Zura Bio Q3 2026 net loss widens to $25.8M
Zura Bio Limited reported a third-quarter 2026 net loss of $25.8 million, or $0.20 per share, compared with $18.0 million, or $0.21 per share, in third-quarter 2025.
Sentiment and the balance of points
Rhea-AI Sentiment reads the wording of the document, how positive or negative its language is on a 1 to 5 scale. The balance of points shown with the takes weighs what the document actually discloses, so the two can disagree, for example when a trial that missed its main goal is described in upbeat language.
Form Type
8-K
Rhea-AI Filing Summary
Zura Bio Limited reported a third-quarter 2026 net loss of $25.8 million, or $0.20 per share, compared with $18.0 million, or $0.21 per share, in third-quarter 2025. Research and development expense was $19.5 million, versus $11.9 million; the increase was primarily driven by continued Phase 2 tibulizumab programs and NEXUS-PMR start-up. General and administrative expense was $9.3 million, versus $7.6 million, primarily due to higher professional fees. Cash and cash equivalents were $187.7 million as of September 30, 2026, and Zura expects its existing cash to support planned operations through at least the end of 2028.
Enrollment is complete in two Phase 2 studies of investigational tibulizumab: TibuSHIELD randomized 247 participants with hidradenitis suppurativa, with topline data on track for Q4 2026, and TibuSURE randomized 91 participants with systemic sclerosis, with topline data on track for H1 2027. The FDA cleared NEXUS-PMR to proceed under an Investigational New Drug application, with initiation on track by year-end 2026. Tibulizumab has not been approved for marketing; Zura is evaluating development approaches for torudokimab and crebankitug.
0 points · 0 major0 major · 1 point
How this balance works
Rhea-AI gives every point it takes from this document a weight. Minor counts 1, Moderate 3 and Major 9, so one Major point outweighs several Minor ones. The bar adds up the weights on each side, and when neither side holds more than 65% of the total the balance reads Mixed.
It reads the document as published, with the same rules for every company, and it does not look at what the market expected or at how the stock traded, so a point can be objectively good on a day the stock falls.
Rhea-AI Sentiment measures something else, the tone of the wording.
Positive
- None.
Negative
- Moderate pointThird-quarter net loss reached $25.8 million, versus $18.0 million in 2025.
Filing Explained
The presentation reports common shares and prefunded warrants; the balance sheet reports 96,306,411 shares issued and outstanding at
8-K Event Classification
3 items: 2.02, 7.01, 9.01
3 items
Item 2.02
Results of Operations and Financial Condition
Financial
Disclosure of earnings results, typically an earnings press release or preliminary financials.
Item 7.01
Regulation FD Disclosure
Disclosure
Material non-public information disclosed under Regulation Fair Disclosure, often investor presentations or guidance.
Item 9.01
Financial Statements and Exhibits
Exhibits
Financial statements, pro forma financial information, or exhibit attachments filed with this report.
Key Figures
Cash and cash equivalents: $187.7 million
Net loss: $25.8 million
Net loss per share: $0.20 per share
+4 more
7 metrics
Cash and cash equivalents
$187.7 million
As of September 30, 2026
Net loss
$25.8 million
Third quarter 2026; compared with $18.0 million in third quarter 2025
Net loss per share
$0.20 per share
Third quarter 2026; compared with $0.21 per share in third quarter 2025
Research and development expenses
$19.5 million
Third quarter 2026; compared with $11.9 million in third quarter 2025
General and administrative expenses
$9.3 million
Third quarter 2026; compared with $7.6 million in third quarter 2025
TibuSHIELD participants randomized
247 participants
Enrollment completed in June 2026
TibuSURE participants randomized
91 participants
Enrollment completed in July 2026
Key Terms
Investigational New Drug application, HiSCR50, modified Rodnan Skin Score (mRSS), bispecific antibody, +1 more
5 terms
Investigational New Drug application regulatory
"cleared to proceed under an Investigational New Drug application"
An investigational new drug application is a formal request made to regulatory authorities to begin testing a new medication in humans. It is a critical step in the drug development process, as approval indicates the drug has passed initial safety checks and can be studied further. For investors, this signals that a potential new treatment is progressing through its early testing stages, which can impact the company's future growth prospects.
