Form 8-K

8-K — Zura Bio Ltd

Accession: 0001104659-26-079538

Filed: 2026-07-01

Period: 2026-07-01

CIK: 0001855644

SIC: 2836 (BIOLOGICAL PRODUCTS (NO DIAGNOSTIC SUBSTANCES))

Item: Regulation FD Disclosure

Item: Financial Statements and Exhibits

Documents

8-K — tm2619483d1_8k.htm (Primary)

EX-99.1 — EXHIBIT 99.1 (tm2619483d1_ex99-1.htm)

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0001855644

2026-07-01

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Warrants [Member]

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington,

D.C. 20549

Form

8-K

Current

Report

Pursuant

to Section 13 or

15(d)

of the Securities Exchange Act of 1934

July 1, 2026

Date of Report (Date of earliest event reported)

Zura Bio Limited

(Exact name of registrant as specified in its charter)

Cayman Islands

001-40598

98-1725736

(State or other jurisdiction of

incorporation)

(Commission

File Number)

(I.R.S. Employer

Identification No.)

1489 W. Warm Springs Rd. #110

Henderson, NV 89014

(Address of principal

executive offices,

including zip code)

(702) 757-6133

(Registrant’s telephone

number, including area code)

(Former name or former address,

if changed since last report)

Check the appropriate box below if the Form 8-K

filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

¨ Written

communication pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

¨ Soliciting

material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

¨ Pre-commencement

communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

¨ Pre-commencement

communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

Title of each class

Trading Symbol(s)

Name

of each exchange on which

registered

Class A Ordinary Shares, par value $0.0001 per share

ZURA

The Nasdaq Stock Market

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405

of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company x

If an emerging growth company, indicate by check mark if the registrant

has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant

to Section 13(a) of the Exchange Act. ¨

Item 7.01.

Regulation FD Disclosure.

On July 1, 2026, Zura Bio Limited (the

“Company”) provided an updated corporate presentation that may be used in connection with upcoming presentations at conferences

and investor meetings. The full text of the Company’s corporate presentation is furnished as Exhibit 99.1 hereto, and incorporated

herein by reference, and may also be accessed through the “News & Events” section of the Company’s website at investors.zurabio.com.

The information furnished under this Item 7.01

(including Exhibit 99.1), shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as

amended, or subject to the liabilities of that section or Sections 11 and 12(a)(2) of the Securities Act of 1933, as amended. The information

in this Item 7.01 (including Exhibit 99.1) shall not be deemed incorporated by reference into any other filing with the Securities and

Exchange Commission made by the Company, whether made before or after the date hereof, regardless of any general incorporation language

in such filing, except as expressly set forth by specific reference in such a filing.

Item 9.01.

Financial Statements and Exhibits.

(d) Exhibits.

Exhibit No.

Description

99.1

Corporate Presentation, dated July 1, 2026

104

Cover Page Interactive Data File (embedded within the Inline XBRL document).

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934,

the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

ZURA BIO LIMITED

Date: July 1, 2026

By:

/s/ Kim Davis

Kim Davis

Chief Operating Officer, Chief Legal Officer and Corporate Secretary

EX-99.1 — EXHIBIT 99.1

EX-99.1

Filename: tm2619483d1_ex99-1.htm · Sequence: 2

Exhibit 99.1

Corporate Overview

July 2026

Nasdaq Ticker: ZURA

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,” “may,” “will,” “could,” “should,” “believe,” “predict,” “potential,” “continue,” “strategy,” “future,” “opportunity,” “would,” “seem,” “seek,” “outlook,” “goal,” “mission,” 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, estimates, and assumptions and, as a result, are subject to risks and

uncertainties that could cause actual results to differ materially from the expected results. These statements are based on various assumptions, whether or not identified in this presentation. These forward-looking statements may include, without

limitation: Zura Bio’s clinical development plans; the design, initiation, conduct, enrollment and timing of its clinical trials; expectations regarding the timing of key milestones and anticipated data readouts; expectations regarding clinical programs,

including the safety, efficacy, and therapeutic potential of Zura Bio’s product candidates; expectations regarding the commercial potential of Zura Bio’s product candidates; expectations regarding data readouts from third parties; expectations

regarding market opportunities, including estimated total addressable markets, competitive landscape, addressable patient populations, or potential clinical differentiation; Zura Bio’s cash resources and projected cash runway; Zura Bio’s business

strategies and objectives; and any other statements that are not historical facts.

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 are difficult or impossible to predict and could differ materially from those expressed or implied in such forward-looking statements, as a result of these risks and uncertainties, which include, but are not limited to: Zura Bio’s

expectations regarding its product candidates and their related benefits, and Zura Bio’s beliefs regarding competing product candidates or approved products, may not be achieved; Zura Bio's vision and strategy may not be successful; the timing of

key events and initiation of Zura Bio's studies, and release of clinical data may take longer than anticipated or may not be achieved at all; the potential general acceptability and maintenance of Zura Bio's product candidates by regulatory authorities,

payors, physicians, and patients may not be achieved; Zura Bio's ability to attract and retain key personnel; Zura Bio's expectations with respect to its future operating expenses, capital requirements and needs for additional financing may not be

achieved; Zura Bio has not completed any clinical trials, and has no products approved for commercial sale; Zura Bio has incurred significant losses since inception, and expects to incur significant losses for the foreseeable future and may not be able

to achieve or sustain profitability in the future; Zura Bio requires substantial additional capital to finance its operations, and if it is unable to raise such capital when needed or on acceptable terms, Zura Bio may be forced to delay, reduce, and/or

eliminate one or more of its development programs or future commercialization efforts; Zura Bio may be unable to renew existing contracts, or enter into new contracts or may experience disputes or other challenges with respect to our vendors or

other third parties; Zura Bio relies on third-party contract development manufacturing organizations for the manufacture of clinical materials; Zura Bio relies on contract research organizations, clinical trial sites, and other third parties to conduct its

preclinical studies and clinical trials; Zura Bio may be unable to obtain regulatory approval for its product candidates, and there may be related restrictions or limitations of any approved products; Zura Bio may be unable to successfully respond to

general economic and geopolitical conditions; Zura Bio may be unable to effectively achieve or manage growth; Zura Bio faces competitive pressures from other companies worldwide; Zura Bio may be unable to adequately protect its intellectual

property rights; and other factors set forth in documents filed, or to be filed by Zura Bio, with the Securities and Exchange Commission (SEC), including the risks and uncertainties described in the “Risk Factors” section of Zura Bio’s Annual Report on

Form 10-K for the year ended December 31, 2025, and other filings with the SEC. 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, which speak only

as of the date made. Zura Bio does not undertake or accept any obligation to update any forward-looking statements, whether as a result of new information, future developments, or otherwise, except as required by law. Zura gives no assurance can

be given that the expectations expressed herein will be achieved orthat deviations from such expectations will not be material.

