion types and predicts treatment resistance

    18 BAFF is elevated across HS lesion types and predicts treatment resistance In acute and chronic HS lesions, BAFF expression tracks with B-cell accumulation, supporting BAFF as a key player in B-cell mediated pathology Sources: 1. Sabat et al., J Allergy Clin Immunol 2023;151:1015-1026; 2. Lowe et

  19. Slide 19: B cells are believed to drive HS pathology via multiple mechanisms

    19 B cells are believed to drive HS pathology via multiple mechanisms BAFF prolongs B cell survival and promotes several effector functions IL-17 drives a feed-forward, self-sustaining inflammatory cycle Neutrophil recruitment & activation B cell survival Antibody release (IgG, IgA1, IgD) Cytokine a

  20. Slide 20: Three B cell-targeting mechanisms demonstrating HS efficacy signal

    20 Three B cell-targeting mechanisms demonstrating HS efficacy signal Pooled placebo (contemporaneous cohorts) 36% Observed sHiSCR50** Responders at Week 16 by Treatment Arm Recent clinical data supports the hypothesis that B cells are key drivers of disease rather than bystanders in HS* (*) Data de

  21. Slide 21: B-cell directed monotherapy absolute response rates across HS trials

    21 Trial PIONEER I Phase 3 PIONEER II Phase 3 SUNRISE Phase 3 SUNSHINE Phase 3 BE HEARD I Phase 3 BE HEARD 2 Phase 3 VELA-1 Phase 3 VELA-2 Phase 3 STOP HS-1 Phase 3 STOP HS-2 Phase 3 LOTUS Phase 2 LOTUS Phase 2 Phase 2 Phase 2 HS- OBTAIN Phase 2 Phase 2 Pilot Week 12 12 16 16 16 16 16 16 12 12 16 16

  22. Slide 22: Orthogonal nature of IL-17 & BAFF pathways increases confidence in potential benefit

    22 Orthogonal nature of IL-17 & BAFF pathways increases confidence in potential benefit over IL-17 inhibition alone Targets distinct biology of HS Tibulizumab is designed to target distinct orthogonal pathways, increasing probability of additive effect Targets IL-17, the most validated MoA in HS IL-

  23. Slide 23: Phase 2 study ongoing in moderate-to-severe HS

    23 Phase 2 study ongoing in moderate-to-severe HS Planned Efficacy Endpoints Primary Endpoint • Percent change from baseline in AN count at Week 16 Additional Endpoints* • HiSCR50 and HiSCR75 • Draining Tunnel Count • IHS4 • DLQI • Skin pain NRS • PK/PD assessments Key Inclusion Criteria • Adults wi

  24. Slide 24: Systemic Sclerosis (SSc)

    \/ zurabio Systemic Sclerosis (SSc)

  25. Slide 25: Systemic sclerosis is a progressive, multisystem autoimmune disease with limited therapeutic options

    25 Systemic sclerosis is a progressive, multisystem autoimmune disease with limited therapeutic options* No therapies are approved that comprehensively address the multisystem pathology of SSc* 300,000 people are estimated to be living with SSc across major markets (US, EU5, Japan) SSc-ILD is a majo

  26. Slide 26: Why SSc requires multi-pathway immune modulation

    26 Why SSc requires multi-pathway immune modulation BAFF- and IL-17–driven inflammation may contribute to vasculopathy and fibrosis, supporting evaluation of multi- pathway therapeutic strategies in SSc Vasculopathy • Immune-mediated endothelial dysfunction contributes to impaired blood flow • Infla

  27. Slide 27: IL-17A is increased in SSc blood and skin and is linked to active and early disease

    27 IL-17A is increased in SSc blood and skin and is linked to active and early disease IL-17A elevated in blood and correlates with disease activity Elevations of IL-17-expressing T cells in skin correlate with early disease IL-17A cytokine elevated in SSc1 Serum IL-17A a predictor and correlate of