HiSCR50 medical
"participants achieving HiSCR50 or HiSCR75"
HiSCR50 is a clinical trial measure used in skin disease studies that means a patient has experienced at least a 50% reduction in the number of painful lumps and boils, without new worsening complications. For investors, HiSCR50 is an objective yardstick of a drug’s effectiveness — hitting this threshold in trials can boost a treatment’s chance of regulatory approval, market acceptance, and commercial value, much like a safety rating improving consumer confidence in a new car model.
modified Rodnan Skin Score (mRSS) medical
"change from baseline in modified Rodnan Skin Score (mRSS) at Week 24"
bispecific antibody technical
"a bispecific antibody designed to neutralize interleukin-17 (IL-17) and BAFF"
A bispecific antibody is a specially designed protein that can attach to two different targets at the same time. Think of it as a custom-made connector that brings two things together—such as a disease cell and an immune system component—helping the body fight illnesses more effectively. For investors, understanding bispecific antibodies is important because they represent innovative therapies that could lead to new treatments and potentially lucrative market opportunities.
open-label extension medical
"OLE open-label extension"
An open-label extension is a continuation of a clinical trial where all participants and researchers know which treatment is being given, often after an initial blinded phase. It allows further study of a drug's long-term safety and effectiveness. For investors, it can indicate ongoing interest and confidence in a product's potential, influencing perceptions of its future value.
Earnings Snapshot
Net loss: $25.8 million · Guidance included
Third quarter 2026
Net loss
$25.8 million
Compared with $18.0 million in third quarter 2025
Net loss per share
$0.20 per share
Compared with $0.21 per share in third quarter 2025
Research and development expenses
$19.5 million
Compared with $11.9 million in third quarter 2025
General and administrative expenses
$9.3 million
Compared with $7.6 million in third quarter 2025
Guidance
Zura expects its existing cash and cash equivalents to support planned operations through at least the end of 2028.
FAQ
AI-generated questions and answers. How Rhea-AI works. Not financial advice.
How much cash does ZURA have, and how long is its runway?
Zura reported $187.7 million in cash and cash equivalents as of September 30, 2026, and expects existing cash and cash equivalents to support planned operations through at least the end of 2028.
How much did ZURA lose in the third quarter of 2026?
Zura reported a third-quarter 2026 net loss of $25.8 million, or $0.20 per share, compared with a net loss of $18.0 million, or $0.21 per share, in the third quarter of 2025.
What is the primary endpoint in ZURA's TibuSHIELD study?
TibuSHIELD's primary endpoint is the percent change from baseline in total abscess and inflammatory nodule count at Week 16. The study will also assess the proportion of participants achieving HiSCR50 or HiSCR75.
What is the primary endpoint in ZURA's TibuSURE study?
TibuSURE's primary endpoint is change from baseline in modified Rodnan Skin Score at Week 24. The study also includes measures of lung involvement.
AI-generated analysis. How Rhea-AI works. Not financial advice.
UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549
______________________________________________________________________
FORM 8-K
______________________________________________________________________
CURRENT REPORT
PURSUANT TO SECTION13 OR 15(D)
OF THE SECURITIES EXCHANGE ACT OF1934
Date of Report (Date of earliest event reported)
(Exact name of registrant as specified in its charter)
______________________________________________________________________
| (State or other jurisdiction of incorporation) | (Commission File Number) | (I.R.S. Employer Identification No.) | ||||||||||||
(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 | ||||||||||||
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 2.02. Results of Operations and Financial Condition.
On October 27, 2026, Zura Bio Limited (the “Company”) issued a press release announcing its third quarter 2026 financial results. A copy of the press release is furnished herewith as Exhibit 99.1 and incorporated herein by reference.
The information furnished under this Item 2.02 (including Exhibit 99.1) shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or subject to the liabilities of that section or Sections 11 and 12(a)(2) of the Securities Act of 1933, as amended (the “Securities Act”). The information in this Item 2.02 (including Exhibit 99.1) shall not be deemed incorporated by reference into any other filing with the Securities and Exchange Commission (the “SEC”) 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 filing.
Item 7.01. Regulation FD Disclosure.
On October 27, 2026, 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 99.2 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 99.2) shall not be deemed “filed” for purposes of Section 18 of the Exchange Act, or subject to the liabilities of that section or Sections 11 and 12(a)(2) of the Securities Act. The information in this Item 7.01 (including Exhibit 99.2) shall not be deemed incorporated by reference into any other filing with the SEC 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 | Press Release dated October 27, 2026 | |||||||
99.2 | Corporate Presentation, dated October 27, 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: October 27, 2026 | By: | /s/ Kim Davis | ||||||
| Kim Davis | ||||||||
| Chief Operating Officer, Chief Legal Officer and Corporate Secretary | ||||||||
Exhibit 99.1
Zura Bio Reports Third Quarter 2026 Financial Results and Recent Corporate Updates
•TibuSHIELD topline data in hidradenitis suppurativa (HS) remains on track for Q4 2026; enrollment completed with 247 participants randomized, exceeding target
•TibuSURE topline data in systemic sclerosis (SSc) remains on track for H1 2027; enrollment completed with 91 participants randomized, exceeding target
•NEXUS-PMR, a Phase 2 study evaluating tibulizumab in polymyalgia rheumatica (PMR), remains on track to initiate by year-end 2026
•Cash and cash equivalents of $187.7 million as of September 30, 2026, which is expected to fund planned operations through at least the end of 2028
HENDERSON, Nev.--(BUSINESS WIRE)--October 27, 2026-- Zura Bio Limited (Nasdaq: ZURA) (“Zura”), a clinical‑stage biotechnology company developing novel and differentiated medicines to meaningfully improve the lives of patients with serious and debilitating autoimmune and inflammatory diseases, today announced financial results for the third quarter ended September 30, 2026, and provided recent corporate updates.