This presentation discusses product candidates that are under clinical investigation and have not been approved for marketing by the U.S. Food and Drug Administration or any other regulatory authority. No representation is made as to the safety,

efficacy, or likelihood of regulatory approval of these product candidates for the uses under investigation. Comparisons across clinical trials or product candidates should be interpreted with caution, as differences in study design, inclusion/exclusion

criteria, patient populations, endpoints, dosing regimens, and other variables may limit interpretability. Statements in this presentation regarding clinical trials involving product candidates originating from third parties (including Eli Lilly, Pfizer and

Novartis) have not been reviewed, verified, or endorsed by such parties.

Zura Bio: advancing a differentiated approach for

complex immune disorders

Our lead program, tibulizumab, is the first and currently only in-class bispecific antibody inhibiting both

the IL-17 and BAFF pathways

▪ Fusion of components from tabalumab, a BAFF-binding antibody, and an IL-17–binding single-chain variable fragment derived from

ixekizumab (marketed as Taltz®, ~$3.6B in global 2025 sales, as reported)

▪ Potent engagement of targets and low immunogenicity observed in completed Phase 1 studies

Tibulizumab has been rationally designed to address complex autoimmune diseases not fully addressed

by single-pathway therapies

▪ Dual-pathway inhibition offers the potential to overcome efficacy ceilings observed with single-pathway inhibition

▪ Potential to modulate both B-cell– and T-cell–driven pathobiology

Initial clinical focus on hidradenitis suppurativa (HS) and systemic sclerosis (SSc), each characterized

by complex immune pathobiology involving both B- and T-cell activation

▪ HS: potential to be the best-in-class treatment by inhibiting two pathways already independently validated

▪ SSc: potential to be first-in-disease treatment able to treat both skin and lung manifestations, where both IL-17 and BAFF have been

implicated

▪ Zura plans to initiate a Phase 2 study for tibulizumab in a third immune-mediated indication by year end 2026

Zura Bio is financed beyond key near-term value inflection points

▪ Topline data expected from HS and SSc phase 2 studies in Q4 2026 and 1H 2027, respectively

▪ ~$225.6M in cash and cash equivalents as of March 31, 2026

▪ Public offering in February 2026 expected to enable the Company to fund planned operations through at least the end of 2028

▪ As a result of recent February 2026 public offering, ~124M shares outstanding (as-converted)*

Nasdaq: ZURA

(*) Shares outstanding as of March 31, 2026; includes 21.2 million shares issued as part of February 2026 financing and ~29.3 million shares issuable upon conversion of outstanding pre-funded warrants

to purchase Class A ordinary shares. This figure does not reflect potential dilution from outstanding stock options or unvested RSUs.

Sources: Zura Bio Ltd., public filings and disclosures; Evaluate Pharma; publicly available information on ixekizumab (Taltz®) and tabalumab.

Acronyms: BAFF, B-cell activating factor; HS, hidradenitis suppurativa; IL-17, interleukin-17; scFv, single-chain variable fragment; SSc, systemic sclerosis.

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

Board of Directors

Nasdaq: ZURA

Executive Team

Kim Davis, JD

Chief Operating Officer, Chief

Legal Officer and Corporate

Secretary

Gary Whale, PhD

Chief Technology Officer

Kiran Nistala, MBBS, PhD

Chief Medical Officer and

Head of Development

Sandeep Kulkarni, MD

Co-Founder, Chief Executive

Officer and Director

Muzammil Mustufa

Chief Business Officer

Acronyms: HS, hidradenitis suppurativa; SSc, systemic sclerosis.

Tibulizumab advancing clinically in high unmet need multi-pathway immune-mediated diseases

Nasdaq: ZURA

A Phase 2 trial in adults with HS

Enrollment completed; 247 participants randomized

Anticipated readout: Q4 2026

Optionality for pipeline expansion into additional autoimmune indications

with complex immune pathobiology

A Phase 2 trial in adults with SSc

On track to complete enrollment early July 2026;

exceeded 80 participant enrollment target

Anticipated readout: 1H 2027

Phase 2 trial in a third immune-mediated indication

Initiation: By year-end 2026

Limits of monotherapy in multi-pathway autoimmune

disease

Acronyms: HS, hidradenitis suppurativa; SSc, systemic sclerosis. 6

Nasdaq: ZURA

Implication: these limitations support therapeutic approaches designed

to address more than one disease-driving pathway with a single agent

▪ Autoimmune diseases, including HS and SSc, are driven by

multiple, intersecting immune pathways, resulting in

biological heterogeneity across patients

▪ Single-pathway biologics may deliver low or inadequate

response rates in complex autoimmune diseases

▪ Even among responders, pathway redundancy and

compensatory signaling can limit depth and durability of

response with monotherapy

Tibulizumab: a single-molecule dual-pathway approach

Tibulizumab is an investigational agent. Its efficacy and safety have not been established or approved by the FDA or any regulatory agency worldwide.

Sources: ClinicalTrials.gov ID NCT06993610; ClinicalTrials.gov ID NCT06843239; Publicly available information on ixekizumab and tabalumab; Benschop et al., mAbs (2019), DOI: 10.1080/19420862.2019.1624463.

Acronyms: Ab, antibody; BAFF, B-cell activating factor; HS, hidradenitis suppurativa; IL-17, interleukin-17; IL-17A/F, interleukin-17A/interleukin-17F heterodimer; scFv, single-chain variable fragment;

SSc, systemic sclerosis.

