Form 8-K

8-K — Zura Bio Ltd

Accession: 0001104659-26-097526

Filed: 2026-08-17

Period: 2026-08-17

CIK: 0001855644

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

Item: Regulation FD Disclosure

Item: Financial Statements and Exhibits

Documents

8-K — tm2623351d1_8k.htm (Primary)

EX-99.1 — EXHIBIT 99.1 (tm2623351d1_ex99-1.htm)

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8-K — FORM 8-K

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0001855644

2026-08-17

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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

August 17, 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) 825-9872

(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 August 17, 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 filed 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 August 17, 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: August 17, 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: tm2623351d1_ex99-1.htm · Sequence: 2

Exhibit 99.1

Corporate Overview

August 2026

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, including regulatory filings

and approval status; 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; Zura Bio’s

expectations regarding the potential general acceptability and maintenance of its 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, its 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 cautions readers 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 Bio gives no assurance that the expectations expressed herein will be achieved or that 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.

Advancing tibulizumab: a potential first- and

only-in-class bispecific antibody

Tibulizumab, a potential first-and only-in-class bispecific

antibody inhibiting IL-17 and

BAFF in development

• IL-17 and BAFF among the most clinically validated pathways in immunologic disorders1,2

• Orthogonal nature of IL-17 and BAFF offers potential to modulate non-redundant pathways

• Potent engagement of targets and low immunogenicity observed in Phase 1

Pipeline in a product potential:

three biologically de-risked and

independent shots on goal

• Hidradenitis suppurativa (HS), systemic sclerosis (SSc) and polymyalgia rheumatica (PMR) span

distinct biology

• Yet each disease leverages existing clinical validation of the IL-17 (HS3,4 and PMR5) or BAFF arm

(SSc6) with strong scientific support for the orthogonal pathway7,8,9

Zura Bio is financed

beyond anticipated key

near-term value inflection points

• Topline data expected from HS and SSc Phase 2 studies in Q4 2026 and H1 2027, respectively

• Three-asset pipeline with optionality across multiple immune-mediated indications

• Cash runway through at least year end 2028

“Biologically de-risked” refers to clinical support for the relevant mechanism(s) of action and is not intended to imply regulatory or clinical success

Sources: 1. Cosentyx®, Taltz®, Bimzelx® Prescribing Information.; 2. Benlysta® Prescribing Information.; 3. Kimball et al. Lancet. 2024; 4. Kimball et al. Lancet. 2023; 5. Stone et al. N Engl J Med. 2026 (REPLENISH); 6. Gordon et al. Arthritis Rheumatol.

2018; 7. Sabat et al. J Allergy Clin Immunol. 2023; 8. Lowe et al. JCI Insight. 2024; 9. van der Geest et al. Rheumatology (Oxford). 2015;10. Zura Bio filings.

Addressing the

distinct biology of

immune-mediated

diseases

Immune-mediated diseases are often driven by multiple,

intersecting immune pathways

Targeting more than one pathway is a rational approach to

address low or inadequate response rates in complex

immune-mediated diseases

Early clinical readouts across a range of immune-mediated

indications have already demonstrated the potential of

bispecific antibodies to break through efficacy ceilings

Untapped market

potential across disease

areas of interest

~$5B

2026

Projected

Mid-2030s

$15B+

TODAY:

Biologic penetration in HS, SSc,

and PMR remains below average1

because current therapies only

partially address the multi-pathway

biology driving these diseases2–9

2030s:

Therapies designed to address

the multi-pathway biology of

each disorder have the

potential to break the response-rate ceiling — expanding the

eligible patient pool, moving into

earlier lines of therapy, and

extending duration of use

SIGNIFICANT GROWTH:

Precedent in adjacent immunology

indications shows each step-change in efficacy — as in

psoriasis and RA — drove a step-change in advanced-therapy

utilization and market size10–13

Both circles represent combined HS, SSc, and PMR global markets1

Sources: 1. Market estimates based on third-party analyses, earnings reports of currently marketed therapies, and published literature, including DRG/Clarivate, Evaluate Pharma, GlobalData, peer-reviewed epidemiology studies, and company

analyses; 2. Kimball et al. Lancet. 2024 (BE HEARD I/II); 3. Kimball et al. Lancet. 2023 (SUNSHINE/SUNRISE); 4. Kimball et al. N Engl J Med. 2016 (PIONEER I/II); 5. Stone et al. N Engl J Med. 2026 (REPLENISH); 6. Spiera et al. N Engl J Med.

2023 (SAPHYR); 7. Khanna et al. Lancet Respir Med. 2020 (focuSSced); 8. Distler et al. N Engl J Med. 2019 (SENSCIS); 9. Fukasawa et al. J Am Acad Dermatol. 2023; 10. Gordon et al. Lancet. 2021 (BE READY); 11. Gordon et al. Lancet. 2018

(UltIMMa 1/2); 12. McInnes et al. Lancet. 2023 (BE OPTIMAL/BE COMPLETE); 13. Mease et al. N Engl J Med. 2015 (FUTURE 1).

Three shots on goal — biologically de-risked, independent, and

fully funded through topline data readouts

A Phase 2 trial in

adults with HS

Anticipated readout:

Q4 2026

A Phase 2 trial in

adults with SSc

Anticipated readout:

H1 2027

A Phase 2 trial in

adults with PMR

Anticipated initiation:

YE 2026

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.

