Zura Bio Limited · NASDAQ:ZURA
Zura Bio — Investor Presentation (August 2026)
51 slides from Zura Bio's investor presentation, August 2026
Slide 1: Corporate Overview
Corporate Overview August 2026
Slide 2: Forward-Looking Statements Disclaimer
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,” “plan
Slide 3: Advancing tibulizumab: a potential first- and only-in-class bispecific antibody
Advancing tibulizumab: a potential first- and only-in-class bispecific antibody Tibulizumab, a potential first- • IL-17 and BAFF among the most clinically validated pathways in immunologic disorders1,2 and only-in-class bispecific • Orthogonal nature of IL-17 and BAFF offers potential to modulate no
Slide 4: Addressing the distinct biology of immune-mediated diseases
Addressing the Immune-mediated diseases are often driven by multiple, distinct biology of intersecting immune pathways immune-mediated diseases Targeting more than one pathway is a rational approach to address low or inadequate response rates in complex immune-mediated diseases Early clinical readou
Slide 5: Untapped market potential across disease areas of interest
Untapped market 2030s: potential across disease Therapies designed to address the multi-pathway biology of areas of interest each disorder have the potential to break the response- $15B+ rate ceiling — expanding the eligible patient pool, moving into earlier lines of therapy, and TODAY: Projected ex
Slide 6: Three shots on goal — biologically de-risked, independent, and fully funded
Three shots on goal — biologically de-risked, independent, and fully funded through topline data readouts A Phase 2 trial in A Phase 2 trial in A Phase 2 trial in adults with HS adults with SSc adults with PMR Anticipated readout: Anticipated readout: Anticipated initiation: Q4 2026 H1 2027 YE 2026
Slide 7: Tibulizumab: Potential first- and only-in-class therapy
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. 7
Slide 8: Tibulizumab is a four-headed hammer designed to inhibit the BAFF and IL-17 pathways
Tibulizumab is a four-headed hammer designed to inhibit the BAFF and IL-17 pathways IL-17A/A & BAFF Addresses disease complexity tabalumab IL-17A/F Aims to target two orthogonal immune pathways Anti-BAFF Ab1 ixekizumab implicated in chronic inflammation and autoimmunity Anti-IL-17 scFv1 Clinically g
Slide 9: Phase 1/1b data support advancement of tibulizumab into Phase 2 development
Phase 1/1b data support advancement of Dose-dependent and comparable BAFF and IL-17 target engagement tibulizumab into Phase 2 development Population Median free target prediction interval* concentration • 78 participants dosed across Phase 1/1b studies 100 mg Q4W 300 mg Q4W concentration %CFB • >98
Slide 10: Broad potential in heterogeneous immune disorders
Broad potential in heterogeneous immune disorders IL-17 BAFF Amplifies inflammation, Promotes autoreactive B cell fibrosis, and tissue destruction survival and function1,2,3 Modulation of Drives recruitment and Promotes maturation, survival, activation of neutrophils independent and function of auto
Slide 11: Ixekizumab contributes a high-efficacy component for IL-17 pathway inhibition
Ixekizumab contributes a high-efficacy component for IL-17 pathway inhibition Multiple Phase 3 High efficacy Broad IL-17 Extensive clinical and programs completed demonstrated pathway inhibition real-world experience • Consistent high efficacy: Demonstrated across multiple PASI 90 at Week 12* (Phase
Slide 12: Tibulizumab potently inhibits IL-17A/A and IL-17A/F
Tibulizumab potently inhibits IL-17A/A and Highest Binding Medium Binding Lowest Binding IL-17A/F: the Affinity Affinity Affinity strongest drivers of IL-17 signaling Target IL-17A/A IL-17A/F IL-17F/F Agent description (KD) (KD) (KD) Anti-BAFF & IL-17 Tibulizumab1 ~14 pM ~90 pM no bindin
Slide 13: Hidradenitis Suppurativa (HS)
Hidradenitis Suppurativa (HS) 13
Slide 14: HS is a chronic, progressive inflammatory condition with high symptom burden