“Our team continues to execute efficiently on our development plan for tibulizumab, and we are excited as we enter this data-rich period for the company. We are on track to report topline results from our TibuSHIELD study in HS later this quarter, followed by topline results from our TibuSURE study in SSc in the first half of 2027,” said Sandeep Kulkarni, M.D., co-founder and Chief Executive Officer of Zura. “We continue to believe deeply in tibulizumab’s potential to address complex immune biology and unmet needs across indications, including in PMR, where we will be starting the NEXUS-PMR study by end of year. With cash runway sufficient to deliver results from all three studies, Zura is in a great position to deliver on tibulizumab’s unique potential.”
PROGRAM UPDATES
Tibulizumab (ZB‑106)
Both ongoing Phase 2 studies of tibulizumab, a bispecific antibody designed to neutralize interleukin-17 (IL-17) and B-cell activating factor (BAFF), are fully enrolled and progressing toward topline data, and Zura also remains on track to initiate a Phase 2 study in PMR, the third indication for tibulizumab, by year-end 2026.
•TibuSHIELD (HS): The Phase 2 clinical study evaluating tibulizumab in adults with hidradenitis suppurativa completed enrollment in June 2026 with 247 participants, exceeding its target. Topline data remains on track for the fourth quarter of 2026 and will include the primary endpoint, percent change from baseline in total abscess and inflammatory nodule count at Week 16, as well as the proportion of participants achieving HiSCR50 or HiSCR75.
•TibuSURE (SSc): The Phase 2 clinical study evaluating tibulizumab in adults with early diffuse cutaneous systemic sclerosis completed enrollment in July 2026 with 91 participants, exceeding its target. Topline data remains on track for the first half of 2027 and will include the primary endpoint, change from baseline in modified Rodnan Skin Score (mRSS) at Week 24, as well as measures of lung involvement.
•NEXUS-PMR (PMR): The Phase 2 clinical study evaluating tibulizumab in adults with polymyalgia rheumatica, an inflammatory disease in which most patients remain dependent on long-term glucocorticoids, has been cleared by the U.S. Food and Drug Administration (FDA) to proceed under an Investigational New Drug application and remains on track to initiate by year-end 2026.
Tibulizumab is an investigational compound and has not been approved for marketing by the FDA or any other regulatory authority.
Additional Clinical-Stage Product Candidates
In addition to tibulizumab, Zura is continuing its evaluation of potential development approaches for torudokimab (ZB‑880) and crebankitug (ZB‑168), informed by current clinical and translational evidence and ongoing assessment of the evolving competitive landscape.
THIRD QUARTER 2026 FINANCIAL RESULTS
Cash Position
As of September 30, 2026, Zura had cash and cash equivalents of $187.7 million. Zura expects that its existing cash and cash equivalents are sufficient to support planned operations through at least the end of 2028.
Research and Development (R&D) Expenses
R&D expenses were $19.5 million for the third quarter of 2026, compared to $11.9 million for the same period in 2025. The increase was primarily driven by the continued execution of Zura’s Phase 2 tibulizumab clinical programs as well as start-up activities for NEXUS-PMR.
General and Administrative (G&A) Expenses
G&A expenses were $9.3 million for the third quarter of 2026, compared to $7.6 million for the same period in 2025. The increase was primarily due to higher professional fees.
Net loss for the third quarter of 2026 was $25.8 million, or $0.20 per share, compared to $18.0 million, or $0.21 per share, for the same period in 2025.
ABOUT ZURA
Zura is a clinical-stage, multi-asset immunology company developing novel dual-pathway antibodies for autoimmune and inflammatory diseases with unmet need. Zura’s pipeline includes product candidates designed to target key mechanisms of immune system imbalance, with the goal of improving efficacy, safety, and dosing convenience for patients.
Zura’s lead product candidate, tibulizumab (ZB-106), is being evaluated in two Phase 2 clinical studies in adults: TibuSHIELD, a study in hidradenitis suppurativa (HS), and TibuSURE, a study in systemic sclerosis (SSc). A third Phase 2 clinical study in polymyalgia rheumatica (PMR), NEXUS-PMR, is planned to begin by year-end 2026. Additional product candidates torudokimab (ZB-880) and crebankitug (ZB-168) have completed Phase 1/1b studies and are being evaluated for their potential across a range of autoimmune and inflammatory conditions.
For more information, please visit www.zurabio.com.