Tibulizumab is a four-headed hammer designed to

inhibit the BAFF and IL-17 pathways

ixekizumab

Anti-IL-17 scFv1

IL-17A/A &

tabalumab IL-17A/F

Anti-BAFF Ab1

BAFF

tibulizumab2,3

Tetravalent bispecific antibody designed to

block BAFF and IL-17–mediated signaling

(IL-17A/A and A/F heterodimers)4

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

Sources: 1. Publicly available information on ixekizumab and tabalumab; 2. ClinicalTrials.gov. NCT06993610.; 3. ClinicalTrials.gov. NCT06843239.;

4. Benschop et al. mAbs. 2019.

Addresses disease complexity

Aims to target two orthogonal immune pathways

implicated in chronic inflammation and autoimmunity

Clinically grounded design

Fusion of a BAFF-binding antibody (tabalumab) with

the IL-17-binding scFv from ixekizumab (ixekizumab

marketed as Taltz®, ~$3.6B in global 2025 sales, as

reported)1,4

Single-entity advantage

Enables dual-pathway modulation without multi-drug

combination complexity

Phase 1/1b data support advancement of

tibulizumab into Phase 2 development

• 78 participants dosed across Phase 1/1b studies

• >98% median trough target engagement for

both IL-17 and BAFF in peripheral blood at

300 mg Q4W

• Mean terminal half-life (t½): 27 days, supporting

once-monthly dosing

• 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

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

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

Modulation of

independent

innate and

adaptive

immune drivers

of disease

IL-17

Amplifies inflammation,

fibrosis, and tissue destruction

Drives recruitment and

activation of neutrophils

Enhances trafficking and cross-talk of immune cells in tissues

Induces pro-inflammatory

protein production, creating a

self-sustaining inflammatory

environment

BAFF

Promotes autoreactive B cell

survival and function1,2,3

Promotes maturation, survival,

and function of autoreactive

B and plasma cells

May promote chronic

maintenance of lymphoid

structures in tissue (TLS)

Persistence of B cells leads to

increased cytokines, T cell activation,

and autoantibodies

Broad potential in heterogeneous immune disorders

Schematic representation of mechanism rationale. Not a clinical efficacy claim. References for B cell axis in HS: 1. Sabat et al. J Allergy Clin Immunol. 2022; 2. Lowe et al. JCI Insight. 2023; 3. Gudjonsson et al. JCI Insight. 2020.

First and only bispecific antibody in development designed to target the orthogonal

IL-17 and B cell pathways

Ixekizumab contributes a high-efficacy component for

IL-17 pathway inhibition

• Consistent high efficacy: Demonstrated across multiple

inflammatory diseases in large Phase 3 programs*1,2

• Validated IL-17 pathway inhibition: Neutralization of IL-17A/A

and IL-17A/F produces robust clinical responses with a well-characterized safety profile1,2,3

• Extensive clinical safety experience: Supported by large

global clinical development programs and post-marketing

datasets across dermatologic and rheumatologic indications*3

• Low incidence of candidiasis relative to IL-17F/F antagonists

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

secukinumab4

PASI 90 at Week 12*

(Phase 3 psoriasis studies)

PASI 90

(%; PBO-adjusted)

100

ixekizumab1,2

UNCOVER-1 UNCOVER-2 UNCOVER-3 PsO1 PsO2

* 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: 1. Griffiths CE et al. Lancet. 2015; 2. Gordon KB et al. N Engl J Med. 2016; 3. Eli Lilly and Company and Novartis. Public disclosures and prescribing information.; 4. Langley RG et al. N Engl J Med. 2014

Tibulizumab potently

inhibits IL-17A/A and

IL-17A/F: the

strongest drivers of

IL-17 signaling

Agent

Target

description

IL-17A/A

(KD)

IL-17A/F

(KD)

IL-17F/F

(KD)

Tibulizumab1 Anti-BAFF & IL-17

bispecific mAb ~14 pM ~90 pM no binding

Secukinumab

(Cosentyx®)

Anti-IL-17A

mAb ~60–90 pM ~2400 pM no binding

Bimekizumab

(Bimzelx®)

Anti-IL-17A/F

mAb ~3.2 pM ~26 pM ~23 pM

Sources: 1. Goedken ER et al. J Pharmacol Exp Ther. 2025; 2. Patel DD et al. Ann Rheum Dis. 2013; 3. Adams R et al. Front Immunol. 2020.

Highest

Binding

Affinity

Medium

Binding

Affinity

Lowest

Binding

Affinity

Hidradenitis Suppurativa (HS)

HS is a chronic, progressive inflammatory

condition with high symptom burden

Patients experience pain in

sensitive, high-friction areas

Patients withdraw from social

interactions due to visible symptoms

Patients struggle with persistent

drainage and odor from lesions

Patients experience prolonged

delays in diagnosis and treatment

Painful nodules and abscesses make

walking, sitting, and arm movement

difficult, limiting daily comfort1

Managing chronic drainage and odor

becomes burdensome, leading to

avoidance of exposure or hiding1

Embarrassment drives social withdrawal,

relationship strain, absenteeism, mental

health consequences2

Delayed diagnosis leads to continued

symptom burden and progression to

more severe disease3

Lesions

commonly

occur in

intertriginous

areas (skin

folds)1

Distinctive for

structural skin

damage driven

by tunneling

and scarring1

Sources: 1. Sabat et al. 14 Lancet. 2025 (Seminar); 2. Kimball et al. J Am Acad Dermatol. 2024; 3. Kokolakis et al. Dermatology. 2020.