HS is a chronic, progressive inflammatory Distinctive for condition with high symptom burden structural skin damage driven by tunneling and scarring1 Patients experience pain in Painful nodules and abscesses make sensitive, high-friction areas walking, sitting, and arm movement difficult, limiting d
Slide 15: How patients are treated today — and the limitations of existing therapies
How patients are treated today — and the limitations of existing therapies Current Treatment Pathway Initial Management Biologics (SoC) Surgery Topicals, oral antibiotics, and in-office Selection driven by access/formulary, not a Reserved for biologic-refractory or procedures (I&D, intralesional cor
Slide 16: Hidradenitis suppurativa: large, underserved market with high unmet need
Hidradenitis suppurativa: large, underserved market with high unmet need $10B Multiple advanced therapies; cycling to innovative options expected to increase as physicians seek durable alternatives Mid-2030s Growth Drivers and Unmet Needs Three advanced therapies (TNF, IL-17) • Despite recent approv
Slide 17: B cells infiltrate and chronically persist in HS lesions
Unlike healthy skin, B cells infiltrate and chronically persist in HS lesions, driving a local amplified and targeted immune response B cells and plasma cells make up B cells expand with In severe disease, B and T cells organize and the bulk of HS cellular infiltrate1 disease progression2 persist in
Slide 18: BAFF is elevated across HS lesion types and predicts treatment resistance
BAFF is elevated across HS lesion types and predicts treatment resistance Elevated BAFF can retain B cells Elevated BAFF is a unique feature of HS in the skin lesions, which predicts TNFi non-response BAFF B cells promotes B B and T cells 800 migrate into organize into tertiary cell HS lesions lymph
Slide 19: B cells are believed to drive HS pathology via multiple mechanisms
B cells are believed to drive HS pathology via multiple mechanisms IL-17 drives a feed-forward, BAFF prolongs B cell Antibody release self-sustaining (IgG, IgA1, IgD) survival and promotes inflammatory cycle several effector functions B cell survival IL-17 Tertiary Lymphoid BAFF B cell Structure Cyt
Slide 20: Recent clinical data supports B cells as key drivers of disease in HS
Recent clinical data supports the hypothesis that B cells are key drivers of disease rather than bystanders in HS* Platform Study Design Observed sHiSCR50** Responders at Week 16 by Treatment Arm1,2 72.7% length varies by cohort (4–84W) Active Follow-up period Pooled placebo Screening Treatment 58.6
Slide 21: B cell directed monotherapy has demonstrated absolute response rates in line with approved assets
B cell directed monotherapy has demonstrated absolute response rates in line with other approved and late-stage assets in HS TNF IL17 Other investigational therapies B cell targeting HiSCR50 Absolute Response Rates Open-label, no 100% placebo arm 90% 85% 80% 67% 70% 70% 64% 59% 56% 59% 60% 59%* 60%
Slide 22: Orthogonal nature of IL-17 and BAFF pathways increases confidence in potential benefit
Orthogonal nature of IL-17 and BAFF pathways increases confidence in potential benefit over IL-17 inhibition alone Targets distinct Targets IL-17, the most BAFF biology of HS validated MoA in HS Tibulizumab is designed to IL-17-binding scFv from Persistence of B cells target distinct orthogonal ixek
Slide 23: Phase 2 study ongoing in moderate-to-severe HS
Phase 2 study ongoing in moderate-to-severe HS Key Inclusion Criteria • Adults with moderate-to-severe HS, defined as: tibulizumab – Hurley Stage II/III (up to 40% Stage III allowed) 300 mg – Total abscess and inflammatory nodule (AN) count ≥5 • Up to 30% of participants may have prior TNF-α inhibit
Slide 24: Systemic Sclerosis (SSc)
\/ zurabio Systemic Sclerosis (SSc)
Slide 25: Systemic sclerosis is a progressive, multisystem autoimmune disease with limited therapeutic options