Nasdaq: ZURA

Addresses disease complexity: aims to

target two distinct immune pathways

implicated in chronic inflammation and

autoimmunity

Clinically grounded design: fusion of a

BAFF-binding antibody (tabalumab) with the

IL-17A-binding scFv from ixekizumab

Single-entity advantage: enables dual-pathway modulation without multi-drug

combination complexity

ixekizumab

Anti-IL-17 scFv

IL-17A & IL-17A/F

tabalumab

Anti-BAFF Ab

BAFF

tibulizumab

Tetravalent bispecific antibody designed to block BAFF and

IL-17A–mediated signaling, including IL-17A/F heterodimers

Inhibition of BAFF and IL-17A in one bispecific antibody

Phase 1/1b data support advancement of tibulizumab into

Phase 2 development

Tibulizumab is an investigational agent. Its efficacy and safety have not been established or approved by the FDA or any regulatory agency worldwide.

(*) Model-predicted median maximum percent change from baseline of free unbound BAFF and IL-17 following the last dose. Values shown reflect steady-state trough suppression.

Sources: Eli Lilly and Company–conducted Phase 1/1b clinical studies; Zura Bio Ltd. internal clinical study reports (CSRs).

Acronyms: ADA, anti-drug antibody; BAFF, B-cell activating factor; CFB, change from baseline; CRP, C-reactive protein; IL-17, interleukin-17; PD, pharmacodynamics; PK, pharmacokinetics; Q4W, once every 4 weeks.

Nasdaq: ZURA

▪ 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): 26.9 days, supporting

once-monthly dosing

▪ Pharmacodynamic activity observed, including B cell

and CRP reductions

▪ Low incidence of treatment-emergent ADAs in

multiple-dose cohorts

▪ Safety profile consistent with published IL-17 and

BAFF pathway experience, with no new or unexpected

safety signals to date

Time (weeks)

Free BAFF concentration

%CFB

Free IL-17 concentration

%CFB

100 mg Q4W 300 mg Q4W

Population prediction interval* Median free target concentration

Dose-dependent and comparable BAFF and IL-17 target engagement

Model-based PK/PD analysis demonstrates a clear exposure–response

relationship, with comparable BAFF and IL-17 suppression and

near-complete target engagement at higher doses

BAFF: a clinically validated immune pathway

central to B cell survival

Sources: Vincent, F.B. et al. (2013), Cytokine & Growth Factor Reviews, DOI:10.1016/j.cytogfr.2013.04.003; Smulski, C.R. and Eibel, H. (2018), Frontiers in Immunology, DOI:10.3389/fimmu.2018.02285;

Matsushita, T. et al. (2005), Arthritis & Rheumatism, DOI:10.1002/art.21526.; Sabat, R. et al. (2023), Journal of Allergy and Clinical Immunology, DOI:10.1016/j.jaci.2022.10.034.

SSc, systemic sclerosis.

Nasdaq: ZURA

BAFF represents a clinically validated immune pathway

addressing a fundamental driver of chronic autoimmune disease biology

▪ BAFF is a non-redundant survival factor supporting

persistence and differentiation of autoreactive B cells

▪ Genetic, translational, and clinical data show that

disruption of BAFF signaling leads to marked reductions in

peripheral B cells

▪ Elevated BAFF levels and B cell dysregulation are reported

across immune-mediated diseases, including HS and SSc

▪ BAFF inhibition targets a core B cell survival pathway

distinct from IL-17–mediated inflammatory signaling

ixekizumab

Anti-IL-17 scFv

tabalumab

Anti-BAFF Ab

BAFF

tibulizumab

Tetravalent bispecific antibody designed to block BAFF and

IL-17A–mediated signaling, including IL-17A/F heterodimers

IL-17A: a clinically validated inflammatory pathway

The IL-17A-binding domain of tibulizumab is derived from ixekizumab.

Sources: Gaffen, S.L. et al. (2014), Nature Reviews Immunology, DOI:10.1038/nri3707; Griffiths, C.E. et al. (2015), The Lancet, DOI:10.1016/s0140-6736(15)60125-8; Blauvelt, A. et al. (2021), Journal of the

American Academy of Dermatology, DOI:10.1016/j.jaad.2020.11.022; Eli Lilly and Company, ixekizumab (Taltz®) Prescribing Information.

Acronyms: Ab, antibody; BAFF, B-cell activating factor; IL-17, interleukin-17; IL-17A, interleukin-17A; IL-17A/F, interleukin-17A/interleukin-17F heterodimer; scFv, single-chain variable fragment.

IL-17A represents a clinically validated inflammatory pathway in autoimmune disease,

with approvals in rheumatology and dermatology

Nasdaq: ZURA

▪ IL-17 is a central amplifier of inflammation across multiple

immune-mediated diseases

▪ IL-17 pathway inhibition has demonstrated efficacy across

multiple inflammatory indications, supported by extensive

clinical experience

▪ Ixekizumab represents a well-established clinical

benchmark for IL-17 pathway inhibition, blocking IL-17A

and IL-17A/F signaling

ixekizumab

Anti-IL-17 scFv

tabalumab

Anti-BAFF Ab

tibulizumab

IL-17A & IL-17A/F

Tetravalent bispecific antibody designed to block BAFF and

IL-17A–mediated signaling, including IL-17A/F heterodimers

Ixekizumab: a high-efficacy clinical benchmark 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

and IL-17A/F produces robust clinical responses with a well-characterized safety profile

▪ Extensive clinical experience: Supported by large global

clinical development programs and post-marketing datasets

across dermatologic and rheumatologic indications*

(*) PASI 90 values represent placebo-adjusted response rates at Week 12 from independent Phase 3 psoriasis trials. Studies were not designed for head-to-head comparison; trial designs, patient

populations, dosing regimens, and placebo response rates differed. Clinical efficacy data shown are limited to psoriasis studies. Efficacy and durability may vary by indication.