How patients are treated today — and the limitations of

existing therapies

Current Treatment Pathway

Initial Management

Topicals, oral antibiotics, and in-office

procedures (I&D, intralesional corticosteroids)

establish control and satisfy payer requirements

before advancing therapy1,2

Biologics (SoC)

Selection driven by access/formulary, not a

strict algorithm: Humira® is declining as HCPs

shift to IL-17s — Cosentyx® first (fast access),

Bimzelx® often 2L+ (preferred efficacy)3,4

Surgery

Reserved for biologic-refractory or

structurally advanced patients with extensive

tunneling and scarring that no longer respond

to medical therapy1,2

Limitations of Current Therapies:

Incomplete,

non-durable control

Many patients never reach high-bar responses (HiSCR75/90) or

lose efficacy over time - driving

recurrent flares, pain, drainage,

and odor3,5

Structural damage

is irreversible

Once disease progresses to

tunnels and scarring, no current

therapy can reverse it1

Patient impact

remains high

Pain and quality of life

impairment can persist

even when objective

measures improve6

Physicians remain only

moderately satisfied

Despite current advancements,

physicians desire new

mechanisms of action that

provide improved efficacy, deeper

and more durable response4

Sources: 1. Zouboulis et al. Lancet. 2025; 2. Alikhan et al. J Am Acad Dermatol. 2019; 3. Kimball et al. Lancet. 2024 (BE HEARD I&II); 4. Zura Bio. Data on file. 2026; 5. Garbayo-Salmons et al. J Eur

Acad Dermatol Venereol. 2025; 6. Ingram et al. Pain Ther. 2025.

Hidradenitis suppurativa: large, underserved market with high

unmet need

Three advanced

therapies (TNF, IL-17)

compete for the

current biologic-treated HS population

Multiple advanced therapies; cycling to

innovative options expected to increase

as physicians seek durable alternatives

Sources: Real-world US claims analysis of HS treatment exposures, Dermatol Ther (Heidelb). 2022. Biologic penetration in moderate-to-severe HS and

market projections ($3B in 2026 to ~$10B by the mid-2030s) are based on internal market research and company analyses. All figures are approximate.

Mid-2030s

$10B

Growth Drivers and Unmet Needs

• Despite recent approvals, HS remains

underdiagnosed and undertreated

• Biologic penetration rate increasing as

treatment options expand

• Novel therapies challenging current

efficacy ceilings; unmet need for deeper

response

~$3B

Today

Unlike healthy skin, B cells infiltrate and chronically persist in HS

lesions, driving a local amplified and targeted immune response

Sources: 1. Gudjonsson et al. JCI Insight. 2020; 2. Lowe et al. JCI Insight. 2020; 3. Lowe et al. JCI Insight. 2024; 4. Yu et al. Immunity. 2024.

In severe disease, B and T cells organize and

persist in tertiary lymphoid structures (TLS)3,4

B cells T cells Proliferating Cells

Immunofluorescence analysis of HS

chronic lesion with tunnel

B cells expand with

disease progression2

Flow cytometry analysis of healthy skin

biopsies, active HS biopsies (inflammatory

nodules), or end stage HS tissue (tunnel

from surgical excision)

B cells and plasma cells make up

the bulk of HS cellular infiltrate1

Imaging CyTOF analysis of HS lesions Plasma cells B cells Monocytes/ macrophages CD8 T cells Neutrophils

Number of cells per mm2

BAFF is elevated across HS lesion types and predicts treatment resistance

In acute and chronic HS lesions, BAFF expression tracks with B cell accumulation,

supporting BAFF as a key player in B cell mediated pathology

Sources: 1. Yu et al. Immunity. 2024 2. Gudjonsson et al. JCI Insight. 2020; 3. Sabat et al. J Allergy Clin Immunol. 2023; 4. Lowe et al. JCI Insight. 2020; 5. Hambly et al. Br J Dermatol. 2022.

Elevated BAFF can retain B cells

in the skin

Elevated BAFF is a unique feature of HS

lesions, which predicts TNFi non-response

• BAFF is absent in healthy skin and in psoriasis

and dermatitis lesions, and B cells transiently

migrate in and out of skin3,4

• BAFF is significantly elevated in all HS lesion

types, and correlates with increases in B cells3,4

• Patients who have higher baseline levels of

BAFF and B cell counts are less likely to

respond to adalimumab4,5

Skin BAFF mRNA (RU)

B cells

migrate into

HS lesions

and initiate

effector

functions1

BAFF

promotes B

cell

accumulation,

maturation,

and

differentiation

B and T cells

organize into tertiary

lymphoid structures

that drive chronic,

local immune

activation1,2

Blood BAFF mRNA

(Normalized counts)

scars

fistulas

abscesses

nodules

P adj=0.005

800

600

400

200

B cells are believed to drive HS pathology via multiple mechanisms

BAFF prolongs B cell

survival and promotes

several effector functions

IL-17 drives a

feed-forward,

self-sustaining

inflammatory cycle

Neutrophil

recruitment

and

activation

B cell

survival

Antibody release

(IgG, IgA1, IgD)

Cytokine and

chemokine

release

T cell

activation

B cell

differentiation

into plasma

cells

IL-17

Th17 Cytokine

production

(IL-6, TNF, TGFb)

BAFF Tertiary Lymphoid

B cell Structure

Three B cell-targeting

mechanisms

demonstrating HS

efficacy signal1,2

Pooled placebo

(contemporaneous

cohorts)

36%

Observed sHiSCR50** Responders at Week 16 by Treatment Arm1,2

Recent clinical data supports the hypothesis that B cells are key

drivers of disease rather than bystanders in HS*

(*) 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. Observed response rates; non-responder imputation applied

(***) Mean results from 25 mg and 100 mg arm shown

Sources: 1. ClinicalTrials.gov. NCT03827798. 2026; 2. Novartis. AAD Annual Meeting. 2024.