Systemic sclerosis is a progressive, multisystem autoimmune disease with limited therapeutic options* approximately Characterized by 300,000 people are estimated to be living with SSc Chronic Inflammation and Fibrosis Across Organs across major markets (US, EU5, Japan)1 Lungs Heart SSc-ILD is a majo
Slide 26: Why SSc requires multi-pathway immune modulation
Why SSc requires multi-pathway Vasculopathy • Immune-mediated endothelial dysfunction immune modulation contributes to impaired blood flow • Inflammatory cytokines (IL-6, IL-17) thought to promote immune cell BAFF- and IL-17–driven infiltration and vascular injury inflammation may contribute to vasc
Slide 27: IL-17A is increased in SSc blood and skin and is linked to active and early disease
IL-17A is increased in SSc blood and skin and is linked to active and early disease IL-17A cytokine elevated in SSc1 Blood IL-17+ cells correlate with disease activity2 Serum IL-17A a predictor and correlate of pulmonary vascular disease1,3 IL-17A elevated in blood and correlates with disease activi
Slide 28: BAFF inhibition reduces profibrotic and B cell signaling genes in SSc skin
BAFF inhibition reduces profibrotic and B cell signaling genes in SSc skin1,2 Hypothesized disease-promoting Belimumab modulated gene profiles roles of B cells3 in post-treatment SSc skin1 RNAseq analysis of skin from patients who demonstrated a 20% reduction in mRSS Indicators of anti- fibrotic eff
Slide 29: IL-17 and BAFF blockade have each shown improvement in skin and lung outcomes in SSc
IL-17 and BAFF blockade have each shown improvement in skin and lung outcomes in SSc BAFF ANTAGONIST IL-17 RECEPTOR ANTAGONIST Belimumab1 Brodalumab2 • In a 52-week, investigator-initiated, single-center, double-blind, placebo- • Met the primary endpoint of reduced mRSS at Week 24 for skin controlle
Slide 30: Phase 2 study ongoing in SSc; enrollment completed
Phase 2 study ongoing in SSc; enrollment completed Key Inclusion Criteria • Adults (18-75 years) with early diffuse cutaneous SSc, enriched for SSc-ILD HRCT (Baseline image) HRCT HRCT • Stable background immunosuppressive or antifibrotic therapy allowed tibulizumab • Disease duration ≤ 7 years 300 m
Slide 31: In Phase 2, lung involvement using qHRCT is a key secondary endpoint
In Phase 2, lung involvement using qHRCT is a key secondary endpoint QILD by HRCT provides a sensitive measure of lung involvement, detecting changes as small as 2%.1 Example of improvement after 24 months of MMF in total lung involvement1 vs Healthy Lung Fibrotic Lung ILD includes various pulmonary
Slide 32: QILD predicts mortality in SSc and closely correlates with FVC
QILD predicts mortality in SSc and closely correlates with FVC — differences of ~2% are clinically meaningful 2 large longitudinal SSc studies (SLS I and SLS 2) showed that Tocilizumab Phase 3 in SSc-ILD ≥2% increase in QILD associated with increased risk of death 1 Approved for SSc-ILD based on FVC
Slide 33: Published SSc disease trajectories validate our Phase 2 enrollment strategy
Published SSc disease trajectories validate our Phase 2 enrollment strategy What the data show PAH • Autoantibody drives disease progression Cutaneous trajectory GI • ATA and RNA Pol III drive the fastest fibrosis • mRSS peaks early, then regresses on its own SRC GI PAH Why our design fits • Stratif
Slide 34: Polymyalgia Rheumatica (PMR)
Polymyalgia Rheumatica (PMR) 34
Slide 35: PMR: inflammatory disease that leads to reduced mobility and loss of independence
PMR: inflammatory disease that leads to reduced mobility, loss of independence, and significant quality of life burden Chronic inflammatory disease Demographics and risk factors • Causes bilateral aching and stiffness in the • Almost exclusively patients over 50; peak onset at shoulders, hip girdle,
Slide 36: PMR represents a 700K+ US patient population with significant headroom
PMR represents a 700K+ US patient population with significant headroom for advanced therapy adoption Today, only 1 FDA-approved biologic2 700K+ PMR is an underserved and underpenetrated disease US PMR Patients1 Advanced therapy market Steroid-dependency3 Standard of care leaves most patients steroid
