Exhibit 99.1
©2023 Zura Bio Ltd. Corporate Overview Last Updated: October 2023 Building the Next Immunology Leader
©2023 Zura Bio Ltd. 2 Forward Looking Statements Disclaimer This communication includes “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,” “may,” “will,” “could,” “should,” “believe,” “predict,” “potential,” “continue,” “strategy,” “future,” “opportunity,” “would,” “seem,” “seek,” “outlook” and similar expressions are intended to identify such forward - looking statements. Forward - looking statements are predictions, projections and other statements about future events that are based on current expectations and assumptions and, as a result, are subject to risks and uncertainties that could cause the actual results to differ materially from the expected results. These statements are based on various assumptions, whether or not identified in this communication. These forward - looking statements are provided for illustrative purposes only and are not intended to serve as, and must not be relied on by an investor as, a guarantee, an assurance, a prediction or a definitive statement of fact or probability. Actual events and circumstances are difficult or impossible to predict and will differ from assumptions. You should carefully consider the risks and uncertainties described in the “Risk Factors” sections of Zura Bio’s recent filings with the SEC. These filings would identify and address other important risks and uncertainties that could cause actual events and results to differ materially from those contained in the forward - looking statements. Many of these factors are outside Zura Bio’s control and are difficult to predict. Many factors could cause actual future events to differ from the forward - looking statements in this communication, including but not limited to: (1) the outcome of any legal proceedings that may be instituted against Zura Bio; (2) volatility in the price of Zura Bio’s securities; (3) the ability of Zura Bio to successfully conduct research and development activities, grow and manage growth profitably, maintain relationships with customers and suppliers, and retain key employees; (4) costs related to financing transactions and the ongoing costs relating to operating as a public company; (5) changes in the applicable laws or regulations; (6) the possibility that Zura Bio may be adversely affected by other economic, business, and/or competitive factors; (7) the risk of downturns and a changing regulatory landscape in the highly competitive industry in which Zura Bio operates; (8) the impact of the global COVID - 19 pandemic; (9) the potential inability of Zura Bio to raise additional capital needed to pursue its business objectives or to achieve efficiencies regarding other costs; (10) the enforceability of Zura Bio’s intellectual property, including its patents, and the potential infringement on the intellectual property rights of others, cyber security risks or potential breaches of data security; and (11) other risks and uncertainties described in the Registration Statement and such other documents filed by Zura Bio from time to time with the SEC. These risks and uncertainties may be amplified by the COVID - 19 pandemic or other unanticipated global disruption events, which may continue to cause economic uncertainty. Zura Bio cautions that the foregoing list of factors is not exclusive or exhaustive and not to place undue reliance upon any forward - looking statements, including projections, which speak only as of the date made. Zura Bio gives no assurance that it will achieve its expectations. Zura Bio does not undertake or accept any obligation to publicly provide revisions or updates to any forward - looking statements, whether as a result of new information, future developments or otherwise, or should circumstances change, except as otherwise required by securities and other applicable laws.
©2023 Zura Bio Ltd. 3 Experienced management team with proven ability to successfully execute and build a leading market position Nasdaq: ZURA Verender Badial Chief Financial Officer Someit Sidhu M.D. Chief Executive Officer and Director Chris Cabell M.D. Chief Medical Officer and Head of Research and Development Gary Whale Ph.D. Chief Technology Officer Mike Howell Ph.D. Chief Scientific Officer and Head of Translational Science Kim Davis Chief Legal Officer Executive Team Board of Directors Amit Munshi Garry Neil, M.D. Jennifer Jarrett Neil Graham, M.D. Parvinder Thiara Sandeep Kulkarni, M.D. Someit Sidhu, M.D. Steve Schoch Chairman Director Director Director Director Director Director Director
©2023 Zura Bio Ltd. Sizeable Total Addressable Market Exists Across Number of Validated Mechanisms 4 Nasdaq: ZURA Room for growth across our three indications Approximately $4 Billion in growth anticipated by 2029 Sources: 1 Based on current annual gross price of marketed products 2 Based on 2023 gross price, adjusted for population and price growth. $ 7 .1 $ 5 .6 $ 8 . 7 $ 5 . 5 $ 4 .5 $ 7 .1 2023 US Total Addressable Market 1 20 29 US Total Addressable Market 2 $17.1 B illion $ 2 1 . 4 Billion alopecia areata hidradenitis suppurativa systemic sclerosis US TAM estimated ~$21 Billion by 2029 2 Systemic sclerosis has unlocked potential with only two specific SSc - ILD approved products