FORWARD-LOOKING STATEMENTS
Any statements contained in this press release that do not describe historical facts may constitute “forward‑looking statements” as that term is defined in the Private Securities Litigation Reform Act of 1995. These statements may be identified by words and phrases such as “anticipate,” “believe,” “continue,” “could,” “designed to,” “expect,” “goal,” “intend,” “may,” “outlook,” “plan,” “potential,” “should,” “will,” and similar expressions, and are based on Zura’s current beliefs and expectations. These forward‑looking statements include, but are not limited to, statements regarding the development and potential therapeutic benefits of Zura’s product candidates; the initiation, timing, progress, design and results of Zura’s current and future clinical trials, including the anticipated reporting of data therefrom; the planned expansion of Zura’s product candidates into additional indications; Zura's evaluation of potential development approaches for its product candidates; the sufficiency of Zura’s cash resources and projected cash runway; and other statements that are not historical facts. These statements involve risks and uncertainties that could cause actual results to differ materially from those reflected in such forward‑looking statements. Risks and uncertainties that may cause actual results to differ materially
include, but are not limited to: uncertainties inherent in the development of therapeutic product candidates, such as the risk that one or more of Zura’s current or future product candidates may not be successfully developed or commercialized; the risk of delay or cessation of any planned clinical trials of Zura’s current or future product candidates; the risk that prior results, including signals of safety, activity or durability of effect observed in preclinical studies or earlier clinical trials, may not be replicated or may not continue in ongoing or future studies or clinical trials; the risk that modeling data indicating therapeutic potential, or clinical evidence from other drug candidates, may not be predictive of results in Zura’s current or future clinical trials; the risk that Zura’s product candidates or procedures in connection with their administration may not have the safety or efficacy profiles anticipated; risks related to the accuracy of Zura’s estimates of expenses, capital requirements and needs for additional financing; changes in expected or existing competition; changes in the regulatory environment; uncertainties related to the timing and outcome of the regulatory approval process; unexpected litigation or other disputes; the impact of macroeconomic conditions on Zura’s business, clinical trials and financial position; and other risks and uncertainties described in Zura’s Annual Report on Form 10‑K for the year ended December 31, 2025, and other filings with the Securities and Exchange Commission. Any forward‑looking statements speak only as of the date of this press release and are based on information available to Zura as of the date hereof. Zura assumes no obligation to, and does not intend to, update any forward‑looking statements, whether as a result of new information, future events or otherwise, except as required by law.
CONTACTS
Investor and media inquiries:
ir@zurabio.com
ZURA BIO LIMITED
CONSOLIDATED BALANCE SHEETS
(In thousands, except share data)
| September 30, 2026 | December 31, 2025 | ||||||||||
| (unaudited) | |||||||||||
| Assets | |||||||||||
| Current assets | |||||||||||
| Cash and cash equivalents | $ | 187,652 | $ | 109,407 | |||||||
| Prepaid expenses and other current assets | 3,940 | 2,903 | |||||||||
| Total current assets | 191,592 | 112,310 | |||||||||
| Property and equipment, net | 153 | 126 | |||||||||
| Other assets | 2,884 | 1,512 | |||||||||
| Total assets | $ | 194,629 | $ | 113,948 | |||||||
| Liabilities and Shareholders’ Equity | |||||||||||
| Current liabilities | |||||||||||
| Accounts payable and accrued expenses | $ | 16,969 | $ | 12,410 | |||||||
| Total current liabilities | 16,969 | 12,410 | |||||||||
| Total liabilities | 16,969 | 12,410 | |||||||||
| Shareholders’ Equity | |||||||||||
| Class A Ordinary Shares, $0.0001 par value; 300,000,000 shares authorized as of September 30, 2026 and December 31, 2025; 96,306,411 and 73,680,710 shares issued and outstanding as of September 30, 2026 and December 31, 2025, respectively | 10 | 7 | |||||||||
| Additional paid-in capital | 478,549 | 326,078 | |||||||||
| Accumulated deficit | (300,899) | (224,547) | |||||||||
| Total shareholders’ equity | 177,660 | 101,538 | |||||||||
| Total liabilities and shareholders’ equity | $ | 194,629 | $ | 113,948 | |||||||