Sources: Griffiths, C.E. et al. (2015), The Lancet, DOI:10.1016/s0140-6736(15)60125-8; Langley, R.G. et al. (2014), New England Journal of Medicine, DOI:10.1056/nejmoa1314258; Gordon, K.B. et al. (2016),

New England Journal of Medicine, DOI:10.1056/nejmoa1512711; Eli Lilly and Company and Novartis public disclosures and prescribing information.

Acronyms: IL-17, interleukin-17; IL-17A, interleukin-17A; IL-17A/F, interleukin-17A/interleukin-17F heterodimer; PASI 90, Psoriasis Area and Severity Index 90% improvement; PBO, placebo; PsO, psoriasis.

Ixekizumab establishes a well-characterized clinical benchmark for IL-17 pathway inhibition

Multiple Phase 3

programs completed

High efficacy

demonstrated

Broad IL-17 pathway

inhibition

Extensive clinical and

real-world experience

Nasdaq: ZURA

secukinumab

PASI 90 at Week 12*

(Phase 3 psoriasis studies)

PASI 90

(%; PBO-adjusted)

ixekizumab

UNCOVER-1 UNCOVER-2 UNCOVER-3 PsO1 PsO2

(*) Clinical studies have shown higher rates of mucocutaneous candidiasis with broader IL-17 pathway inhibition that includes IL-17F.

Sources: Benschop, R.J. et al. (2019), mAbs, DOI:10.1080/19420862.2019.1624463; Adams, R. et al. (2020), Frontiers in Immunology, DOI:10.3389/fimmu.2020.01894.

Acronyms: BAFF, B-cell activating factor; HS, hidradenitis suppurativa; IL, interleukin; IL-17A, interleukin-17A; IL-17F, interleukin-17F; IL-17A/A, interleukin-17A homodimer; IL-17A/F, interleukin-17A/interleukin-17F heterodimer; IL-17F/F, interleukin-17F homodimer; KD

, dissociation constant; mAb, monoclonal antibody; pM, picomolar.

Tibulizumab is the first and only in-class

bispecific antibody targeting IL-17 and BAFF

IL-17 pathway

B-Cell–driven

inflammation

Agent Target description IL-17A/A

(KD

)

IL-17A/F

(KD

)

IL-17F/F*

(KD

)

Tibulizumab Anti-BAFF & IL-17

bispecific mAb ~14 pM ~90 pM no binding BAFF

Secukinumab

(Cosentyx®)

Anti-IL-17A

mAb ~60–90 pM ~2400 pM no binding no

Bimekizumab

(Bimzelx®)

Anti-IL-17A/F

mAb ~3.2 pM ~26 pM ~23 pM no

Nasdaq: ZURA

IL-17–only approaches

▪ Inhibits IL-17A signaling with

varying affinity

▪ May also inhibit IL-17A/F or IL-17F

to further suppress the IL-17

pathway

▪ Does not address additional

disease drivers

Tibulizumab (anti-IL-17 + BAFF)

▪ Inhibits key IL-17 ligands

(IL-17A/A and IL-17A/F)

▪ Adds BAFF pathway inhibition

(B-cell biology)

▪ Is designed to address multiple

disease drivers

Tibulizumab targets two potentially high-value autoimmune

market opportunities

Nasdaq: ZURA

Source: Market estimates based on third-party analyses and published literature, including DRG/Clarivate, Evaluate Pharma, GlobalData, peer-reviewed epidemiology studies, and company analyses.

Acronyms: TAM, total addressable market.

Potential significant multi-billion-dollar market opportunities

▪ Growing biologics market supported by increasing

diagnosis and utilization

▪ Chronic inflammatory disease with durable treatment

demand and high unmet need

▪ Heterogeneous disease biology creates opportunity

beyond single-pathway approaches

Large and expanding chronic disease

HIDRADENITIS SUPPURATIVA

~$8B projected by the mid-2030s

ESTIMATED TAM

▪ Rare autoimmune disease with significant unmet need

and limited effective treatment options

▪ Specialist-managed market with concentrated

prescribing and premium pricing dynamics

▪ Multisystem inflammatory and fibrotic manifestations

contribute to substantial disease burden

High-value orphan autoimmune opportunity

SYSTEMIC SCLEROSIS

~$4B projected by mid-2030s

ESTIMATED TAM

A dual-pathway approach in HS

tibulizumab

ZB-106

Anti-BAFF + IL-17

▪ First and currently only in-class bispecific antibody designed to target BAFF and

IL-17 signaling, including IL-17A and IL-17A/F

▪ Phase 2 clinical trial (TibuSHIELD) ongoing; topline data anticipated in Q4 2026

Tibulizumab is an investigational agent. Its efficacy and safety have not been established or approved by the FDA or any other regulatory agency worldwide.

Nasdaq: ZURA | www.zurabio.com

HS is a complex and relapsing disease

The interplay of acute lesions, chronic inflammation, and complex immune drivers makes

HS uniquely challenging, and highlights the opportunity for biology-driven solutions

Patient experience

▪ HS affects ~1% of the population and is

widely underdiagnosed

▪ Painful nodules and abscesses form in

sensitive areas

▪ Lesions may progress to tunnels and

scarring

▪ Acute flares coexist with chronic

inflammation

▪ Delayed diagnosis and variable treatment

response

Underlying biology

▪ HS lesions are driven by a

diverse, dynamic immune

microenvironment

▪ Prominent immune signatures:

Th1/Th17, neutrophils, B cells

▪ Chronic immune activity

underlies persistent, relapsing

disease course

Sources: Moran, B. et al. (2017), Journal of Investigative Dermatology, DOI:10.1016/j.jid.2017.05.033; Banerjee, A. et al. (2017), Immunological Investigations, doi:10.1080/08820139.2016.1230867; Sabat, R. et al. (2023),

Journal of Allergy and Clinical Immunology, DOI:10.1016/j.jaci.2022.10.034; Garg, A. et al. (2017), JAMA Dermatology, DOI:10.1001/jamadermatol.2017.0201; Ingram, J.R. (2020), British Journal of Dermatology,

DOI:10.1111/bjd.19435; Midgette, B. et al. (2022), British Journal of Dermatology, DOI:10.1111/bjd.21798; Sabat, R. et al. (2020), Nature Reviews Disease Primers, DOI:10.1038/s41572-020-0149-1; MEDACorp

key opinion leader (KOL) discussions.