©2023 Zura Bio Ltd. Clinical stage pipeline targeting key immunology pathways 5 ZURA BIO PROGRAM INDICATION EXPECTED KEY MILESTONES Preclinical NEXT CLINICAL PHASE Phase 1 Phase 2 Phase 3 ZB - 106 tibulizumab Anti - BAFF x IL - 17 systemic sclerosis Transition asset from Eli - Lilly Open IND rheumatology division Phase 2 study initiation, to enable seamless transition to Ph3 2H - 24’ hidradenitis suppurativa Transition asset from Eli - Lilly Open IND dermatology division 2H - 24’ Phase 2 initiation 2H - 24’ ZB - 168 Anti - IL - 7R alopecia areata Transition asset from Pfizer Open IND dermatology division Completed technology transfer to CDMO Phase 2 initiation* 1H - 24’ ZB - 880 torudokimab Anti - IL - 33 allergy / respiratory Conduct all necessary CMC and regulatory tasks to prepare the asset for Phase 2 readiness** (*) pending expected phase 2 external catalysts in atopic dermatitis (AD) and ulcerative colitis (UC) (**) pending expected phase 2 and 3 external catalysts in asthma and chronic obstructive pulmonary disease (COPD) Nasdaq: ZURA Sources: Zura Internal Data and Planning. Current development plans and trial designs are subject to change due to factors such as regulatory feedback
©2023 Zura Bio Ltd. 6 ZB - 106 Program: External Catalyst ZB - 168 Program: External Catalyst ZB - 880 Program: External Catalyst L EG END: Sources: ClinicalTrial.gov, Company Press Release Abbreviations: AA, alopecia areata; AD, atopic dermatitis; COPD, chronic obstructive pulmonary disease; HS, hidradenitis suppurativa, PsA, psoriatic arthritis; SLE, systemic lupus erythematosus; UC, ulcerative colitis 2024 2025 Q1 Q2 Q3 Q4 Q1 Q2 (1Q - 2024) Topline data from Ph2b/3 in PsA Acelyrin, izokibep ( IL - 17 ) (4Q - 2024) Topline Ph2b/3 in Uveitis Acelyrin, izokibep ( IL - 17 ) (3Q - 2024) Topline Ph2 in Plaque psoriasis Dice (part of Eli Lilly), DC - 806 ( IL - 17 ) (3Q - 2024) Topline Ph3 in Asthma Astra Zeneca / Amgen, tezepelumab ( TSLP ) (3Q - 2024) Ph2 in SLE Novartis, Ianalumab (VAY736) ( BAFF ) & iscalimab (CFZ533) ( anti - CD40 ) (1Q - 2024) Topline Ph2 in COPD Astra Zeneca / Amgen, tezepelumab ( TSLP ) (1Q - 2024) Topline data from Ph2b in PsA MoonLake, sonelokimab ( IL - 17 ) (3Q - 2024) Topline in Ph2a in AA Q - 32 Bio/Horizon (part of Amgen), ADX - 914 ( IL - 7 / TSLP ) (1Q/2Q - 2024) Topline in Ph2 in AD Q - 32 Bio/Horizon (part of Amgen), ADX - 914 ( IL - 7 / TSLP ) (4Q - 2024) Topline in Ph1b / 2a in AA Inmagene, IMG - 007 ( OX40 ) (2Q - 2025) Ph3 in COPD (AERIFY - 1 / AERIFY - II) Sanofi/Regeneron, itepekimab ( anti - IL - 33 mAb ) Nasdaq: ZURA Key External Catalysts Through 1H - 2025 (4Q - 2023 to 1Q - 2024) Topline Ph2 in UC OSE Immunotherapeutics , OSE - 127 (anti - IL - 7R mAb ) (1Q/2Q - 2024) Initiate Ph1/2 trial in AA Nektar Therapeutics, rezpegaldesleukin (Ongoing through Q4 - 2026) Topline Readouts in Multi - year B - cell Platform Study in HS Novartis, CFZ533, LYS006, MAS825, LOU064 and VAY736
©2023 Zura Bio Ltd. Paradigm shift for patients Our approach could signify a paradigm shift for patients suffering from severe and intricate autoimmune diseases. These patients currently find their needs unmet by the conventional "single” pathway approach. Pioneering dual pathway biology Integrating two validated mechanisms in disease indications where each has demonstrated individual efficacy Potent molecules with highly validated pathways Our clinical - stage assets are positioned as potentially best - in - class in pathways driving efficacy, aiming to profoundly alter the trajectory of chronic autoimmune diseases . Pioneering dual pathway biology Potential best - in - class potency on clinically validated pathways Paradigm shift for complex diseases 7 Our Strategic Approach
©2023 Zura Bio Ltd. Paradigm shifting not incrementalism 8 Nasdaq: ZURA PATIENTS NEED A PARADIGM SHIFT Hidradenitis suppurativa • IL - 17 treatments seem to have reached their efficacy ceiling • Overall disease burden still exists • Persistent inflammatory burden remains with a B - cell driven component Systemic sclerosis • Skin, lung, kidney and other organs are affected by SSc • Two drugs approved for severe lung complications (SSc - ILD) • No treatment addresses the disease across multiple organ systems, currently, only lung complications are being addressed Broader efficacy Works in more patients not just certain subsets Deeper efficacy Raising the efficacy bar for all patients Effi cacy Tox Patient tolerability and safety Tox Alopecia areata • Efficacy bar is set at the low or mid dose of JAK inhibitors (JAKi) • The JAKi class carries black box warnings limiting broad adoption for AA • Efficacious, safer and better tolerated treatments are needed CURRENT APPROACHES ARE INCREMENTAL Sources: Company Presentations, Publications and Research.