ZURA BIO LIMITED
CONSOLIDATED STATEMENTS OF OPERATIONS
(Unaudited)
(In thousands, except share and per share data)
| For the Three Months Ended September 30, | For the Nine Months Ended September 30, | ||||||||||||||||||||||
| 2026 | 2025 | 2026 | 2025 | ||||||||||||||||||||
| Operating expenses: | |||||||||||||||||||||||
| Research and development | $ | 19,491 | $ | 11,948 | $ | 54,943 | $ | 31,126 | |||||||||||||||
| General and administrative | 9,282 | 7,571 | 28,650 | 25,709 | |||||||||||||||||||
| Total operating expenses | 28,773 | 19,519 | 83,593 | 56,835 | |||||||||||||||||||
| Loss from operations | (28,773) | (19,519) | (83,593) | (56,835) | |||||||||||||||||||
| Other (income), net | |||||||||||||||||||||||
| Interest income | (1,759) | (1,526) | (4,998) | (5,060) | |||||||||||||||||||
| Other expense (income), net | 32 | 47 | (941) | (300) | |||||||||||||||||||
| Total other (income), net | (1,727) | (1,479) | (5,939) | (5,360) | |||||||||||||||||||
| Loss before income taxes | (27,046) | (18,040) | (77,654) | (51,475) | |||||||||||||||||||
| Income tax benefit | (1,221) | — | (1,302) | — | |||||||||||||||||||
| Net loss | $ | (25,825) | $ | (18,040) | $ | (76,352) | $ | (51,475) | |||||||||||||||
| Accretion of redeemable noncontrolling interest to redemption value | — | (2,828) | — | (2,828) | |||||||||||||||||||
| Adjustment of redeemable noncontrolling interest | — | 831 | — | 831 | |||||||||||||||||||
| Net loss attributable to Class A Ordinary Shareholders of Zura | $ | (25,825) | $ | (20,037) | $ | (76,352) | $ | (53,472) | |||||||||||||||
| Net loss per share attributable to Class A Ordinary Shareholders of Zura, basic and diluted | $ | (0.20) | $ | (0.21) | $ | (0.62) | $ | (0.57) | |||||||||||||||
| Weighted-average Class A Ordinary Shares used in computing net loss per share attributable to Class A Ordinary Shareholders of Zura, basic and diluted | 127,712,533 | 94,564,632 | 122,303,170 | 93,941,675 | |||||||||||||||||||
Corporate Overview October 2026
2 Forward-Looking Statements Disclaimer This presentation contains “forward-looking statements” within the meaning of the “safe harbor” provisions of the Private Securities Litigation Reform Act of 1995. Words such as “expect,” “estimate,” “project,” “budget,” “forecast,” “anticipate,” “intend,” “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.
3 Advancing tibulizumab: a potential first- and only-in-class bispecific antibody Tibulizumab, a potential first- and only-in-class bispecific antibody inhibiting IL-17 and BAFF in development • IL-17 and BAFF among the most clinically validated pathways in immunologic disorders1,2 • Orthogonal 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 “Bio logically de-risked” refers to clinica l support for the relevant mechanism(s) of action and is not intended to imply regulatory or clin ical success Sources: 1. Cosentyx®, Taltz®, Bimzelx® Prescribing Information; 2 . Benlysta® Prescribing Information; 3 . Kimball et a l. Lancet. 2024; 4. Kimball et al. Lancet. 2023; 5. Stone et al. N Engl J Med. 2026 (REPLENISH); 6. Gordon et a l. 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.
4 Addressing the distinct biology of immune-mediated diseases Immune-mediated diseases are often driven by multiple, intersecting immune pathways Targeting more than one pathway is a rational approach to address low or inadequate response rates in complex immune-mediated diseases Early clinical readouts across a range of immune-mediated indications have already demonstrated the potential of bispecific antibodies to break through efficacy ceilings
5 Untapped market potential across disease areas of interest ~$5B 2026 Projected Mid-2030s $15B+ TODAY: Biologic penetration in HS, SSc, and PMR remains below average1 because current therapies only partially address the multi-pathway biology driving these diseases2–9 2030s: Therapies designed to 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-par ty 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 a l. Lancet. 2023 (BE OPTIMAL/BE COMPLETE); 13. Mease et al. N Engl J Med. 2015 (FUTURE 1).
6 Three shots on goal – biologically de-risked, independent, and fully funded through topline data readouts A Phase 2 trial in adults with HS Anticipated readout: Q4 2026 A Phase 2 trial in adults with SSc Anticipated readout: H1 2027 A Phase 2 trial in adults with PMR Anticipated initiation: YE 2026
7 Tibulizumab: Potential first- and only-in-class therapy Tibulizumab is an investigational agent. Its efficacy and safety have not been established or approved by the FDA or any other regulatory agency worldwide.