W–5 D1 Screening

Active

Treatment

Corresponding

Placebo

W16

Follow-up period

length varies by cohort (4

–84W)

PEA EOS

Common design applied across 5 cohorts of the Novartis platform study; each

cohort tested a different drug against its own randomized placebo arm.1

Platform Study Design

51.6%

72.7%

48.5%

58.6%

46.9%

32.0%

ianalumab

(VAY736)

BAFF-R

N=32

remibrutinib

(LOU064)

BTKi

N=33

remibrutinib

(LOU064)

BTKi

N=33

iscalimab

(CFZ533)

anti-CD-40

N=29

MAS825

IL-1β / IL-18

N=33

LYS006

LPA1

N=27

25 mg 100 mg

Trial

PIONEER I

Phase 3

PIONEER II

Phase 3

SUNRISE

Phase 3

SUNSHINE

Phase 3

HEARD I

Phase 3

HEARD 2

Phase 3

VELA-1

Phase 3

VELA-2

Phase 3

STOP

HS-1

Phase 3

STOP

HS-2

Phase 3

LOTUS

Phase 2

LOTUS

Phase 2

Phase 2 Phase 2 HS-OBTAIN

Phase 2

Pilot

Week 12 12 16 16 16 16 16 16 12 12 16 16 16 16 16 16 16 16 16 12

Active arm 153 163 180 181 289 291 283 276 202 208 83 84 37 39 58 32 33 33 29 20

B cell directed monotherapy has demonstrated absolute response

rates in line with other approved and late-stage assets in HS

42%

59%

42% 45% 48% 52% 51%

56%

41% 42%

59%

64%

60%

49%

67%

52%

70%

49%

59%

85%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

HiSCR50 Absolute Response Rates

secukinumab2

adalimumab1

bimekizumab3

sonelokimab4 povorcitinib5

Novartis platform study

lutikizumab7

abdakibart6

brivekimig8

ianalumab9 remibrutinib10 fostamatinib11 iscalimab9

Sources: 1. Kimball AB et al. N Engl J Med. 2016; 2. Kimball AB et al. Lancet. 2023; 3. Kimball AB et al. Lancet. 2024; 4. Porter ML, Kimball AB et al. SHSA Annual Meeting. 2025; 5. Porter ML et al. Nat Med. 2026; 6. Avalo Therapeutics. LOTUS

Topline Presentation. 2026; 7. Kimball AB et al. JAMA Dermatol. 2026; 8. Sanofi. HS-OBTAIN Phase 2a Readout. 2025; 9. ClinicalTrials.gov. NCT03827798. 2026; 10. Kimball AB et al. AAD Annual Meeting. 2024; 11. Jepsen R et al. J Am Acad

Dermatol. 2023.

Open-label, no

placebo arm

TNF IL17 Other investigational therapies B cell targeting

* sHiSCR50: modified HiSCR50 omitting the “no increase in abscess count” criterion; For all studies, HiSCR50 was the primary endpoint except LOTUS (abdakibart; HiSCR75) and the Novartis platform study (ianalumab, remibrutinib, iscalimab; sHiSCR50). Note: Data are

derived from separate clinical trials with differences in design and patient populations. No head-to-head clinical trials have been conducted to date; cross-trial comparison limitations exist.

Investigational drug Placebo response rate

Orthogonal nature of IL-17 and BAFF pathways increases

confidence in potential benefit over IL-17 inhibition alone

Targets distinct

biology of HS

Tibulizumab is designed to

target distinct orthogonal

pathways, increasing

probability of additive effect

Targets IL-17, the most

validated MoA in HS

IL-17-binding scFv from

ixekizumab (a potent

IL-17 pathway inhibitor)

BAFF

Persistence of B cells

leads to increased

cytokines, T cell activation,

and autoantibodies

De-risked, biologically relevant approach to potentially break through efficacy ceilings in HS

Phase 2 study ongoing in

moderate-to-severe HS

Efficacy Endpoints

Primary Endpoint

• Percent change from baseline in AN count at Week 16

Additional Endpoints*

• HiSCR50 and HiSCR75

• Draining Tunnel Count

• IHS4

• DLQI

• Skin pain NRS

• PK/PD assessments

Key Inclusion Criteria

• Adults 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

Efficacy Period

(16 weeks)

OLE

(16 weeks)

Study timeline (weeks)

1:1:1

tibulizumab

150 mg

placebo

N = 247

participants

tibulizumab

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 =

* Includes secondary and exploratory endpoints

Systemic Sclerosis (SSc)

Systemic sclerosis is a progressive, multisystem autoimmune

disease with limited therapeutic options*

No therapies are approved that comprehensively

address the multisystem pathology of SSc*2

300,000

people are estimated to be living with SSc

across major markets (US, EU5, Japan)1

SSc-ILD is a major

cause of morbidity and

mortality in SSc. Two

disease-modifying

treatments are

approved for SSc-ILD2

Lungs

Skin

Characterized by

Chronic Inflammation and

Fibrosis Across Organs

Skin fibrosis

contributes to

functional impairment,

disability, and reduced

quality of life

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

Sources: 1. Clarivate/DRG (accessed 19-Aug-2024); 2. Public regulatory disclosures and prescribing information.