©2023 Zura Bio Ltd. Pioneering Dual Pathway Biology 9 Sources: 1 Liu, Ling, et al. Journal of Inflammation Research, doi:10.2147/jir.s100940. 2 Manetta, Joseph et al. Journal of Inflammation Research, doi:10.2147/jir.s67751. 3 Benschop, Robert J., et al. mAbs, doi:10.1080/19420862.2019.1624463. (*) Figure Generated with BioRender Nasdaq: ZURA ZB - 106 tabalumab ZB - 106 + IL - 17A tabalumab + IL - 17A ZB - 106 T A L TZ ® TALTZ® + BAFF ZB - 106 + BAFF ZB - 106 is an IgG - scFv engineered by the fusion of ixekizumab (TALTZ®) and tabalumab 1, 2, 3 T A L T Z ® Anti - IL - 17 scFv Anti - BAFF Ab t a b a l um a b tibulizumab Anti BAFFxIL17 x ZB - 106 neutralizes IL - 17A or BAFF regardless of whether the other binding sites are occupied x ZB - 106 binds in the same way as Taltz and tabalumab with the same number of binding sites x Activity is mediated through direct target engagement and not ADCC x t 1/2 is 26.9 days IL - 17 * BAFF * ZB - 106 inhibits BAFF - mediated proliferation in T1165 cells in an IL - 17 independent manner 3 ZB - 106 inhibits IL - 17 mediated CXCL1 in epithelial cells in a BAFF independent manner 3
TALTZ® Anti - IL - 17 scFv Anti - BAFF Ab t a ba l u m a b IL - 17 tibulizumab: BAFF / IL - 17 BAFF ZB - 168: IL - 7R / TSLP torudokimab: IL - 33 / RAGE Potent molecules with highly validated pathways Nasdaq: ZURA DOSING TO DATE 2 o 78 Participants Dosed Across Three Ph1/1b studies 57 participants with single dose 21 participants with multiple dose up to 12 weeks POTENCY 93 Participants Dosed 60 participants with single dose 33 participants with multiple doses up to 12 weeks 244 Participants Dosed 81 participants with single dose 163 participants with multiple doses up to 52 weeks IL - 17 binds to IL - 17A preventing IL - 17A/A and IL - 17A/F heterodimerization 1 • ZB - 168 is nearly 10 - fold more potent than AZ/AMG’s tezepelumab, and tezepelumab does not inhibit IL - 7 signaling • ZB - 168 is >300 - fold more potent than Q32Bio / Horizon’s ADX - 914 in TSLP - induced markers, but similar in IL - 7 - induced pSTA5 8 Torudokimab was 2.9 and 5.5 - fold more potent than etokimab and itepekimab , respectively, inhibiting IL - 33 - induced GM - CSF production by human mast cells ha lf - lif e ( t 1/2 ) UPB - 101 ( α - TS LP R) t eze p el u m ab (TSLP) b e mp i k i ba rt (IL - 7R α ) ZB - 168 (I L - 7R α ) Antibody k on (M - 1 s - 1 ) k off (s - 1 ) k d (pM) t oru d o kimab Potency α - TSLPR mAb TSLP mAb IL - 7R α mAb IL - 7R α mAb tibulizumab 26.9 days torudokimab (LY3375880) 1.7 x 10 6 6.7 x 10 - 5 39 7.5 ng / ml / 0.05nM (CCL17) (5) 11 ng / ml / 0.07nM (CCL22) (5) 0.08 nM (CCL2) (8) TS LP - I nd u ced Signals 16.1 ng / ml / 0.1nM (CCL17) (7) 67 ng / ml / 0.44nM (CCL17) (7) 24 nM (CCL2) ( 8) etokimab (AnaptysBio) 9.4 x 10 5 1.2 x 10 - 4 112 2.9x sonelokimab 11 - 12 days itepekimab (Regeneron) 7.6 x 10 5 1.6 x 10 - 4 215 5.5x izokibep ~11 days 0.6 nM (IL - 7 at 0.25ng/ml) (8) 2.1 nM (IL - 7 at 2.5ng/ml) (8) search, doi:10.2147/jir.s677 oi:10.1124/jpet.121.000686 Sources: 1 Liu, Ling, et al. Journal of Inflam 6 Herold, Kevan C., et al. JCI Insight, doi:10.1 mation Research, doi:10.2147/jir.s100940. 2 IB an 172/jci.insight.126054. 7 Numazaki, Mako, et al. Jo IL - 7 - Induced Signals d CSR, 3 Manetta, Jose urnal of Pharmacolo Neg ph et al. Journal o gy and Experimen Neg f Inflammation Re tal Therapeutics, d 0.46nM (pSTAT5) (6) 51. 4 Benschop, Robert J., et al. m . 8. BMS patent https://patents.go Abs, doi:10.1080/19420862.2019.1624463. 5 Z gle.com/patent/WO2020154293A1/en ura Internal Dat a. ©2 023 Zura Bio Ltd. 10 IL - 7R TSLPR γ c
©2023 Zura Bio Ltd. ZB - 106 is Clinically De - Risked Through Ph1b 11 ▪ SAD Studies: No deaths or SAEs ▪ MAD study: No deaths, single related SAE of neutropenia with resolution ▪ Most frequent TEAE: Headache, transient neutropenia, nausea, diarrhea ▪ No TEAE of infection at target doses ▪ In the MAD study, one participant had TE - ADAs detected at a low titer ▪ t 1/2 is 26.9 days ▪ Bioavailability after SC doses was 62.9% ▪ At doses tested there is evidence of maximum target engagement with clinical safety supporting 6 - fold “window” between max target engagement and max human dose tested Established dosing regimen ▪ In Ph1b healthy volunteer study in RA participants there was multiple impacts on PD markers: - Decrease in CD20+ B - cells with higher doses generally associated with larger changes from baseline - Decrease in hs - CRP AUC was associated with higher ZB - 106 AUCs 78 Participants Dosed Across Three Ph1/1b studies 57 participants with single dose; 21 participants with multiple dose up to 12 weeks PHARMACOKINETICS PHARMACODYNAMICS SAFETY and ADA Demonstrated PD in participants in Ph1b Safety / ADA profile in line with TALTZ® ZB - 106 is a highly validated molecule that enables the opportunity to deliver on the promise of both IL - 17 and BAFF inhibition in autoimmune disease Nasdaq: ZURA Abbreviations: MAD, multiple ascending dose; SAD, single ascending dose