8 Tibulizumab is a four-headed hammer designed to inhibit the BAFF and IL-17 pathways ixekizumab Anti-IL-17 scFv1 IL-17A/A & IL-17A/Ftabalumab Anti-BAFF Ab1 BAFF tibulizumab2,3 Tetravalent bispecific antibody designed to block BAFF and IL-17–mediated signaling (IL-17A/A and A/F heterodimers)4 Tibulizumab is an investigational agent. Its efficacy and safety have not been established or approved by the FDA or any other regulatory agency wor ldwide. Sources: 1. Publicly available information on ixekizumab and tabalumab; 2. ClinicalTrials.gov. NCT06993610.; 3 . Clinica lTria ls.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
9 Phase 1/1b data support advancement of tibulizumab into Phase 2 development • 78 participants dosed across Phase 1/1b studies • >98% median trough target engagement for both IL-17 and BAFF in peripheral blood at 300 mg Q4W • Mean terminal half-life (t½): 27 days, supporting once-monthly dosing • 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) F re e B A F F c o n c e n tr a ti o n % C F B F re e I L -1 7 c o n c e n tr a ti o n % C F B 100 mg Q4W 300 mg Q4W 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 wor ldwide. * 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 stud ies; Zura Bio internal clin ical study reports (CSRs).
10 Modulation of independent innate and adaptive immune drivers of disease IL-17 Amplifies inflammation, fibrosis, and tissue destruction Drives recruitment and activation of neutrophils Enhances trafficking and cross- talk of immune cells in tissues Induces pro-inflammatory protein production, 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 a l. JCI Insight. 2020. First and only bispecific antibody in development designed to target the orthogonal IL-17 and B-cell pathways
11 Ixekizumab contributes a high-efficacy component for IL-17 pathway inhibition • Consistent high efficacy: Demonstrated across multiple inflammatory diseases in large Phase 3 programs*1,2 • Validated IL-17 pathway inhibition: Neutralization of IL-17A/A and IL-17A/F produces robust clinical 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) P A S I 9 0 (% ; P B O -a d ju s te d ) 0 10 20 30 40 50 60 70 80 90 100 ixekizumab1,2 PsO1 PsO2UNCOVER-2 UNCOVER-3UNCOVER-1 * 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 compar ison; 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. Gr iffiths et al. Lancet. 2015; 2. Gordon et al. N Engl J Med. 2016; 3. Eli L illy and Company and Novar tis. Public disclosures and prescrib ing information.; 4. Langley et al. N Engl J Med. 2014.
12 Tibulizumab potently inhibits IL-17A/A and IL-17A/F: the strongest drivers of IL-17 signaling Agent Target description IL-17A/A (KD) IL-17A/F (KD) IL-17F/F (KD) Tibulizumab1 Anti-BAFF & IL-17 bispecific mAb ~14 pM ~90 pM no binding Secukinumab (Cosentyx®)2 Anti-IL-17A mAb ~60–90 pM ~2400 pM no binding Bimekizumab (Bimzelx®)3 Anti-IL-17A/F mAb ~3.2 pM ~26 pM ~23 pM Sources: 1. Goedken et al. J Pharmacol Exp Ther. 2025; 2. Patel e t al. Ann Rheum Dis. 2013; 3. Adams et al. Front Immunol. 2020. Highest Binding Affinity Medium Binding Affinity Lowest Binding Affinity
13 Hidradenitis Suppurativa (HS)
14 Patients experience pain in sensitive, high-friction areas Patients withdraw from social interactions due to visible symptoms Patients struggle with persistent drainage and odor from lesions Patients experience prolonged delays in diagnosis and treatment Painful nodules and abscesses make walking, 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, and mental health consequences2 Delayed diagnosis leads to continued symptom burden and progression to more severe disease3 HS is a chronic, progressive inflammatory condition with high symptom burden Lesions commonly occur in intertriginous areas (skin folds)1 Sources: 1. Sabat et al. Lancet. 2025 (Seminar); 2. Kimball et al. J Am Acad Dermatol. 2024; 3. Kokolakis et a l. Dermatology. 2020. Distinctive for structural skin damage driven by tunneling and scarring1
15 How patients are treated today – and the limitations of existing therapies Current Treatment Pathway Initial Management Topicals, oral antibiotics, and in-office procedures (I&D, intralesional corticosteroids) establish control and satisfy payer requirements before advancing therapy1,2 Biologics (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 a l. J Eur Acad Dermatol Venereol. 2025; 6. Ingram et al. Pain Ther. 2025.