Heart

Kidney

Liver

Stomach

approximately

Why SSc requires

multi-pathway

immune modulation

BAFF- and IL-17–driven

inflammation may

contribute to vasculopathy

and fibrosis, supporting

evaluation of multi-pathway therapeutic

strategies in SSc

Vasculopathy

• Immune-mediated endothelial dysfunction

contributes to impaired blood flow

• Inflammatory cytokines (IL-6, IL-17)

thought to promote immune cell

infiltration and vascular injury

Inflammation

• BAFF signaling supports

survival of autoreactive B cells

• Elevated autoantibody

production and cytokine

networks (including IL-6, IL-17)

are observed in SSc

Fibrotic Remodeling

• Fibroblast activation contributes to

progressive tissue fibrosis

• IL-17 activates inflammatory

pathways in fibroblasts;

autoantibodies promote fibrosis

• Excess extracellular matrix deposition

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

IL-17A is increased in SSc blood and skin and is linked to active

and early disease

IL-17A elevated

in blood and

correlates with

disease activity

Elevations of

IL-17-expressing

T cells in skin

correlate with

early disease

IL-17A cytokine elevated in SSc1 Serum IL-17A a predictor and correlate of pulmonary

vascular disease1,3

Blood IL-17+ cells correlate with disease activity2

IL-17A+ cells increased in SSc skin4,5 IL-17A+ cells increased in early disease skin2

Sources: 1. Seki et al. Cytokine. 2024; 2. Yang et al. Arthritis Res Ther. 2014; 3. Ono et al. Sci Rep. 2024; 4. Lonati et al. PLoS One. 2014; 5. Deng et al. Front Immunol. 2025.

Healthy SSc Morphea

Healthy SSc

BAFF inhibition reduces profibrotic and B cell signaling genes

in SSc skin1,2

Sources: 1. Gordon et al. Arthritis Rheumatol. 2018; 2. Matsushita et al. Arthritis Rheum. 2006; 3. Matsushita et al. Sci Adv. 2018.

Belimumab modulated gene profiles

in post-treatment SSc skin1

RNAseq analysis of skin from patients

who demonstrated a 20% reduction in mRSS

Hypothesized disease-promoting

roles of B cells3

Baseline 52 weeks

Indicators of anti-fibrotic effect

Indicators of B cell

inhibition effect

IL-17 and BAFF blockade have each shown improvement in skin

and lung outcomes in SSc

Sources: 1. Gordon JK et al. Arthritis Rheumatol. 2018; 2. Fukasawa T et al. Ann Rheum Dis. 2022.

IL-17 RECEPTOR ANTAGONIST

Brodalumab2

• Met the primary endpoint of reduced mRSS at Week 24 for skin

involvement, and 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

Phase 3 brodalumab trial (24 weeks)2

Δ -21.2 units Δ +5.2%

mRSS FVC (% predicted)

BAFF ANTAGONIST

Belimumab1

• 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

Phase 2 belimumab IIT trial (52 weeks)1

mRSS

Δ -7.0 units

FVC (% predicted)

Δ +7.0%

Phase 2 study ongoing in SSc;

enrollment completed

* Includes secondary and exploratory endpoints

Endpoints and Stratification

Primary Endpoint

• Change from baseline in mRSS at Week 24

Additional Endpoints*

• qHRCT lung imaging

• FVC

• HAQ-DI

• revised CRISS

Stratification factors

• Presence of ILD (yes/no)

• Duration of disease (≥ or <2 years)

• Anti-RNA polymerase III (+/-)

Key Inclusion Criteria

• Adults (18-75 years) with early diffuse

cutaneous SSc, enriched for SSc-ILD

• Stable background immunosuppressive or

antifibrotic therapy allowed

• Disease duration ≤ 7 years

• mRSS 15-45 at screening

Efficacy Period

(24 weeks)

OLE

(28 weeks)

1:1

tibulizumab

300 mg

placebo

N = 91

participants

tibulizumab

300 mg

SC dosing

at study visit =

Study timeline (weeks) 0 52

Week 52

Final OLE study visit

(no SC dose)

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

(Baseline image) HRCT

HRCT HRCT

In Phase 2, lung involvement using qHRCT is a key

secondary endpoint

Sources: 1. Goldin J et al. Ann Am Thorac Soc. 2018; 2. Zura Bio. Data on file. 2026.

ILD includes various pulmonary disorders marked by

inflammation and progressive lung fibrosis, resulting in

restrictive lung function and 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%.1

Example of improvement after 24 months of

MMF in total lung involvement1

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).

QILD predicts mortality in SSc and closely correlates with FVC —

differences of ~2% are clinically meaningful

Sources: 1. Volkmann E et al. CHEST. 2022; 2. Kafaja S et al. Am J Respir Crit Care Med. 2018; 3. Goldin J et al. Ann Am Thorac Soc. 2018; 4. ACTEMRA® (tocilizumab) Prescribing Information.; 5. Roofeh D et al. Arthritis Rheumatol. 2021.

2 large longitudinal SSc studies (SLS I and SLS 2) showed that

≥2% increase in QILD associated with increased risk of death1

Tocilizumab Phase 3 in SSc-ILD

Approved for SSc-ILD based on FVC (% predicted)

• -6.4% (PBO) vs. 0.1% (tocilizumab) over 48 weeks4

Patients were also evaluated by HRCT for QILD:5

• Greater QILD was associated with worse FVC at Baseline

• Significant improvement from Baseline

(-1.8%) with tocilizumab; treatment difference of 3.3%

• QILD is highly correlated with FVC2,3

• Clinically meaningful FVC changes were associated with

2% QILD change2

Published SSc disease trajectories validate our Phase 2

enrollment strategy

What the data show

• Autoantibody drives disease progression

• ATA and RNA Pol III drive the fastest fibrosis

• mRSS peaks early, then regresses on its own

Why our design fits

• Stratification factors designed to reduce

confounders

• Targets the active window: mRSS 15-45, ≤7

years

• Maximizes the probability of success for skin

primary endpoint

– Exclude anti-centromere

– Include all participants with anti-RNA pol-III up to 2

years duration, after which require severe disease

Source: Lescoat et al. Semin Immunopathol. 2025.