©2023 Zura Bio Ltd. Combining IL - 17 and BAFF Neutralization in a Murine Model of Arthritis Enables Improvement in Therapeutic Benefit 12 ▪ Rheumatoid arthritis is a prototypic autoimmune disease where individually targeting IL - 17 - mediated inflammation or depleting B cells has been clinically validated ▪ The collagen - induced arthritis (CIA) murine model is similarly characterized by increased IL - 17 production and B cells that drive disease pathogenesis ▪ Surrogate antibodies were used to evaluate whether neutralization of IL - 17 and BAFF was superior to targeting individual pathways ▪ Mice were injected with anti - IL - 17A and/or anti - BAFF on days 22, 29, and 36 ▪ Blockade of both IL - 17A and BAFF was associated with reduced: ▪ Disease severity ▪ Inflammation in the hind paw (histology score) ▪ Anti - collagen antibodies histology score anti - collagen antibody (mg/mL) anti - BAFF + anti - IL - 17 Sources: Zura Internal Data, IND Briefing
©2023 Zura Bio Ltd. Potential First - in - Class, Dual Antagonist Combining tabalumab and TALTZ® ZB - 1 0 6 tibulizumab Anti - BAFF x IL - 17 systemic sclerosis (SSc)
©2023 Zura Bio Ltd. zz zz zz zz 14 Systemic sclerosis is a rare & life - threatening disease with no approved therapy ~200,000 people with SSc in US, EU and Japan 1 40 - 60% mortality in 10 years 2 Zero SSc - specific * drugs approved $2B+ annual potential market opportunity Rare and life - threatening autoimmune disease characterized by tissue inflammation and fibrosis 01 One of the deadliest of the rheumatic diseases 02 Associated with severe disability, fibrosis - related organ failure, and premature death • Up to 50% of patients develop interstitial lung disease (ILD), the most common cause of mortality in these patients • Severe impact on patients’ lives with a variable constellation of symptoms, including Raynaud’s phenomenon, arthritis, painful ulcers on fingers and toes, thickening and scarring of the skin, shortness of breath, hypertension, and severe fatigue High unmet medical need with no approved therapy 01 Standard of care relies upon off label use of immunosuppressive agents 02 Symptom management with pain relief through nonsteroidal, anti - inflammatory medications or corticosteroids 03 Two disease - modifying drugs are approved for severe lung complications of the disease (SSc - ILD), but no effective treatment exists that combats the disease across organ systems. Sources: Medscape, BMJ best practice 1 Health Advanced, LLC; Lenabasum Commercial Market Assessment. 2 Tyndall et al, 2010 3 Bergamasco, A. et al., Clin Epidemiol. 2019 Apr 18;11:257 - 273 4 Zura Bio internal analysis and benchmarking, 5 Internal assumption based on demand research and rare disease analogues (*) no effective treatment exists that combats the disease across organ systems ZB - 106 | SSc
©2023 Zura Bio Ltd. IL - 17 efficacy in SSc Role of BAFF in SSc IL - 17 and BAFF Inhibition Have Shown Efficacy in Placebo Controlled Trials in systemic sclerosis (SSc) 15 S t rom al cells T1 - IFN BAF F P l a sm a cell C XC R5 + T fh cell T LS GC B cell C XC L1 3 • Brodalumab treatment in SSc leads to improved clinical outcomes 1 • IL - 17 known to play key role in the fibrotic process of various organs like lung, kidney, heart and skin • Th17 cell – derived IL - 17 was significantly higher in the skin and serum of SSc patients 2 Sources: 1 Fukasawa, T., et al. Annals of the Rheumatic Diseases, doi:10.1136/annrheumdis - 2022 - eular.2519. 2 Yang, Xiaoqin, et al. Arthritis Research Therapy, doi:10.1186/ar4430. 3 Ebata, Satoshi, et al. The Lancet Rheumatology, doi:10.1016/s2665 - 9913(21)00107 - 7. 4 Sato, Shinichi, et al. Molecular Immunology, doi:10.1016/j.molimm.2004.06.025. 5 Senécal, Jean - Luc, et al. Journal of Scleroderma and Related Disorders, doi:10.1177/2397198319870667. 6 Sato, Shinichi,, et al. The Journal of Immunology, doi:10.4049/jimmunol.165.11.6635. 7 Gordon, Jessica K., et al. Arthritis Rheumatology, doi:10.1002/art.40358. • Belimumab therapy shows efficacy in open label studies and one single center PBO study 7 • Belimumab has been granted ODD by FDA and a Phase 2/3 had been initiated in SSc - ILD by GSK • SSc patients have B cell abnormalities characterized by chronic hyper - reactivity of memory B cells 4 • BAFF and auto - antibodies are key biomarkers in SSc 5,6 ZB - 106 has the potential to treat the Th17 and BAFF components of SSc ZB - 106 | SSc Stromal cells Plasma cell C X CR 5 + T fh c e l l