  28. Slide 28: BAFF inhibition reduces profibrotic and B cell signaling genes in SSc skin

    28 BAFF inhibition reduces profibrotic and B cell signaling genes in SSc skin2 Sources: 1. Matsushita et a l, Sclerosis 2026; 2. Gordon et a l., Arthritis and Rheumato logy 2018 Belimumab modulated gene profiles in post-treatment SSc skin2 RNAseq analysis of skin from patients who demonstrated a 20%

  29. Slide 29: IL-17 and BAFF blockade have each improved skin and lung outcomes in SSc

    29 IL-17 and BAFF blockade have each improved skin and lung outcomes in SSc Sources: 1. Fukasawa T, et al. Ann Rheum Dis 2022, doi:10.1136/annrheumdis-2022-eular.2519 (NCT03957681); 2. Gordon JK, et al. Ar thr itis Rheumatol 2018;70:308-316 (NCT01670565) IL-17 RECEPTOR ANTAGONIST Brodalumab • Met th

  30. Slide 30: Phase 2 study ongoing in SSc; enrollment completed

    30 Phase 2 study ongoing in SSc; enrollment completed * Includes secondary and exploratory endpoints Endpoints and Stratification Primary Endpoint • Change from baseline in mRSS at Week 24 Additional Endpoints * • qHRCT lung imaging • FVC • HAQ-DI • revised CRISS Stratification factors • Presence of

  31. Slide 31: In Phase 2, lung involvement using qHRCT is a key secondary endpoint

    31 In phase 2, lung involvement using qHRCT is a key secondary endpoint Sources: 1. Goldin J, et al. Ann Am Thorac Soc 2018, doi:10.1513/annalsats.201802-079OC; 2. Zura Bio, data on file , 2026 ILD includes various pulmonary disorders marked by inflammation and progressive lung fibrosis, resulting i

  32. Slide 32: QILD predicts mortality in SSc and closely correlates with FVC

    32 QILD predicts mortality in SSc and closely correlates with FVC — differences of ~2% are clinically meaningful Sources: 1. Volkmann E, et al. CHEST 2022; 2. Kafaja S, et al. Am J Respir Crit Care Med 2018; 3. Goldin J, et a l. Ann Am Thorac Soc 2018; 4. Actemra USPI; 5. Roofeh D, et a l. Arthritis

  33. Slide 33: Published SSc disease trajectories validate our Phase 2 enrollment strategy

    33 Published SSc disease trajectories validate our Phase 2 enrollment strategy What the data show • Autoantibody drives disease progression • ATA and RNA Pol III drive the fastest fibrosis • mRSS peaks early, then regresses on its own Why our design fits • TibuSURE stratification factors designed to

  34. Slide 34: Polymyalgia Rheumatica (PMR)

    34 Polymyalgia Rheumatica (PMR)

  35. Slide 35: PMR: inflammatory disease that leads to reduced mobility and significant quality of life burden

    35 PMR: inflammatory disease that leads to reduced mobility, loss of independence, and significant quality of life burden Hot-spots of pain & stiffness Chronic inflammatory disease • Causes bilateral aching and stiffness in the shoulders, hip girdle, neck and torso • Systemic inflammation is present

  36. Slide 36: PMR represents a 700k+ US patient population with significant headroom

    36 PMR represents a 700k+ US patient population with significant headroom for advanced therapy adoption Today, only 1 FDA-approved biologic2 PMR is an underserved and underpenetrated disease Need for more effective therapies3,4,5 Even with use of on and off-label therapies, complete and sustained re

  37. Slide 37: Current reliance on steroids leads to long-term dependence, relapse, and toxicity

    37 Current reliance on steroids provides short-term relief but leads to long-term dependence, relapse, and toxicity Steroids-associated toxicities are common (e.g., insomnia, weight gain, hyperglycemia, osteoporosis, and infections) and can be problematic in the PMR age demographic due to high rates

  38. Slide 38: BAFF and IL-17 believed to contribute to PMR pathology

    38 BAFF and IL-17 believed to contribute to PMR pathology IL-17 is elevated in blood & tissue around PMR joints and correlates with disease activity3,4 IL-17 BAFF B cell Th17 IL-6 IL-6 activates Promotes differentiation amplifies Elevated BAFF strongly correlates with disease activity and key PMR bi