16 Hidradenitis suppurativa: large, underserved market with high unmet need Three advanced therapies (TNF, IL-17) compete for the current biologic- treated HS population Multiple advanced therapies; cycling to innovative options expected to increase as physicians seek durable alternatives Sources: Real-world US claims analysis of HS treatment exposures, Garg et al. Dermatol Ther (Heidelb). 2023. Biologic penetration in moderate-to- severe HS and market projections ($3B in 2026 to ~$10B by the mid-2030s) are based on in ternal 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
17 Unlike healthy skin, B cells infiltrate and chronically persist in HS lesions, driving a local amplified and targeted immune response Sources: 1. Gudjonsson et al. JCI Insight. 2020; 2. Lowe et al. JCI Insight. 2020; 3. Lowe et al. JCI Insight. 2024; 4. Yu et al. Immunity. 2024. In severe disease, B and T cells organize and persist in tertiary lymphoid structures (TLS)3,4 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 P la s m a c e lls B c e ll s M o n o c y te s / m a c ro p h a g e s C D 8 T c e lls N e u tr o p h ils N u m b e r o f c e lls p e r m m 2
18 BAFF is elevated across HS lesion types and predicts treatment resistance In acute and chronic HS lesions, BAFF expression tracks with B-cell accumulation, supporting BAFF as a key player in B-cell-mediated pathology Sources: 1. Yu et al. Immunity. 2024; 2. Gudjonsson et a l. JCI Insight. 2020; 3. 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 S k in B A F F m R N A ( R U ) S k in B A F F m R N A ( R U ) 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 B lo o d B A F F m R N A (N o rm a li z e d c o u n ts ) scars fistulas abscesses nodules P adj=0.005 800 600 400 200 0
19 B cells are believed to drive HS pathology via multiple mechanisms BAFF prolongs B-cell survival and promotes several effector functions IL-17 drives a feed-forward, self-sustaining inflammatory cycle Neutrophil recruitment and activation B-cell survival Antibody release (IgG, IgA1, IgD) Cytokine and chemokine release T-cell activation B-cell differentiation into plasma cells IL-17 Th17 Cytokine production (IL-6, TNF, TGFβ) BAFF Tertiary Lymphoid StructureB cell
20 Three B-cell-targeting mechanisms demonstrating HS efficacy signal1,2 Pooled placebo (contemporaneous cohorts) 36% Observed sHiSCR50** Responders at Week 16 by Treatment Arm1,2 Recent clinical data support the hypothesis that B cells are key drivers of disease rather than bystanders in HS* (*) Data der ived from a randomized, placebo-controlled, multi-arm hidradenitis suppurativa platform study (ClinicalTrials.gov Identifier: NCT03827798). Repor ted results are based on information posted on ClinicalTr ials.gov (as of 09-Jan-2026) and are subject to sponsor quality review and potential update. Results are descrip tive and not powered for formal cross-arm compar isons. (**) 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 arms shown Sources: 1. ClinicalTr ials.gov. NCT03827798. 2026; 2. Novartis. AAD Annual Meeting. 2024. R W–5 D1 S c re e n in g Active Treatment Corresponding Placebo W16 F o llo w -u p p e ri o d le n g th v a ri e s b y c o h o rt ( 4 – 8 4 W ) 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
21 Trial PIONEER I Phase 3 PIONEER II Phase 3 SUNRISE Phase 3 SUNSHINE Phase 3 BE HEARD I Phase 3 BE HEARD II Phase 3 VELA-1 Phase 3 VELA-2 Phase 3 STOP HS-1 Phase 3 STOP HS-2 Phase 3 LOTUS Phase 2 LOTUS Phase 2 Phase 2 Phase 2 HS- OBTAIN Phase 2 Phase 2 Pilot Week 12 12 16 16 16 16 16 16 12 12 16 16 16 16 16 16 16 16 16 12 N 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% 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% * * H iS C R 5 0 A b s o lu te R e s p o n s e R a te s secukinumab2 adalimumab1 bimekizumab3 sonelokimab4 povorcitinib5 Novartis platform study lutikizumab7abdakibart6 remibrutin ibbrivekimig8 ianalumab9 re ibrutin ib10 fostamatinib11isca limab9 Sources: 1. Kimball et al. N Engl J Med. 2016; 2. Kimball et al. Lancet. 2023; 3. Kimball et al. Lancet. 2024; 4. Porter et al. SHSA Annual Meeting. 2025; 5. Porter et al. Nat Med. 2026; 6. Avalo Therapeutics. LOTUS Topline Presentation. 2026; 7. Kimball et al. JAMA Dermatol. 2026; 8. Sanofi. HS-OBTAIN Phase 2a Readout. 2025; 9. ClinicalTrials.gov. NCT03827798. 2026; 10. Kimball et al. AAD Annual Meeting. 2024; 11. Jepsen et al. J Am Acad Dermatol. 2023. Open-label, no placebo arm TNF IL-17 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
22 Orthogonal nature of IL-17 and BAFF pathways increases confidence in potential benefit over IL-17 inhibition alone Targets distinct biology of HS Tibulizumab is designed to target distinct orthogonal pathways, increasing probability of additive effect Targets IL-17, the most validated MoA in HS 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