Acronyms: HS, hidradenitis suppurativa; Th1, T helper 1 cell; Th17, T helper 17 cell.

tibulizumab | ZB-106

A dual-pathway approach to hidradenitis suppurativa

Targeting immune drivers of chronic inflammation and tissue damage

Disease

▪ Chronic, inflammatory skin disease with

recurrent painful lesions

▪ Significant impact on quality of life and

long-term morbidity

Biology

▪ Heterogeneous disease driven by

activation of multiple immune pathways

▪ BAFF elevation and associated B cell

dysregulation observed in HS lesions

▪ IL-17A–driven inflammation implicated

in dysfunction of neutrophils,

macrophages, and keratinocytes

Program

▪ Tibulizumab (BAFF + IL-17A bispecific

antibody)

▪ Phase 2 TibuSHIELD clinical study in

adults with HS; topline data expected

Q4 2026

Th17 cell

IL-17A

B cell

tibulizumab | ZB-106

Acronyms: BAFF, B cell activating factor; HS, hidradenitis suppurativa; IL-17A, interleukin-17A; Th17, T helper 17 cells.

Neutrophils and B cells represent orthogonal immune

drivers in HS

Sources: Rumberger, B.E. et al. (2020), Inflammation Research, DOI:10.1007/s00011-020-01381-7; Sabat, R. et al. (2023), Journal of Allergy and Clinical Immunology, doi:10.1016/j.jaci.2022.10.034;

Macchiarella, G. et al. (2023), Journal of Investigative Dermatology, DOI:10.1016/j.jid.2022.08.051; Gudjonsson, J.E. et al. (2020), JCI Insight, doi:10.1172/jci.insight.139930; Rastrick, J. et al. (2024),

British Journal of Dermatology, DOI:10.1093/bjd/ljae442.

Acronyms: BAFF, B-cell activating factor; B cell, B lymphocyte; HS, hidradenitis suppurativa; IL-17, interleukin-17; IL-17A, interleukin-17A; NETosis, neutrophil extracellular trap formation; T cell, T lymphocyte;

TLS, tertiary lymphoid structure.

IL-17 and BAFF act through distinct pathways

that drive neutrophil- and B cell–mediated immune pathology in HS

Neutrophils:

▪ Abundant in HS lesions and sinus tracts

▪ Amplify acute inflammatory flares and tissue damage

▪ Driven in part by IL-17A–mediated recruitment and

activation

B cells:

▪ Activated and persistent in HS lesions

▪ Contribute to chronic immune activation

▪ Supported by BAFF-mediated survival and

pro-inflammatory functions

tibulizumab | ZB-106

Neutrophils and B cells are rare in

healthy skin but infiltrate HS lesions

IL-17A– and B cell–associated pathways contribute to

inflammation in HS

Sources: Novartis, AAD Annual Meeting 2024; ClinicalTrials.gov ID NCT03827798; Sabat, R. et al. (2023), Journal of Allergy and Clinical Immunology, DOI:10.1016/j.jaci.2022.10.034; Macchiarella, G. et

al. (2023), Journal of Investigative Dermatology, DOI:10.1016/j.jid.2022.08.051.

Acronyms: BAFF, B cell activating factor; BAFF-R, B cell activating factor receptor; BTK, Bruton’s tyrosine kinase; HS, hidradenitis suppurativa; IL-17, interleukin-17; IL-17A, interleukin-17A.

HS is characterized by IL-17A–mediated inflammation, with emerging clinical evidence supporting B cell–

pathways, underscoring the approach for multi-pathway strategies

▪ B cells and plasma cells infiltrate acute and

chronic HS lesions and contribute to

persistent immune activation

▪ BAFF expression aligns with B-cell and

plasma-cell signatures in human HS tissue

▪ Elevated BAFF provides a biological link

between B-cell accumulation and chronic

immune persistence

▪ Clinical activity observed with multiple B

cell–targeted approaches in HS, including

BTK inhibition (remibrutinib) and BAFF-R

inhibition (ianalumab)

B cell / BAFF-associated biology

Emerging clinical evidence

▪ Elevated IL-17 pathway activity

observed in HS lesions

▪ Amplifies macrophage and

neutrophil-driven inflammation

and keratinocyte activation

▪ Clinical efficacy demonstrated

with IL-17 pathway inhibitors

IL-17A biology

Clinically validated

tibulizumab | ZB-106

Increasing clinical evidence for B cell–related pathways in

hidradenitis suppurativa*

tibulizumab | ZB-106

(*) Data derived from a randomized, placebo-controlled, multi-arm hidradenitis suppurativa platform study (ClinicalTrials.gov Identifier: NCT03827798). Reported results are based on information posted on

ClinicalTrials.gov (as of 09-Jan-2026) and are subject to sponsor quality review and potential update. Results are descriptive and not powered for formal cross-arm comparisons.

(**) sHiSCR50: ≥50% reduction in abscess and inflammatory nodule count, with no increase in abscesses or draining fistulas, assessed using a simplified lesion-count methodology.

Sources: Novartis, AAD Annual Meeting 2024; ClinicalTrials.gov ID: NCT03827798.

Acronyms: BAFF-R, B-cell activating factor receptor; BTK, Bruton’s tyrosine kinase; CD40, cluster of differentiation 40; HS, hidradenitis suppurativa; IL-1β, interleukin-1 beta; IL-18, interleukin-18;

LPA1, lysophosphatidic acid receptor 1; sHiSCR50, Simplified Hidradenitis Suppurativa Clinical Response (50%).

72.7%

48.5%

58.6%

51.6% 46.9%

32.0% 36.0%

remibrutinib (LOU064)

BTKi

25 mg

remibrutinib (LOU064)

BTKi

100 mg

iscalimab (CFZ533)

anti-CD-40

ianalumab (VAY736)

BAFF-R

MAS825

IL-1β / IL-18

LYS006

LPA1

Pooled placebo

(contemporaneous

cohorts)

Observed sHiSCR50** Responders at Week 16 by Treatment Arm

(Observed response rates; non-responder imputation applied)

Observations:

▪ Data show that B-cell–associated pathways (BTK, BAFF-R, CD40) demonstrate numerically higher sHiSCR50 response rates than pooled

placebo in this HS platform study.