Cutaneous trajectory

PAH

Cutaneous trajectory

SRC GI PAH

Myocardial ILD

Joints

Cutaneous trajectory

PAH

SRC GI

Joints

Pericarditis

Early-stage (0-3 years) Late-stage

Polymyalgia Rheumatica (PMR)

PMR: inflammatory disease that leads to reduced mobility,

loss of independence, and significant quality of life burden

Hot-spots of

pain and stiffness

Chronic inflammatory disease

• Causes bilateral aching and stiffness in the

shoulders, hip girdle, neck and torso1,2

• Systemic inflammation is present with increased

erythrocyte sedimentation rate (ESR) and C-reactive

protein (CRP) levels1,2

• Driven by innate and adaptive immune activation3,4

Demographics and risk factors

• Almost exclusively patients over 50; peak onset at

ages 70-802,5

• Women are more likely to develop PMR than men5

• Highly comorbid population6

Signs and symptoms

• Morning stiffness/stiffness with inactivity is a hallmark1,2

• Proximal stiffness makes daily activities difficult (e.g.,

dressing, overhead reaching)2

• Nonspecific systemic signs: malaise, fatigue, low-grade

fever, weight loss1,2

Steroid dependency, relapse-prone

• Rapid symptom improvement on low-to-moderate

corticosteroid doses2,7

• 40-60% of patients relapse during steroid tapering4,7

• Many patients remain on steroids for 5+ years 4,7

Sources: 1. Dasgupta et al. Ann Rheum Dis. 2012; 2. Dejaco et al. Lancet. 2017; 3. Weyand & Goronzy. N Engl J Med. 2014; 4. Floris et al. Clin Rheumatol. 2022; 5. Raheel et al.

Arthritis Care Res (Hoboken). 2017; 6. Partington et al. Semin Arthritis Rheum. 2020; 7. Dejaco et al. Ann Rheum Dis. 2015.

PMR represents a 700K+ US patient population with significant

headroom for advanced therapy adoption

Today, only 1 FDA-approved biologic2

PMR is an underserved and underpenetrated disease

Need for more effective therapies3,4,5

Even with use of on and off-label therapies, complete and

sustained remission remains inconsistent – HCPs are looking for

more reliable options

Steroid-dependency3

Standard of care leaves most patients steroid-dependent

700K+

US PMR Patients1

Advanced therapy market

remains underpenetrated

Sources: 1. Lawrence et al. Arthritis Rheum. 2008; 2. KEVZARA® (sarilumab) Prescribing Information. Sanofi/Regeneron; 3. Floris et al. Clin Rheumatol. 2022; 4. Spiera et al. N Engl J Med. 2023; 5. Zura Bio. Data on file. 2026.

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 osteoporosis, hypertension, or T2D

Median time to permanent

glucocorticoid discontinuation

Due to high relapse rates during taper,

many patients remain on steroids to

manage PMR even after 5 years3

Relapse on steroid taper

Patients are forced back to

higher doses of glucocorticoids

with no clear end in sight

50%1

The plan to reduce was difficult. I

started reducing by like half a mg a week. The

reduction was difficult because the pain kept

returning. I couldn’t get away from the pain.”

- PMR Patient4

I’m on prednisone, and it does awful

things to you. The side effects are really nasty. If

there was anything I could take or do to get

rid of those side effects, I would do it in a

minute. But at this point, apparently, there isn’t

anything that my physician knows about.”

- PMR Patient4

Sources: 1. Spiera et al. N Engl J Med. 2023; 2. Devauchelle-Pensec et al. Ann Rheum Dis. 2018; 3. Camellino et al. Front

Med (Lausanne). 2022; 4. Zura Bio. Data on file. 2026.

Over

6 Yrs2

Approx.

Targeting BAFF and IL-17 may help address both immune

dysregulation and inflammation in PMR

Sources: 1. van der Geest et al. Arthritis Rheumatol. 2014; 2. van der Geest et al. Rheumatology (Oxford). 2015; 3. Reitsema et al. Front Immunol. 2022; 4. Ramiro et al. Rheumatol Ther. 2025.

B cell homeostasis and trafficking

is dysregulated1,2

Circulating B cells:

Traffic out of blood during active disease

and return in remission1,2

May be acting as antigen presenting cells

and cytokine producers (including TNF

and IL-6) in sites of inflammation1,2

BAFF correlates with disease

activity1,2

Serum BAFF is:

Elevated in newly diagnosed PMR1,2

Decreased during remission1,2

Correlated with ESR, CRP, and IL-6

↓may lead to

↑ B cell survival

↑ B cell activation

↑ Cytokine production

↑ Interactions with T cells

IL-17 may amplify local and

systemic inflammation3,4

IL-17 and IL-17-producing cells (e.g.

Th17, MAIT) are:

Elevated in circulation3,4

Present in synovial fluid3,4

↓may lead to

↑ IL-6, IL-8, TNF, and other inflammatory

mediators

↑ number and activation of myeloid cells

IL-17 and B cell targeted therapies have shown positive

glucocorticoid-sparing effects in PMR

* Sustained remission defined as remission that occurred by week 12 and was sustained until week 52, without recurrence of PMR and

no new diagnosis of GCA; complete sustained remission defined as sustained remission plus no ESR/CRP elevation at Week 52

** 52 week results shown from extension phase of BRIDGE-PMR

Sources: 1. Stone et al. N Engl J Med. 2026 (REPLENISH); 2. Marsman et al. Lancet Rheumatol. 2021 (BRIDGE-PMR); 3. Bolhuis et al. Lancet Rheumatol. 2023 (BRIDGE-PMR 1-year extension); 4. REDUCE-PMR-1. NCT05533125.