©2023 Zura Bio Ltd. 16 Rituximab CD20 B - cell depleter ▪ Multiple Studies demonstrated effectiveness of rituximab in SSc (mainly open label and observational) ▪ The most compelling data comes from the DESIRES double blind – placebo - controlled trial in 56 pts with SSc ▪ Primary endpoint: mRSS change after 24 weeks of treatment ▪ Rituximab - 6.30 points vs. PBO +2.14 points (p < 0.0001) ▪ 48 / 56 participants had SSc - ILD 2.96% FVC improvement at 24 weeks vs. PBO (p=0.04) Belimumab BAFF antagonist ▪ 52 - week, investigator initiated, single center, double blind, placebo - controlled pilot study in 20 participants with dcSSC on MMF ▪ No significant difference of AEs in active and placebo arms ▪ Both treatment groups experienced improvements in mRSS favoring belimumab ( - 10 vs - 3; p=NS) ▪ All secondary endpoints favored belimumab with statistical significance in 2 endpoints: SHAQ DI and VAS Raynaud’s phenomenon ▪ Orphan Drug Designation granted ▪ P 2/3 RCT has been initiated for SSc - ILD CD20+ B cells in HS Lesions Brodalumab IL - 17 receptor antagonist ▪ Achieved primary endpoint of treatment difference of least square mean: −21.2 [95% CI - 23.9, 18.5]; P<0.0001), and demonstrated a rapid, sustained reduction in mRSS over 52 weeks 1 ▪ Demonstrated therapeutic effects on lung/respiratory functions, digital ulcers, the symptoms of gastroesophageal reflux disease, and QOL without noteworthy safety concerns ZB - 106 | SSc Sources: 1 Fukasawa, T., et al. Annals of the Rheumatic Diseases, doi:10.1136/annrheumdis - 2022 - eular.2519. 2 Gordon, Jessica K., et al. Arthritis Rheumatology, doi:10.1002/art.40358. 3 Ebata, Satoshi, et al. The Lancet Rheumatology, doi:10.1016/s2665 - 9913(21)00107 - 7. IL - 17 and BAFF Inhibition Have Shown Efficacy in Placebo Controlled Trials in systemic sclerosis (SSc)
©2023 Zura Bio Ltd. Phase 2 SSc Trial Design* 17 ZB - 106 | SSc KEY SAFETY ENDPOINTS KEY EFFICACY ENDPOINTS DOUBLE BLIND, PLACEBO - CONTROLLED TRIAL EFFICACY PERIOD (24 / 52 WEEKS) P L A C E B O ZB - 106 DOSE LEVEL 2 ZB - 106 DOSE LEVEL 1 R • FVC, DLCO • ACR - CRISS • Change in mRSS • SHAQ DI • VAS (RP, Pain, Ulcers, Breathing) • PK / PD assessments • General Safety and Tolerability • Severe infection • Neutropenia • ADA / nAb (*) Trial design is subject to change due to factors such as regulatory feedback
©2023 Zura Bio Ltd. Potential First - in - Class, Dual Antagonist Combining tabalumab and TALTZ® ZB - 1 0 6 tibulizumab Anti - BAFF x IL - 17 hidradenitis suppurativa (HS)
©2023 Zura Bio Ltd. Overview of hidradenitis suppurativa (HS) 19 Estimated ~300K people living with Hidradenitis suppurativa in the U.S. (1 - 2% global prevalence) Average of 7 years to diagnose globally High unmet need >50% patients still left inadequately treated According to HiSCR 75 data CURRENT TREATMENTS ONLY AIM TO MANAGE SYMPTOMS AND INCLUDE PALLIATIVE CARE SUCH AS OTC EYEDROPS, TOPICAL CYCLOSPORINE AND OFF - LABEL STEROIDS OR IMMUNOSUPPRESSANTS TO MANAGE SYSTEMIC SYMPTOMS DISEASE OVERVIEW ▪ Hidradenitis suppurativa is an inflammatory follicular skin disease ▪ Skin lesions develop in axillae, in the groin, and under the breasts, are formed as a result of inflammation & infection of sweat glands and are characterized by: - Recurrent boil - like nodules and abscesses that culminate in pus - like discharge - Difficult - to - heal open wounds (sinuses) and scarring - Increased Th1/Th17 and B cell mediated inflammation 1 - 3 - Disproportionately affects women between adolescent age to 55 years of age 4, 5 CLINICAL OPPORTUNITY ZB - 106 | HS Sources: 1 Moran, Barry, et al. Journal of Investigative Dermatology, doi:10.1016/j.jid.2017.05.033. 2 Banerjee, Anirban, et al. Immunological Investigations, doi:10.1080/08820139.2016.1230867. 3 Sabat, Robert, et al. Journal of Allergy and Clinical Immunology, doi:10.1016/j.jaci.2022.10.034. 4 Garg, Amit, et al. JAMA Dermatology, doi:10.1001/jamadermatol.2017.0201. 5 Ingram, John R. British Journal of Dermatology, doi:10.1111/bjd.19435.