▪ BAFF-R inhibition (ianalumab) shows numerically meaningful observed activity, supporting a potential role for B-cell survival pathways in HS.

▪ IL-1β / IL-18 inhibition (MAS825) shows more modest observed activity with limited separation from pooled placebo.

HS landscape: multiple approved and late-stage therapies

highlight ongoing need for differentiation

tibulizumab | ZB-106

Company

Asset Tibulizumab

(ZB-106)

Adalimumab

(Humira®)

Secukinumab

(Cosentyx®)

Bimekizumab

(Bimzelx®) Sonelokimab Remibrutinib Brivekimig

(SAR444245) AVTX-009 Lutikizumab

(ABT-981)

Zasocitinib

(TAK-279)

Mechanism of Action

Anti-BAFF

and IL-17

bispecific

mAb

Anti-TNFα

mAb

Anti-IL-17A

mAb

Anti-IL-17A /F

mAb

Anti-IL-17A/F

Nanobody

Covalent BTK

inhibitor

TNFα / OX40L

bispecific

mAb

Anti-IL-1β

mAb

IL-1α / IL-1β

mAb

TYK2

inhibitor

Stage of Development Phase 2 Approved Approved Approved Phase 3 Phase 3 Phase 2 Phase 2 Phase 3 Phase 2

Route of Administration SC SC SC SC SC PO SC SC SC PO

Dosing Frequency Q4W

(studied) Q2W–Q4W Q4W Q2W → Q4W Q2W / Q4W

(studied) QD Q4W

(studied) Q2W–Q4W QW–Q2W QD

Note: Approved and development status reflect HS or broader inflammatory indications as publicly reported; dosing regimens shown represent studied or labeled schedules and may vary by program. Table is

descriptive and not intended to imply direct comparison between products.

Sources: Company public disclosures, prescribing information, conference presentations, and ClinicalTrials.gov.

Acronyms: BAFF, B cell activating factor; BTK, Bruton’s tyrosine kinase; HS, hidradenitis suppurativa; IL-1α, interleukin-1 alpha; IL-1β, interleukin-1 beta; IL-17, interleukin-17; IL-17A, interleukin-17A;

IL-17A/F, interleukin-17A/interleukin-17F heterodimer; IV, intravenous; mAb, monoclonal antibody; OX40L, OX40 ligand; PO, oral administration; QD, once daily; QW, once weekly;

Q2W, once every two weeks; Q4W, once every four weeks; SC, subcutaneous; TNFα, tumor necrosis factor alpha; TYK2, tyrosine kinase 2.

(*) Includes secondary and exploratory endpoints

Acronyms: AN, abscess and inflammatory nodule; DLQI, Dermatology Life Quality Index; HiSCR50, Hidradenitis Suppurativa Clinical Response ≥50%; HiSCR75, Hidradenitis Suppurativa Clinical Response ≥75%;

HS, hidradenitis suppurativa; IHS4, International Hidradenitis Suppurativa Severity Score System; NRS, Numeric Rating Scale; OLE, open-label extension; PK, pharmacokinetics;

PD, pharmacodynamics; SC, subcutaneous; TNF-α, tumor necrosis factor alpha.

tibulizumab | ZB-106

KEY INCLUSION CRITERIA

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

▪ Other symptom and lesion-based measures per protocol

▪ 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

exposure

▪ Additional eligibility criteria per protocol

Randomized, double-blind, placebo-controlled, three-arm study

16-week primary efficacy period followed by a 16-week OLE

Tibulizumab dose: 150 mg and 300 mg SC

Dose selection informed by Phase 1 PK/PD and target engagement data

Efficacy Period (16 weeks) OLE (16 weeks)

Study timeline

(weeks)

1:1:1

tibulizumab (n ≈ 75)

150 mg

n ≈ 225 placebo (n ≈ 75)

participants

tibulizumab (n ≈ 75)

300 mg

tibulizumab

150 mg

0 2 4 8 12 16 20 24 28 32

Week 32

Final OLE study visit

(no SC dose)

SC dosing

at study visit =

Phase 2 study in moderate-to-severe

hidradenitis suppurativa

A dual-pathway approach in SSc

tibulizumab

ZB-106

Anti-BAFF + IL-17

▪ First and currently only in-class bispecific antibody designed to target BAFF

and IL-17 signaling, including IL-17A and IL-17A/F

▪ Phase 2 clinical trial (TibuSURE) ongoing; topline data anticipated in 1H 2027

Tibulizumab is an investigational agent. Its efficacy and safety have not been established or approved by the FDA or any other regulatory agency worldwide.

Systemic sclerosis is a progressive, multisystem

autoimmune disease with limited therapeutic options*

(*) Two therapies are approved for SSc-ILD; however, no treatment approved for SSc addresses multiple organ systems.

Sources: Clarivate/DRG (accessed 19 August 2024); public regulatory disclosures and prescribing information.

Acronyms: CGA, Clinical Global Assessment; EU5, five major European markets (France, Germany, Italy, Spain, United Kingdom); FVC, forced vital capacity; HAQ-DI, Health Assessment Questionnaire Disability

Index; ILD, interstitial lung disease; mRSS, modified Rodnan Skin Score; PtGA, Patient Global Assessment; SSc, systemic sclerosis; US, United States.

Systemic Sclerosis (SSc) is a Rare,

Serious Multisystem Autoimmune Disease

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)

TibuSURE Phase 2 Trial Evaluates Key Domains of Systemic Sclerosis

Other Organs

Heart

Kidney

Liver

Stomach

SSc-ILD is a major cause of

morbidity and mortality in SSc.