Phase 3 REPLENISH trial (52 weeks, N = 381, 1:1:1 ratio) Percentage of patients

41%

28%

41%

25% 20%

100

Sustained remission Complete sustained

remission

89%

43%

52%

86%

43%

54%

78%

24%

34%

100

Remission by Wk 12 No signs or symptoms,

Wks 12–52

No ESR/CRP elevation,

Wks 12–52

Secukinumab 300 mg Secukinumab 150 mg Placebo

IL-17A inhibitor – relapsing PMR (Phase 3)

Secukinumab1

• Met the primary endpoint of sustained remission at Week 52 and all key secondary endpoints

• Demonstrated a meaningful glucocorticoid-sparing effect while maintaining disease control

• Secukinumab has been filed in the US and EU for approval in PMR

Phase 2 BRIDGE-PMR (52 weeks**) and Phase 3 REDUCE-PMR-1 (52 weeks) IITs Glucocorticoid-free remission (PMR-AS <10, No current GC use)

48%

21%

48%

35%

100

Rituximab Phase 2 Placebo (BRIDGE-PMR)

Rituximab Phase 3 Placebo (REDUCE-PMR-1)

Anti-CD20 – newly diagnosed PMR (Phase 2 & 3)

Rituximab

• Anti-CD20 clinical evidence that B cells drive PMR

• BRIDGE-PMR (Phase 2 IIT) demonstrated that a single rituximab infusion

increased glucocorticoid-free remission at 21 weeks and produced durable

benefit through one year2,3

• REDUCE-PMR-1 (Phase 3 IIT) showed trend in favor of rituximab4

Remission Outcomes at Week 52* Components of remission, Weeks 12-52*

BRIDGE-PMR

(N = 47, 1:1 ratio)

REDUCE-PMR-1

(N = 116, 1:1 ratio)

Despite IL-17 advances, the unmet need for PMR remains

significant

Source: Stone et al. N Engl J Med. 2026 (REPLENISH).

• Glucocorticoids control

PMR but cannot be

withdrawn: three in four

patients on taper alone

needed escape or rescue

therapy by Week 52

• IL-17 provides real but

partial benefit: More than

half of participants in

secunikumab arms do not

reach sustained remission

Proposed PMR Phase 2 study to be initiated by year end 2026

Key Inclusion Criteria

• Diagnosis of PMR according to the 2012

provisional ACR/EULAR classification criteria

• History of treatment for ≥8 weeks for PMR

with prednisone ≥10 mg/day

• ≥1 episode of PMR relapse at a prednisone

dose ≥5 mg/day

Key Efficacy Endpoints

Primary endpoint:

• Sustained remission at Week 52 defined as:

– Clinical remission at Week 12 maintained

to Week 52

– No use of escape or rescue therapy

– No new diagnosis of Giant Cell Arteritis

Key secondary endpoints:

• Complete sustained remission at Week 52

• Time to the first use of escape or rescue

treatment up to Week 52

• Cumulative glucocorticoid dose

tibulizumab

300 mg

1:1:1

steroid taper

placebo

Study timeline

(weeks)

0 24 52

BLINDED EFFICACY PERIOD

tibulizumab

150 mg

~150-180 total

participants

Efficacy Period

(52 weeks) SC dosing

at study visit =

Study timeline (weeks) 0 52

Week 80

Final OLE

study visit

(no SC dose)

2 4 8 12 16 20 24 28 32 36 40 44 48 56 60 64 68 72 76 80

OLE Period

(28 weeks)

tibulizumab

Summary & Milestones

Executive Team and Board of Directors

Amit Munshi

Chairman

Sandeep Kulkarni, MD

Co-Founder, CEO & Director

Dan Becker, MD, PhD

Director

Mark Eisner, MD, MPH

Director

Jennifer Jarrett

Director

Ajay Nirula, MD, PhD

Director

Steve Schoch

Director

Parvinder Thiara

Director

Kim Davis, JD

Chief 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

Executive Team Board of Directors

Multiple potential near-term clinical milestones and strong pipeline

for the future

TARGET DISCOVERY PHASE 1 PHASE 2 PHASE 3

Tibulizumab (ZB-106) Anti-BAFF and IL-17

Anti-BAFF and IL-17

Crebankitug (ZB-168) Anti-IL-7Rα

Torudokimab (ZB-880) Anti-IL-33

Hidradenitis Suppurativa

Systemic Sclerosis

Polymyalgia Rheumatica

TibuSURE Readout H1 2027

TibuSHIELD Readout Q4 2026

Anticipated Study Initiation YE 2026

Phase 2 ready

Crebankitug: Phase 2 ready multi-functional antibody with

potential in dermatology and beyond

TSLP binds to its specific

receptor, TSLPR, initiating a

signaling process that is

optimized when IL-7Rα

integrates into the complex

• TSLP activates signaling

pathways primarily associated

with type 2 immunity

• TSLP pathways are commonly

linked to allergic responses and

certain inflammatory conditions

IL-7Rα combines with the

common gamma chain (γc)

to form the IL-7 receptor

complex

• IL-7 signaling is vital for the

development, survival, and

balance of T cells

• IL-7 is implicated in many

autoimmune and inflammatory

diseases due to its central role in

T cell development

T cell

JAK3 JAK1 JAK1 JAK2

IL-7Rα

Dendritic cell

IL-7 TSLP

Crebankitug inhibits two distinct cytokine pathways, IL-7 and TSLP, through a single target

Source: Markovic et al. Front Immunol. 2020.

About IL-33 and torudokimab

Growing clinical validation of IL-33 targeting in respiratory:

• Potential for first-in-class opportunities

• Validated pathways in COPD and asthma6

Torudokimab: Phase 2 ready IL-33 targeting antibody with

potential in respiratory disease and beyond

Sources: 1. Cohen ES et al. Nat Commun. 2015; 2. Liew et al. Nat Rev Immunol. 2010; 3. Zura Bio. Data on file. 2026; 4. Laquer et al. Br J Dermatol. 2022; 5. Okragly et

al. J Inflamm Res. 2021; 6. Wechsler et al. NEngl J Med. 2021.