  39. Slide 39: IL-17 and B-cell targeted therapies have shown positive glucocorticoid-sparing effects in PMR

    39 IL-17 and B-cell targeted therapies have shown positive glucocorticoid-sparing effects in PMR Sources: 1. Stone et al., N Engl J Med 2026, DOI:10.1056/NEJMoa2602567 (REPLENISH; NCT05767034); 2 . Marsman et al., Lancet Rheumatol 2021;3:e758-e766 (BRIDGE-PMR); 3. Bolhuis et al., Lancet Rheumatol 20

  40. Slide 40: Proposed PMR Phase 2 study to be initiated by year end 26

    40 Proposed PMR Phase 2 study to be initiated by year end 2026 Key Inclusion Criteria • Diagnosis of PMR according to the 2012 provisional ACR/EULAR classification criteria • History of treatment for ≥8 weeks for PMR with prednisone ≥10 mg/day • ≥1 episode of PMR relapse at a prednisone dose ≥5 mg/d

  41. Slide 41: Summary & Milestones

    \/ zurabio Summary & Milestones

  42. Slide 42: Executive Team and Board of Directors

    42 Executive Team and Board of Directors Amit Munshi Chairman Sandeep Kulkarni, MD Co-Founder, CEO & Director Dan Becker, MD, PhD Director Mark Eisner, MD, MPH Director Jennifer Jarrett Director Ajay Nirula, MD, PhD Director Steve Schoch Director Parvinder Thiara Director Kim Davis, JD Chief Operati

  43. Slide 43: Multiple potential near-term clinical milestones and strong pipeline for future

    43 Multiple potential near-term clinical milestones and strong pipeline for future TARGET DISCOVERY PHASE 1 PHASE 2 PHASE 3 Tibulizumab (ZB-106) Anti-BAFF and IL-17 Anti-BAFF and IL-17 Anti-BAFF and IL-17 Crebankitug (ZB-168) Anti-IL-7Rα Torudokimab (ZB-880) Anti-IL-33 Hidradenitis Suppurativa Syste

  44. Slide 44: Crebankitug: Phase 2 ready multi-functional antibody

    44 Crebankitug: Phase 2 ready multi-functional antibody with potential in dermatology & beyond TSLP binds to its specific receptor, TSLPR, initiating a signaling process that is optimized when IL-7Rα integrates into the complex • TSLP activates signaling pathways primarily associated with type 2 imm

  45. Slide 45: About IL-33 and torudokimab

    45 About IL-33 and torudokimab Growing clinical validation of IL-33 targeting in respiratory: • Potential for first-in-class opportunities • Validated pathways in COPD and asthma6 Torudokimab: Phase 2 ready IL-33 targeting antibody with potential in respiratory disease and beyond Sources: 1. Cohen E

  46. Slide 46: Key Takeaways

    46 Key Takeaways Clear differentiation Tibulizumab is a potential first and currently only in-class bispecific antibody in development designed to simultaneously target IL-17– mediated signaling and BAFF, addressing immune complexity beyond single- pathway approaches Defined, anticipated clinical ca

  47. Slide 47: Appendix

    \/ zurabio Appendix

  48. Slide 48: Cash and Shares Outstanding

    48 Cash and Shares Outstanding Cash and cash equivalents balance $205.1M (as of 6/30/26) Number of shares (M) Common stock 95.4 Prefunded warrants 29.3 Total Outstanding 124.7

  49. Slide 49: Glossary

    49 Glossary Ab antibody ACA anti-centromere antibodies ACR American College of Rheumatology ADA anti-drug ant ibody AN abscess and inflammatory nodule A-RNA-Pol-III anti-RNA polymerase 3 antibodies ATA anti-topoisomerase antibodies BAFF B cell act ivating factor BAFF-R B-cell activat ing factor rece

  50. Slide 50: www.zurabio.com

    Nasdaq: ZURA | www.zurabio.com

Zura Bio — Investor Presentation (August 2026) on 6ix