Two disease-modifying treatments

are approved for SSc-ILD

Lungs

Skin

Characterized by Chronic Inflammation and Fibrosis Across Organs

Skin fibrosis contributes to

functional impairment, disability,

and reduced quality of life

FVC

Forced Vital

Capacity

mRSS

modified Rodnan

Skin Score

HAQ-DI

Health Assessment

Questionnaire Disability Index

PtGA

Patient

Global Assessment

CGA

Clinical

Global Assessment

Lung Function Skin Fibrosis Functional Impact Patient-Reported Outcome Clinician-Reported Outcome

tibulizumab | ZB-106

A dual-pathway approach in systemic sclerosis

Targeting immune drivers of autoimmunity, inflammation, and fibrosis

Disease

▪ Severe, progressive, multisystem

autoimmune disease

▪ Core features: inflammation,

vasculopathy, and fibrosis

▪ No therapies are approved that

comprehensively address the

multisystem pathology of SSc*

Program

▪ Tibulizumab (BAFF + IL-17A bispecific

antibody)

▪ Phase 2 TibuSURE clinical study; topline

data expected 1H 2027

Biology

▪ Inflammation plays a key role in fibrosis

and vasculopathy

▪ Autoreactive B cells and autoantibodies

are key inflammatory signature

▪ IL-17 pathway elevation observed in SSc

patients

Th17 cell

IL-17A

B cell

(*) Two therapies are approved for SSc-ILD; however, no treatment approved for SSc addresses multiple organ systems.

Acronyms: BAFF, B cell activating factor; IL-17A, interleukin-17A; SSc, systemic sclerosis; Th17, T helper 17 cells.

tibulizumab | ZB-106

IL-17A and BAFF/B cells contribute to inflammation,

vasculopathy, and fibrosis in systemic sclerosis

Core Disease Features

▪ SSc is characterized by chronic inflammation, vasculopathy, and progressive fibrosis

▪ Infiltration of activated immune cells (macrophages, T cells, B cells) creates a persistent inflammatory tissue

environment

BAFF / B Cell Biology

▪ BAFF is elevated in SSc and supports survival and activation of autoreactive B cells

▪ Activated B cells produce autoantibodies and inflammatory cytokines (e.g., IL-6) associated with fibrosis and

vascular dysfunction

IL-17A Biology

▪ IL-17A has been reported to be elevated in subsets of patients with SSc

▪ Preclinical studies suggest IL-17A can activate fibroblasts and endothelial cells, promoting inflammation,

immune cell recruitment, and tissue remodeling

tibulizumab | ZB-106

Sources: Seki, N. et al. (2024), Cytokine, DOI:10.1016/j.cyto.2024.156534; Ono, Y. et al. (2024), Scientific Reports, DOI:10.1038/s41598-024-76987-6; Lonati, P.A. et al. (2014), PLoS ONE,

DOI:10.1371/journal.pone.0105008; Deng, C.-C. et al. (2025), Frontiers in Immunology, DOI:10.3389/fimmu.2024.1522076; Kurasawa, K. et al. (2000), Arthritis & Rheumatism, 43(11), pp. 2455–

2463. doi:10.1002/1529-0131(200011)43:11<2455::aid-anr12>3.0.co;2-k.

Acronyms: BAFF, B cell activating factor; IL-6, interleukin-6; IL-17A, interleukin-17A; SSc, systemic sclerosis.

Targeting interconnected immune pathways in systemic

sclerosis

BAFF- and IL-17–driven inflammation may contribute to vasculopathy and fibrosis,

supporting evaluation of multi-pathway therapeutic strategies in SSc

▪ BAFF signaling supports

survival of autoreactive B cells

▪ Elevated autoantibody

production and cytokine

networks (including IL-6, IL-17)

are observed in SSc

▪ Immune-mediated endothelial dysfunction

contributes to impaired blood flow

▪ Inflammatory cytokines (IL-6, IL-17) thought

to promote immune cell infiltration and

vascular injury

▪ Fibroblast activation contributes to

progressive tissue fibrosis

▪ Excess extracellular matrix deposition

(e.g., collagen) is characteristic of SSc

INFLAMMATION

VASCULOPATHY

FIBROTIC REMODELING

Sources: Allanore, Y. et al. (2015), Nature Reviews Disease Primers, DOI:10.1038/nrdp.2015.2; Distler, J.H. et al. (2019), Nature Reviews Rheumatology, DOI:10.1038/s41584-019-0322-7; Asano, Y. and Sato,

S. (2015), Seminars in Immunopathology, DOI:10.1007/s00281-015-0505-5; Varga, J. and Abraham, D. (2007), Journal of Clinical Investigation, DOI:10.1172/jci31139.

Acronyms: BAFF, B cell activating factor; IL-6, interleukin-6; IL-17, interleukin-17; SSc, systemic sclerosis.

tibulizumab | ZB-106

Separately inhibiting IL-17A or BAFF has shown efficacy in

placebo-controlled trials for systemic sclerosis

Sources: Fukasawa, T. et al. (2022), Annals of the Rheumatic Diseases, doi:10.1136/annrheumdis-2022-eular.2519; ClinicalTrials.gov ID NCT03957681; Gordon, J.K. et al. (2018), Arthritis & Rheumatology,

DOI:10.1002/art.40358; ClinicalTrials.gov ID NCT01670565.

Acronyms: BAFF, B cell activating factor; dcSSc, diffuse cutaneous systemic sclerosis; FVC, forced vital capacity; IL-17A, interleukin-17A; IIT, investigator-initiated trial; mRSS, modified Rodnan Skin Score;

MMF, mycophenolate mofetil; NS, not significant; QOL, quality of life; SHAQ-DI, Scleroderma Health Assessment Questionnaire–Disability Index; SSc, systemic sclerosis; VAS, visual analog scale.