IL-33

IL-33 is a damage-associated “alarmin”

cytokine released by stressed or injured tissues

that activates immune cells through the ST2

receptor to promote inflammation, immune

responses, tissue repair, and fibrosis1,2

Torudokimab

Torudokimab is a fully human monoclonal

antibody that binds and neutralizes IL-335

Clinical Results

Torudokimab was well tolerated in Phase 1

and Phase 2 trials conducted by Eli Lilly3,4

• 141 healthy volunteers in Phase 1 study

• 103 participants with moderate to severe

atopic dermatitis in Phase 2

• Target engagement confirmed with binding to

IL-33 and downstream biomarker reductions3

• Treatment-emergent ADA had no apparent

impact on PK or target engagement

Key Takeaways

Clear

differentiation

Tibulizumab is a potential first

and currently only in-class

bispecific antibody in

development designed to

simultaneously target IL-17–

mediated signaling and BAFF,

addressing immune

complexity beyond single-pathway approaches

Defined, anticipated

clinical catalysts

Three independent Phase 2

trials (TibuSHIELD,

TibuSURE, and NEXUS-PMR*) evaluating a dual-pathway strategy in diseases

with significant unmet need

and potential multi-billion-dollar market opportunities

Portfolio

optionality

Multi-pathway immune

biology provides potential for

expansion into additional

immune-mediated indications

* NEXUS-PMR Phase 2 trial planned to be initiated by year end 2026

Appendix

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

Glossary

Ab antibody

ACA anti-centromere antibodies

ACR American College of Rheumatology

ADA anti-drug antibody

AN abscess and inflammatory nodule

A-RNA-Pol-III anti-RNA polymerase 3 antibodies

ATA anti-topoisomerase antibodies

BAFF B cell activating factor

BAFF-R B cell activating factor receptor

BTK Bruton’s tyrosine kinase

BTKi Bruton’s tyrosine kinase inhibitors

CCL17 C-C motif chemokine ligand 17

CD3/8/19/20/40/45 cluster of differentiation 3/8/19/20/40/45

CFB change from baseline

COPD chronic obstructive pulmonary disease

CRISS Combined Response Index in Systemic Sclerosis

CRP C-reactive protein

CyTOF cytometry by time-of-flight

dcSSc diffuse cutaneous systemic sclerosis

DLCO diffusing capacity of the lung for carbon monoxide

DLQI Dermatology Life Quality Index

ESR erythrocyte sedimentation rate

EULAR European Alliance of Associations for Rheumatology

FDA Food and Drug Administration

FVC forced vital capacity

GC glucocorticoid

GI gastrointestinal

HAQ-DI Health Assessment Questionnaire Disability Index

HCP healthcare professional

HiSCR50 Hidradenitis Suppurativa Clinical Response ≥50%

HiSCR75 Hidradenitis Suppurativa Clinical Response ≥75%

HRCT high-resolution computed tomography

HS hidradenitis suppurativa

I&D incision and drainage

lcSSc limited cutaneous systemic sclerosis

IgA1, D, G immunoglobulin A1, D, and G

IHS4 International Hidradenitis Suppurativa

Severity Score System

IIT investigator-initiated trial

IL-1β interleukin 1 beta

IL-6 interleukin 6

IL-7Rα interleukin 7 receptor alpha

IL-8 interleukin 8

IL-10 interleukin 10

IL-17 interleukin 17

IL-18 interleukin 18

IL-33 interleukin 33

ILD interstitial lung disease

JAK Janus kinase

KD dissociation constant

LPA1 lysophosphatidic acid receptor 1

mAb monoclonal antibody

MAIT Mucosal-associated invariant T cells

MMF mycophenolate mofetil

mRNA messenger RNA

MoA mechanism of action

mRSS Modified Rodnan Skin Score

N number of subjects

NETosis neutrophil extracellular trap formation

NPX normalized protein expression

NRS Numeric Rating Scale

NS not significant

OLE open-label extension

P p-value

PAH pulmonary arterial hypertension

PASI Psoriasis Area and Severity Index

PASI 90 Psoriasis Area and Severity Index 90% improvement

PBO placebo

PD pharmacodynamics

PK pharmacokinetics

pM picomolar

PMR polymyalgia rheumatica

PsO psoriasis

Q2W once every 2 weeks

Q4W once every 4 weeks

qHRCT quantitative high-resolution computed tomography

QILD quantitative interstitial lung disease

QLF quantitative lung fibrosis

QOL quality of life

R randomization

RA rheumatoid arthritis

RNA ribonucleic acid

RU relative units

SC subcutaneous

scFv single-chain variable fragment

SHAQ-DI Scleroderma Health Assessment Questionnaire–

Disability Index

sHiSCR50 Simplified Hidradenitis Suppurativa

Clinical Response (50%)

sHiSCR75 Simplified Hidradenitis Suppurativa

Clinical Response (75%)

sHiSCR90 Simplified Hidradenitis Suppurativa

Clinical Response (90%)

SLE systemic lupus erythematosus

SLS Scleroderma Lung Study

SoC standard of care

SRC scleroderma renal crisis

SSc systemic sclerosis

SSc-ILD systemic sclerosis-associated interstitial lung disease

ST2 suppression of tumorigenicity 2

T2D type 2 diabetes

TARC thymus and activation-regulated chemokine

TGFβ transforming growth factor beta

Th17 T helper 17 cells

TLS tertiary lymphoid structure

TNF tumor necrosis factor

TNFi tumor necrosis factor inhibitor

TNF-α tumor necrosis factor alpha

TSLP thymic stromal lymphopoietin

VAS visual analog scale

Nasdaq: ZURA | www.zurabio.com

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