Zura Bio Limited · NASDAQ:ZURA
Zura Bio — Investor Presentation (October 2026)
51 slides from Zura Bio's investor presentation, Oct 27, 2026
Slide 1: Corporate Overview October 2026
Corporate Overview October 2026
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
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
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
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 remains below average1 because current therapies only partially address the multi-pathway biology driving these diseases2–9 2030s: Therapies designed to ad
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: H1 2027 A Phase 2 trial in adults with PMR Anticipated initiation: YE 202
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.
Slide 8: Tibulizumab is a four-headed hammer designed to inhibit BAFF and IL-17
8 Tibulizumab is a four-headed hammer designed to inhibit the BAFF and IL-17 pathways ixekizumab Anti-IL-17 scFv1 IL-17A/A & IL-17A/Ftabalumab Anti-BAFF Ab1 BAFF tibulizumab2,3 Tetravalent bispecific antibody designed to block BAFF and IL-17–mediated signaling (IL-17A/A and A/F heterodimers)4 Tibuli
Slide 9: Phase 1/1b data support advancement of tibulizumab into Phase 2
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
Slide 10: Modulation of independent innate and adaptive immune drivers of disease
10 Modulation of independent innate and 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, crea
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*1,2 • Validated IL-17 pathway inhibition: Neutralization of IL-17A/A and IL-17A/F produces robust clinical respons
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
Slide 13: Hidradenitis Suppurativa (HS)
13 Hidradenitis Suppurativa (HS)
Slide 14: HS is a chronic, progressive inflammatory condition with high symptom burden
14 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 delays in diagnosis and treatment Painful nodules and abscesses make walking
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 therapy1,2 Biologics
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; cycling to innovative options expected to increase as physicians seek durable alternatives Sources: R
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; 4. Yu et al. Immunity. 2024. In severe disease
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. Yu et al. Immunity. 2024; 2. Gudjonsson et a l. JCI Insight. 2020; 3
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 and activation B-cell survival Antibody release (IgG, IgA1, IgD) Cytokine
Slide 20: Three B-cell-targeting mechanisms demonstrating HS efficacy signal
20 Three B-cell-targeting mechanisms demonstrating HS efficacy signal1,2 Pooled placebo (contemporaneous cohorts) 36% Observed sHiSCR50** Responders at Week 16 by Treatment Arm1,2 Recent clinical data support the hypothesis that B cells are key drivers of disease rather than bystanders in HS* (*) Da
Slide 21: B-cell-directed monotherapy response rates in line with approved HS assets
21 Trial PIONEER I Phase 3 PIONEER II Phase 3 SUNRISE Phase 3 SUNSHINE Phase 3 BE HEARD I Phase 3 BE HEARD II 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 1
Slide 22: Orthogonal nature of IL-17 and BAFF pathways increases confidence
22 Orthogonal nature of IL-17 and 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 I
Slide 23: Phase 2 study ongoing in moderate-to-severe HS
23 Phase 2 study ongoing in moderate-to-severe HS Key Inclusion / Exclusion Criteria • Adults with moderate-to-severe HS, defined as: – Hurley Stage II/III (up to 40% Stage III allowed) – Total abscess and inflammatory nodule (AN) count ≥5 • Up to 30% of participants may have prior TNF-α inhibitor e
Slide 24: Systemic Sclerosis (SSc)
\/ zurabio Systemic Sclerosis (SSc)
Slide 25: Systemic sclerosis is a progressive, multisystem autoimmune disease
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*2 300,000 people are estimated to be living with SSc across major markets (US, EU5, Japan)1 SSc-ILD is a ma
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
Slide 27: IL-17A is increased in SSc blood and skin
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
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 skin1,2 Sources: 1. Gordon et a l. Arthritis Rheumatol. 2018; 2. Matsushita et a l. Arthritis Rheum. 2006; 3. Matsushita et al. Sci Adv. 2018. Belimumab modulated gene profiles in post-treatment SSc skin1 RNAseq analysis of ski
Slide 29: IL-17 and BAFF blockade have each shown improvement in skin and lung outcomes