©2023 Zura Bio Ltd. 20 RECENT HS DATA C om p a n y Asset h umir a cosentyx bimzelx bimzelx sonelokimab sonelokimab i z o k ib e p i z o k ib e p fo s t a m a t i n i b M ec Admi P Do Total Efficacy ( H i SCR 5 0 ) Efficacy ( H i S C R75) Safety / T o lera b ili t y hanism TNF - α IL - 17 A IL - 17 A/F IL - 17 A/F IL - 17 A/F IL - 17 A/F IL - 17 A/A IL - 17 A/A SYK inhibitor nistration SC SC/IV SC SC SC SC SC SC PO hase PIONEER I & II Phase 3 SUNSHINE & SUNRISE Phase 3 BE HEARD I & II Phase 3 Phase 2 Phase 2 Part A Phase 2 Part B Phase 2b Part A Phase 2b Part B Phase 2 sing 40mg QW for 12W 30mg Q2W for 16W 320mg Q2W for 16W 320mg Q2W for 12W 120mg Q2W for 12W 120mg Q2W for 24W 160mg QW for 12W 160 mg Q2W or QW for 12W 150 mg BID for 12W Patients n = 633 n = 360 est. n = 579 n = 88 n = 234 n = 234 n = 30 n = 175 n = 20 Non - Pl ac e bo Adjusted 42% - 59% 42% - 45% 48% - 52% 63% 66% 76% 71% 42% - 46% 85% Placebo Adjust ed 16% - 31% 11% + 19% - 20% 35% 38% 48% N/A 1% - 5% N/A Non - Pl ac e bo Adjusted N/A N/A 33 - 36% 50% 43% 57% 57% 34% - 39% 70% Placebo Adjust ed N/A N/A 15% - 20% 29% 29% N/A N/A 5% - 10% N/A Most Common AEs Hea dac h e 9% - 13% Hea dac h e 9% - 12% Hi d ra d e n itis 7% - 9% I nfec t ions 44% Naso p ha r y n gitis 16% Naso p ha r y n gitis 12% Injection site reactions TBD Na u sea 30% Candidiasis 0% 1 0% - 3% 1 4% - 7% 9% 10.5% >10% 0% 2 TBD 0% ZB - 106 | HS Phase 2 data show IL - 17 efficacy ceiling may have been reached | Fostamatinib data provide evidence of B - Cell importance Multiple P3 Studies Show IL - 17 is Clinically Validated Pathway to Treat HS Sources: Company Presentations, Publications and Research. 1 Represents data from psoriasis trial. 2 Represents safety data from psoriatic arthritis trial.
©2023 Zura Bio Ltd. B Cell Signaling Potentiates HS Disease 21 ZB - 106 | HS Sources: 1 Van der Zee, H.H., et al. British Journal of Dermatology, doi:10.1111/j.1365 - 2133.2011.10698. 2 Rumberger et al. 2020. J Inflam Research; 3 Sabat, Robert, et al. Journal of Allergy and Clinical Immunology, doi:10.1016/j.jaci.2022.10.034. 4 Gudjonsson, Johann E., et al. JCI Insight, doi:10.1172/jci.insight.139930. 5 Seigel et al 2023. JCutanMedicSurgery; 6 Jepsen et al. 2023. JAAD Pathogenic Role for B Cells and Plasma Cells ▪ CD20+ B and CD138+ Plasma Cells are increased in chronic HS lesions 1 ▪ B cell depletion with rituximab provided therapeutic benefit with 4 out of 5 cases reporting complete remission of HS lesions 5 CD20+ B cells in HS Lesions Clinical Benefit of Targeting B Cells BAFF Drives B Cell Activation and Inflammation ▪ Increased BAFF expression in HS lesions and tunnels 2 - 4 ▪ Neutralization of BAFF in HS lesional explants reduced the expression of B & plasma cell gene signatures 2 BAFF gene expression in HS BAFF is essential for B cell activation Week 12 % Achieving HiSCR50 % Achieving HiSCR75 Fostamatinib (SYK inhibition) 6 85% 70% ▪ Modulating B cell function using fostamatinib (SYK inhibition) provided therapeutic benefit in HS 6 ▪ B cell depletion with rituximab provided therapeutic benefit 5 ▪ 4/5 cases report complete remission of HS lesions 5 B cell disruption is efficacious in HS Baseline W1 W2 W6 W 8 W12 0 50 1 00 H i S C R5 0 H iS CR 75 H iS CR 90 W4 W5 T im e p o in t Percentage of Participants Achieving Clinical Outcome (%)
©2023 Zura Bio Ltd. Dermal Tunnels: Role in HS Pathogenesis 22 Sources: 1 Frew et al. 2021 Clin Exper Derm; 2 Sabat et al JACI 2023; 3 Moran et al. JID 2017; 4 Gudjonsson et al. 2020; 5 Jepsen et al. 2023. JAAD Treatment with fostamatinib (SYK Inhibitor) significantly reduced IHS4 scores and draining tunnel counts 5 Dermal tunnels in HS are characterized by increased numbers of neutrophils and B cells that produce high levels of BAFF 2,4 Recent literature highlights the role of dermal tunnels in the pathogenesis of HS 1, 2 The presence of dermal tunnels increased the amount of time needed to achieve HiSCR50 with adalimumab 3 One significant drawback of the HiSCR is the lack of a dynamic measurement of draining tunnel; therefore, not fully capturing the anti - inflammatory properties of a therapeutic The International Hidradenitis Suppurativa Severity Score System (IHS 4 ) was developed to assess inflammatory nodules ( 1 point), abscesses ( 2 points) and draining tunnels ( 4 points) ZB - 106 | HS