IL-17 RECEPTOR ANTAGONIST – PHASE 3

Brodalumab

▪ Met the primary endpoint of reduced mRSS at Week 24 for skin involvement, and

demonstrated improvement in FVC as a secondary endpoint reflecting lung

function

▪ Also showed therapeutic effects on lung/respiratory functions, digital ulcers,

symptoms of gastroesophageal reflux disease, and QOL without noteworthy

safety concerns

Δ -21.2 units Δ +5.2%

CLINICAL PRECEDENT

Phase 3 brodalumab trial (24 weeks)

mRSS FVC (% predicted)

BAFF ANTAGONIST

Belimumab

▪ In a 52-week, investigator-initiated, single-center, double-blind, placebo-controlled pilot trial involving 20 participants with dcSSc on background MMF

▪ Both treatment groups experienced improvements in mRSS, favoring belimumab

(-10 vs. -3; p = NS)

▪ Secondary endpoints were met with statistical significance in two endpoints:

SHAQ-DI and VAS Raynaud’s phenomenon

CLINICAL PRECEDENT

Phase 2 belimumab IIT trial (52 weeks)

mRSS FVC (% predicted)

Δ -7.0 units

Δ +7.0%

tibulizumab | ZB-106

(*) Includes secondary and exploratory endpoints

Acronyms: CRISS, Combined Response Index in Systemic Sclerosis; FVC, forced vital capacity; HAQ-DI, Health Assessment Questionnaire Disability Index; HRCT, high-resolution computed tomography;

ILD, interstitial lung disease; mRSS, modified Rodnan Skin Score; OLE, open-label extension; PK/PD, pharmacokinetics/pharmacodynamics; qHRCT, quantitative high-resolution computed

tomography; R, randomization; SC, subcutaneous; SSc, systemic sclerosis.

Phase 2 study in

diffuse cutaneous systemic sclerosis

KEY INCLUSION CRITERIA

PLANNED EFFICACY ENDPOINTS

PRIMARY ENDPOINT

▪ Change from baseline in mRSS at Week 24

ADDITIONAL ENDPOINTS*

▪ qHRCT lung imaging

▪ FVC

▪ HAQ-DI

▪ revised CRISS (rCRISS)

▪ Adults (18–75 years) with early diffuse cutaneous SSc,

enriched for SSc-ILD

▪ Stable background immunosuppressive or antifibrotic therapy

▪ Anti-centromere antibody negative

▪ Disease duration ≤ 7 years

▪ mRSS 15–45 at screening

▪ Additional eligibility criteria per protocol

Randomized, double-blind, placebo-controlled design

24-week primary efficacy period, followed by 28-week OLE

Tibulizumab dose: 300 mg SC

Dose selection informed by Phase 1 PK/PD and target engagement data

tibulizumab | ZB-106

n ≈ 80

participants

Efficacy Period (24 weeks)

Baseline

image

HRCT

1:1

tibulizumab (n ≈ 40)

300 mg

placebo (n ≈ 40)

OLE (28 weeks)

tibulizumab

300 mg

HRCT HRCT

Week 52

(no SC dose)

0 2 4 8 12 16 20 24 28 32 36 40 44 48 52

Study

timeline

SC dosing (weeks)

at study visit =

modified Rodnan Skin Score (mRSS):

Endpoint for assessing skin thickness and fibrosis

Severe skin thickening and tightening restricts movement

and causes painful ulcers on the hands and fingers,

significantly impairing daily activities and quality of life.

Fine Wrinkles

(0/3)

Severe Thickness

(3/3)

The mRSS assesses skin thickness in systemic sclerosis patients

by evaluating 17 body sites (e.g., face, chest, abdomen, arms,

legs). Each site is scored from 0 to 3.

The total score ranges from 0 to 51, with higher scores indicating

greater skin involvement.

17 Surface Anatomic Areas of the Body

2 Moderate Thickness

1 Mild Thickness

3 Severe Thickness

0 Normal Skin

Face

Anterior chest

Abdomen

Upper arm

Forearm

Hand

Fingers

Thigh

Leg

Foot

Upper arm

Forearm

Hand

Fingers

Thigh

Leg

Foot

with inability to pinch

the skin into a fold

Sources: Khanna, D. et al. (2017), Journal of Scleroderma and Related Disorders, doi:10.5301/jsrd.5000231; Ferreli, C. et al. (2018), Clinical Reviews in Allergy & Immunology, doi:10.1007/s12016-017-8625-4.

tibulizumab | ZB-106

In phase 2, lung involvement using qHRCT is a key secondary

endpoint

Sources: Goldin, J. et al. (2018), Annals of the American Thoracic Society, doi:10.1513/annalsats.201802-079OC; Zura Bio internal planning.

Acronyms: ILD, interstitial lung disease; MMF, mycophenolate mofetil; qHRCT, quantitative high-resolution computed tomography; QILD, quantitative interstitial lung disease; QLF, quantitative lung fibrosis;

SSc, systemic sclerosis.

ILD includes various pulmonary disorders marked by

inflammation and progressive lung fibrosis, resulting in

restrictive lung function and impaired gas exchange.

SSc often leads to ILD due to immune system dysregulation

and subsequent lung interstitial fibrosis.

Healthy Lung Fibrotic Lung

QILD by HRCT provides a sensitive measure of lung

involvement, detecting changes as small as 2%.

Example of improvement after 24 months of MMF in total lung involvement

The blue and red areas show QLF, while the yellow area shows quantitative ground

glass. The entire colored area represents QILD. After 24 months, QLF areas decreased (arrow in B).

tibulizumab | ZB-106

Key takeaways

Clear differentiation

Tibulizumab is the first and currently only in-class bispecific

antibody designed to simultaneously target BAFF and IL-17–

mediated signaling, addressing immune complexity beyond single-pathway approaches

Acronyms: BAFF, B cell activating factor; IL-17, interleukin-17.

Defined, anticipated near-term clinical catalysts

Two independent Phase 2 trials (TibuSHIELD and TibuSURE)

evaluating a dual-pathway strategy in diseases with significant

unmet need and potential multi-billion dollar market opportunities

Platform optionality

Multi-pathway immune biology provides potential for expansion into

additional autoimmune indications, subject to clinical validation

Nasdaq: ZURA

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Jul. 01, 2026

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Jul. 01, 2026

Entity File Number

001-40598

Entity Registrant Name

Zura Bio Limited

Entity Central Index Key

0001855644

Entity Tax Identification Number

98-1725736

Entity Incorporation, State or Country Code

Entity Address, Address Line One

1489 W. Warm Springs Rd.

Entity Address, Address Line Two

#110

Entity Address, City or Town

Henderson

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89014

City Area Code

702

Local Phone Number

757-6133

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ZURA

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NASDAQ

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