29 IL-17 and BAFF blockade have each shown improvement in skin and lung outcomes in SSc Sources: 1. Gordon et a l. Arthritis Rheumatol. 2018; 2. Fukasawa et al. Ann Rheum Dis. 2022. IL-17 RECEPTOR ANTAGONIST Brodalumab2 • Met the primary endpoint of reduced mRSS at Week 24 for skin involvement, and
Slide 30: Phase 2 study ongoing in SSc; enrollment completed
30 Phase 2 study ongoing in SSc; enrollment completed * Includes secondary and exploratory endpoints Key Inclusion Criteria • Adults (18–75 years) with early diffuse cutaneous SSc, enriched for SSc-ILD • Stable background immunosuppressive or antifibrotic therapy allowed • Disease duration ≤ 7 years
Slide 31: 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 et al. Ann Am Thorac Soc. 2018; 2. Zura Bio. Data on file. 2026. ILD includes various pulmonary disorders marked by inflammation and progressive lung fibrosis, resulting in restrictive lung function and impair
Slide 32: QILD predicts mortality in SSc and correlates with FVC
32 QILD predicts mortality in SSc and closely correlates with FVC – differences of ~2% are clinically meaningful Sources: 1. Volkmann et al. CHEST. 2022; 2. Kafaja et al. Am J Respir Crit Care Med. 2018; 3. Goldin et al. Ann Am Thorac Soc. 2018; 4. ACTEMRA® ( tocilizumab) Prescribing Information.; 5
Slide 33: Published SSc disease trajectories validate our enrollment strategy
33 Published SSc disease trajectories validate our Phase 2 enrollment strategy What the data show • The type of autoantibody drives disease progression, with cutaneous trajectory peaking early in certain patients • ATA (anti-topoisomerase antibody) and A-RNA Pol-III (anti-RNA polymerase 3 antibody)
Slide 34: Polymyalgia Rheumatica (PMR)
34 Polymyalgia Rheumatica (PMR)
Slide 35: PMR: inflammatory disease with reduced mobility and 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 and stiffness Chronic inflammatory disease • Causes bilateral aching and stiffness in the shoulders, hip girdle, neck, and torso1,2 • Systemic inflammation is p
Slide 36: PMR represents a 700K+ US patient population
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 r
Slide 37: Reliance on steroids leads to dependence, relapse, and toxicity
37 Current reliance on steroids provides short-term relief but leads to long-term dependence, relapse, and toxicity Steroid-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
Slide 38: Targeting BAFF and IL-17 in PMR
38 Targeting BAFF and IL-17 may help address both immune dysregulation and inflammation in PMR Sources: 1. van der Geest et al. Arthritis Rheumatol. 2014; 2. van der Geest et al. Rheumatology (Oxford). 2015; 3. Reitsema et al. Front Immunol. 2022; 4. Ramiro et al. Rheumatol Ther. 2025. B-cell homeos
Slide 39: IL-17 and B-cell-targeted therapies show glucocorticoid-sparing effects in PMR
39 IL-17 and B-cell-targeted therapies have shown positive glucocorticoid-sparing effects in PMR * Sustained remission defined as remission that occurred by Week 12 and was sustained until Week 52, without recurrence of PM R and no new diagnosis of GCA; complete sustained remission defined as sustai
Slide 40: Despite IL-17 advances, the unmet need for PMR remains significant
40 Despite IL-17 advances, the unmet need for PMR remains significant Source: Stone et a l. N Engl J Med. 2026 (REPLENISH). • Glucocorticoids control PMR but cannot be withdrawn: three in four patients on taper alone needed escape or rescue therapy by Week 52 • IL-17 inhibition provides meaningful b
Slide 41: Proposed PMR Phase 2 study to be initiated by year-end 2026
41 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
Slide 42: Summary & Milestones
\/ zurabio Summary & Milestones
Slide 43: Executive Team and Board of Directors
43 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
Slide 44: Multiple near-term clinical milestones and strong pipeline
44 Multiple potential near-term clinical milestones and strong pipeline for the 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 S
Slide 45: Crebankitug: Phase 2-ready multi-functional antibody
45 Crebankitug: Phase 2-ready multi-functional antibody with potential in dermatology and 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 i
Slide 46: About IL-33 and torudokimab
46 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
Slide 47: Key Takeaways
47 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
Slide 48: Appendix
\/ zurabio Appendix
Slide 49: Cash and Shares Outstanding
49 Cash and Shares Outstanding Cash and cash equivalents balance $187.7M (as of 9/30/26) Number of shares (M) Common stock 96.3 Prefunded warrants 29.3 Total Outstanding 125.6
Slide 50: Glossary
50 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 activat ing factor BAFF-R B-cell activat ing factor rece
Slide 51: www.zurabio.com
Nasdaq: ZURA | www.zurabio.com