©2023 Zura Bio Ltd. Phase 2 HS Trial Design* 23 ZB - 106 | HS KEY SAFETY ENDPOINTS KEY EFFICACY ENDPOINTS EFFICACY PERIOD (12 / 24 WEEKS) P L A C E B O ZB - 106 DOSE LEVEL 2 ZB - 106 DOSE LEVEL 1 Moderate to Severe HS Total abscess and inflammatory count (AN) ≥ 5 KEY INCLUSION CRITERIA DOUBLE BLIND, PLACEBO - CONTROLLED TRIAL ~60 p ar t i c i p an t s R per arm • HiSCR (50, 75, 100) • Improvement in baseline AN counts • I H S4 • PGA • DLQI • PK / PD assessments • General Safety and Tolerability • Severe infection • Neutropenia Hurley Stage II/III (*) Trial design is subject to change due to factors such as regulatory feedback
©2023 Zura Bio Ltd. A Potential Best - in - Class Anti - IL - 7R Inhibiting Both IL - 7 and TSLP Pathways ZB - 1 6 8 Anti - IL - 7R alopecia areata (AA)
©2023 Zura Bio Ltd. 25 Cytokine Signaling via IL - 7 and TSLP Pathways ZB - 168 | AA IL - 7R α is a key receptor in immune regulation, central to the signaling of cytokines IL - 7 and TSLP Positioning ZB - 168 for diverse immune - related and autoimmune conditions Commonly tied to allergic responses and specific inflammatory scenarios This assembled complex initiates pathways primarily linked to type 2 im m u n it y TSLP binds to its dedicated receptor, TSLPR. For optimal signaling, IL - 7R α joins the mix, creating a composite complex with TSLPR and TSLP TSLP IL - 7 R α collaborates with the common gamma chain ( γ c) to establish the IL - 7 receptor complex IL - 7 Vital for the growth, sustenance, and balance of T - cells Triggers a sequence of cellular events, notably JAKs & STATs T - Cell
©2023 Zura Bio Ltd. 26 Potential Therapeutic Franchises for ZB - 168 ZB - 168 | AA Sources: 1 ClinicalTrials.gov database Explore the potential indication space Solid biologic rationale for IL - 7 / TSLP E x p ec t ed Clinical Readout 1 Alopecia areata (and other Dermatology) Ulcerative colitis (and other GI) Asthma (and other Respiratory)
©2023 Zura Bio Ltd. 27 Redefining Treatment Standards for alopecia areata ZB - 168 | AA Alopecia areata H i g h CD8 T effector memory CD4 T reg ZB - 16 8 I L - 7 R α L ow I L - 7 R α Universalis T o t a l is A r eat a Z B - 1 68 1, 2 Targets the T effector memory Preserves the T r eg Autoimmune disease with 2% of population affected, 30 - 40% with >50% scalp hair loss. Characterized by patchy areata or complete hair loss on scalp (totalis) or complete hair loss all over body (universalis) Significant impact to physical, psychosocial and overall productivity Invasion of T - cells Loss of immune p r ivi l e g e P re s er v a t i o n of hair follicle T i me / T reg T effector memory 1.5 1.0 0 70 Sources: 1 Williams, Jason H., et al. The AAPS Journal, doi:10.1208/s12248 - 019 - 0401 - 3. 2 Herold, Kevan C., et al. JCI Insight, doi:10.1172/jci.insight.126054.
©2023 Zura Bio Ltd. 28 Anti - TSLPR t e z e p e l u m a b IgG ZB - 168 1 00 50 0 - 50 4 2 - 2 - 4 %Inhibition 0 Log (nm) % inhibition of TSLP stimulated CCL17 secretion from human monocytes ZB - 168 is Potentially Best - in - Class Asset at TSLP Inhibition ZB - 168 | AA ▪ ZB - 168 is nearly 10 - fold more potent than AZN / AMGN’s tezepelumab, and tezepelumab does not inhibit IL - 7 signaling ▪ ZB - 168 is >300 - fold more potent than Q32 Bio / Horizon’s bempikibart (formerly ADX - 914) in TSLP - induced markers, but similar in IL - 7 - induced pSTAT5 4 UPB - 101 ( α - T SL P R) teze p e l u mab (TSLP) b e mpik i ba r t (IL - 7R α ) ZB - 168 (I L - 7R α ) α - TSLPR mAb TSLP mAb IL - 7R α mAb IL - 7R α mAb 7.5 ng / ml / 0.05nM (CCL17) (1) T SL P - I n duced Signals 16.1 ng / ml / 0.1nM (CCL17) (3) 67 ng / ml / 0.44nM (CCL17) (3) 24 nM ( CC L2) ( 4) 11 ng / ml / 0.07nM (CCL22) (1) 0.08 nM (CCL2) (4) 0.6 nM I L - 7 - I n duce d Signals Neg Neg (IL - 7 at 0.25ng/ml) (4) 2.1 nM 0.46nM (pSTAT5) (2) (IL - 7 at 2.5ng/ml) (4) In 2023, Zura Bio and Benaroya Research Institute (BRI) initiated a sponsored research collaboration to delve deeper into the role of IL - 7R α in TSLP and IL - 7 signaling pathways. This collaboration aims to enhance understanding of the roles IL - 7 and TSLP play in immunological diseases and the potential benefit from targeting IL - 7R ⍺ , which is required for the signaling of both pathways. Sources: 1 Zura Internal Data, 2 Herold, Kevan C., et al. JCI Insight, doi:10.1172/jci.insight.126054. . 3 Numazaki, Mako, et al. Journal of Pharmacology and Experimental Therapeutics, doi:10.1124/jpet.121.000686. 4 Yamniuk, Aaron P., et al. Antibodies against Il - 7r Alpha Subunit and Uses Thereof. 18 May 2021.