Slide 37: Current reliance on steroids provides short-term relief but leads to long-term dependence
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 of
Slide 38: Targeting BAFF and IL-17 may help address both immune dysregulation and inflammation in PMR
Targeting BAFF and IL-17 may help address both immune dysregulation and inflammation in PMR B cell homeostasis and trafficking BAFF correlates with disease IL-17 may amplify local and is dysregulated1,2 activity1,2 systemic inflammation 3,4 Serum BAFF is: Elevated in newly diagnosed PMR1,2 IL-17 and
Slide 39: IL-17 and B cell targeted therapies have shown glucocorticoid-sparing effects in PMR
IL-17 and B cell targeted therapies have shown positive glucocorticoid-sparing effects in PMR IL-17A inhibitor – relapsing PMR (Phase 3) Anti-CD20 – newly diagnosed PMR (Phase 2 & 3) Secukinumab1 Rituximab • Met the primary endpoint of sustained remission at Week 52 and all key secondary endpoints •
Slide 40: Despite IL-17 advances, the unmet need for PMR remains significant
Despite IL-17 advances, the unmet need for PMR remains significant • Glucocorticoids control PMR but cannot be withdrawn: three in four patients on taper alone needed escape or rescue therapy by Week 52 • IL-17 provides real but partial benefit: More than half of participants in secunikumab arms do
Slide 41: Proposed PMR Phase 2 study to be initiated by year end 2026
Proposed PMR Phase 2 study to be initiated by year end 2026 ~150-180 total tibulizumab participants 300 mg Key Inclusion Criteria tibulizumab tibulizumab • Diagnosis of PMR according to the 2012 R 150 mg provisional ACR/EULAR classification criteria 1:1:1 • History of treatment for ≥8 weeks for PMR
Slide 42: Summary & Milestones
\/ zurabio Summary & Milestones
Slide 43: Executive Team and Board of Directors
Executive Team and Board of Directors Executive Team Board of Directors Amit Munshi Chairman Sandeep Kulkarni, MD Co-Founder, CEO & Director Dan Becker, MD, PhD Director Mark Eisner, MD, MPH Sandeep Kim Davis, JD Muzammil Kiran Nistala, Gary Whale, PhD Director Kulkarni, MD Chief Operating Officer,
Slide 44: Multiple potential near-term clinical milestones and strong pipeline for the future
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 Hidradenitis Suppurativa TibuSHIELD Readout Q4 2026 Anti-BAFF and IL-17 Systemic Sclerosis TibuSURE Readout H1 2027 Anti-BAFF and IL-1
Slide 45: Crebankitug: Phase 2 ready multi-functional antibody
Crebankitug: Phase 2 ready multi-functional antibody with potential in dermatology and beyond Crebankitug inhibits two distinct cytokine pathways, IL-7 and TSLP, through a single target IL-7 IL-7Rα TSLP IL-7Rα combines with the IL-7 TSLP TSLP binds to its specific common gamma chain (γc) receptor, T
Slide 46: Torudokimab: Phase 2 ready IL-33 targeting antibody
Torudokimab: Phase 2 ready IL-33 targeting antibody with potential in respiratory disease and beyond About IL-33 and torudokimab IL-33 Clinical Results IL-33 is a damage-associated “alarmin” Torudokimab was well tolerated in Phase 1 cytokine released by stressed or injured tissues and Phase 2 trials
Slide 47: Key Takeaways
Key Takeaways Clear Defined, anticipated Portfolio differentiation clinical catalysts optionality Tibulizumab is a potential first Three independent Phase 2 Multi-pathway immune and currently only in-class trials (TibuSHIELD, biology provides potential for bispecific antibody in TibuSURE, and NEXUS-
Slide 48: Appendix
\/ zurabio Appendix
Slide 49: Cash and Shares Outstanding
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 50: Glossary
Glossary Ab antibody HiSCR75 Hidradenitis Suppurativa Clinical Response ≥75% NRS Numeric Rating Scale sHiSCR90 Simplified Hidradenitis Suppurativa Clinical Response (90%) ACA anti-centromere antibodies HRCT high-resolution computed tomography NS not significant SLE systemic lupus erythematosus ACR A
Slide 51: Nasdaq: ZURA www.zurabio.com
Nasdaq: ZURA | www.zurabio.com