©2023 Zura Bio Ltd. 29 Current treatments involving JAK inhibitors ZB - 168 | AA JAK inhibitors block multiple pathways by targeting JAK1 and JAK2, which are involved in numerous cytokine signaling processes. This broad action will/can inadvertently suppress beneficial immune responses. Concerns with JAK Inhibitors 1 2 Broad Action Black Box Warnings 3. Thrombosis Patients on JAK inhibitors face a heightened risk of blood clots. 4. Increased Mortality Particularly in older patients with cardiovascular risk factors, there's an associated higher risk of death. 1. Infections JAK inhibitors can/will increase the risk of serious infections due to their immunosuppressive nature. 2. Malignancy Their use has been linked to an elevated risk of certain cancers
©2023 Zura Bio Ltd. Phase 2 AA Trial Design* 30 (*) Trial design is subject to change due to factors such as regulatory feedback KEY SAFETY ENDPOINTS • General Safety and Tolerability • Severe infection • Neutropenia • ADA / nAb ZB - 168 | AA KEY EFFICACY ENDPOINTS • Percent change in SALT score • ClinRo • Proportion of patients with pre - specified SALT reductions • Scalp Hair Assessment • Biomarkers PART B: RANDOMIZED TRIAL PART A: OPEN - LABEL TRIAL EFFICACY PERIOD (24 WEEKS) ZB - 168 DOSE ~30 E participants ~ 40 p ar t i c i p an t s per arm P L A C E B O ZB - 168 DOSE LEVEL 3 ZB - 168 DOSE LEVEL 1 ZB - 168 DOSE LEVEL 2 EFFICACY PERIOD (24 / 36 WEEKS) R
©2023 Zura Bio Ltd. Targeting Anti - IL - 33, an Alarmin with Potential in Multiple Indications ZB - 880 t or u do k i m a b Anti - IL - 33 allergy / respiratory Indications
©2023 Zura Bio Ltd. Mechanism of Action About ZB - 880 (torudokimab) Initial Focus on Respiratory, Dermatologic, Gastrointestinal and Orphan Autoimmune Indications ZB - 880 Asset Overview 32 Sources: 1. Cohen et al. 2015 Nature, 2. https://clinicaltrials.gov/ct2/show/NCT03913260; https://clinicaltrials.gov/ct2/show/NCT03343587; https://clinicaltrials.gov/ct2/show/NCT03831191, Section 6.1, DSUR for period 23 - Sep - 2019 to 22 - Sep - 2020, 3. doi.org/10.1111/bjd.21631 4. Okragly et al Journal of Inflammation Research 2021:14 3823 – 3835, 5.. doi:10.1056/NEJMoa2024257 01 IL - 33 implicated in driving Th2 biology through ST2 and Th1/Th17 through alternative signaling 1 02 Well tolerated in Ph1 and Ph2 trials conducted by Eli Lilly 2 03 The target engagement evaluation suggested binding to IL - 33 and treatment emergent ADA had no apparent impact on PK or target engagement 141 healthy volunteers in Ph1 study 103 participants with moderate to severe atopic dermatitis in Ph2 Analyses confirmed key biomarker reductions (IL - 13, periostin and CCL17/TARC) and no ADA impact 3 Potential utility in diseases driven by epithelial inflammation 1 01 Potential for 1st - in - class opportunities 02 Validated pathways in COPD4 and asthma 5 01 Inhibition of IL - 33 blocks both ST2 and RAGE signaling 4
©2023 Zura Bio Ltd. ZB - 880 IL - 33 Pathway 33 Sources: 1. Chan, 2019. Frontiers Immunol, 2. doi.org/10.1016/j.cyto.2022.155891, 3. https://doi.org/10.1038/ng.323 and doi:10.1016/j.jaci.2020.04.051 , 4. .:https://doi.org/10.1016/S2213 - 2600(22)00005 - 4; doi:10.1056/NEJMoa2024257 and doi: 10.1126/scitranslmed.aax2945 , 5. Sci Trans Med., Zura Bio Internal data, 6. doi: 10.1111/imm.12174; https://doi.org/10.3389/fphys.2021.781012 and https://doi.org/10.3389/fmed.2021.739489 IL - 33 is a member of the IL - 1 cytokine family that is constitutively expressed in structural and lining cells including fibroblasts, endothelial, and epithelial cells of skin, gastrointestinal tract, and lungs 1 IL - 33 is released from the epithelium by disease exacerbating environmental factors and is an important amplifier of innate inflammation during exacerbations 2 Polymorphisms in IL - 33 and ST2 are associated with increased eosinophil production as well as respiratory diseases such as COPD and severe asthma IL - 33 inhibition clinically validated in severe asthma, COPD3, and subsets of other epithelial disorders 4 Pre - clinical data demonstrates superior activity of torudokimab compared with etokimab suggesting the potential for best - in - class activity 5 Emerging biology suggests expanding opportunity for IL - 33 in fibrotic and autoimmune conditions 6
©2023 Zura Bio Ltd. ZB - 880 Has Potential for “Best - in - Class” Activity 34 Torudokimab was 2.9 and 5.5 - fold more potent than etokimab and itepekimab , respectively, inhibiting IL - 33 - induced GM - CSF production by human mast cells Sources: Zura Bio Internal data Antibody k on (M - 1 s - 1 ) k off (s - 1 ) k d (pM) Torudokimab Potency torudokimab (LY3375880) 1.7 x 10 6 6.7 x 10 - 5 39 etokimab (AnaptysBio) 9.4 x 10 5 1.2 x 10 - 4 112 2.9x itepekimab (Regeneron) 7.6 x 10 5 1.6 x 10 - 4 215 5.5x