23 Phase 2 study ongoing in moderate-to-severe HS Key Inclusion / Exclusion Criteria • Adults with moderate-to-severe HS, defined as: – Hurley Stage II/III (up to 40% Stage III allowed) – Total abscess and inflammatory nodule (AN) count ≥5 • Up to 30% of participants may have prior TNF-α inhibitor exposure • Prior IL-17 use excluded • Stable GLP-1 use allowed (at least 6 months) • Stable antibiotic use allowed (at least 4 weeks) • Additional eligibility criteria per protocol 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 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 2 4 8 12 160 20 24 28 32 Week 32 Final OLE study visit (no SC dose) SC dosing at study visit = * Includes secondary and exploratory endpoints R
24 Systemic Sclerosis (SSc)
25 Systemic sclerosis is a progressive, multisystem autoimmune disease with limited therapeutic options* No therapies are approved that comprehensively address the multisystem pathology of SSc*2 300,000 people are estimated to be living with SSc across major markets (US, EU5, Japan)1 SSc-ILD is a 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 multip le organ systems. Sources: 1. Clarivate/DRG (accessed 19-Aug-2024); 2. Public regulatory disclosures and prescribing information. Heart Kidney Liver Stomach approximately
26 Why SSc requires multi-pathway immune modulation BAFF- and IL-17–driven inflammation may contribute to vasculopathy and fibrosis, supporting evaluation of multi- pathway therapeutic strategies in SSc Vasculopathy • Immune-mediated endothelial dysfunction contributes to impaired blood flow • 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
27 IL-17A is increased in SSc blood and skin and is linked to active and early disease IL-17A elevated in blood and correlates with disease activity Elevations of IL-17-expressing T cells in skin correlate with early disease IL-17A cytokine elevated in SSc1 Serum IL-17A a predictor and correlate of 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 a l. Arthritis Res Ther. 2014; 3. Ono et a l. Sci Rep. 2024; 4. Lonati et al. PLoS One. 2014; 5. Deng et al. Front Immunol. 2025. Healthy SSc Morphea Healthy SSc
28 BAFF inhibition reduces profibrotic and B-cell signaling genes in SSc skin1,2 Sources: 1. Gordon et a l. Arthritis Rheumatol. 2018; 2. Matsushita et a l. Arthritis Rheum. 2006; 3. Matsushita et al. Sci Adv. 2018. Belimumab modulated gene profiles in post-treatment SSc skin1 RNAseq analysis of 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
29 IL-17 and BAFF blockade have each shown improvement in skin and lung outcomes in SSc Sources: 1. Gordon et a l. Arthritis Rheumatol. 2018; 2. Fukasawa et al. Ann Rheum Dis. 2022. IL-17 RECEPTOR ANTAGONIST Brodalumab2 • Met the primary endpoint of reduced mRSS at Week 24 for skin involvement, and 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 +5.2%Δ −21.2 units mRSS FVC (% predicted) BAFF ANTAGONIST Belimumab1 • 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 (52 weeks)1 mRSS Δ −7.0 units FVC (% predicted) Δ +7.0%
30 Phase 2 study ongoing in SSc; enrollment completed * Includes secondary and exploratory endpoints Key Inclusion Criteria • Adults (18–75 years) with early diffuse cutaneous SSc, enriched for SSc-ILD • Stable background immunosuppressive or antifibrotic therapy allowed • Disease duration ≤ 7 years • mRSS 15–45 at screening • Additional eligibility criteria per protocol 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 (+/−) 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 28 36 4420 24 32 40 48 (Baseline image) HRCT R HRCTHRCT
31 In Phase 2, lung involvement using qHRCT is a key secondary endpoint Sources: 1. Goldin et al. Ann Am Thorac Soc. 2018; 2. Zura Bio. Data on file. 2026. ILD includes various pulmonary disorders marked by inflammation and progressive lung fibrosis, resulting in restrictive lung function and impaired gas exchange. SSc often leads to ILD due to immune system dysregulation and subsequent lung interstitial fibrosis. vs 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).
32 QILD predicts mortality in SSc and closely correlates with FVC – differences of ~2% are clinically meaningful Sources: 1. Volkmann et al. CHEST. 2022; 2. Kafaja et al. Am J Respir Crit Care Med. 2018; 3. Goldin et al. Ann Am Thorac Soc. 2018; 4. ACTEMRA® ( tocilizumab) Prescribing Information.; 5 . Roofeh et al. Arthritis Rheumatol. 2021. Two large longitudinal SSc studies (SLS I and SLS II) 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
33 Published SSc disease trajectories validate our Phase 2 enrollment strategy What the data show • The type of autoantibody drives disease progression, with cutaneous trajectory peaking early in certain patients • ATA (anti-topoisomerase antibody) and A-RNA Pol-III (anti-RNA polymerase 3 antibody) endotypes have worst skin disease Why our design fits • Stratification factors designed to reduce confounders • Targets the active window: mRSS 15–45, ≤7 years • Improves probability of success for skin primary endpoint – Excludes anti-centromere antibody (ACA) positive participants – Allows all anti-topoisomerase participants – Includes all participants with anti-RNA Pol-III up to 2 years' duration, after which severe disease is required Source: Lescoat et al. Semin Immunopathol. 2025. Cutaneous trajectoryGI PAH Cutaneous trajectory PAH GISRC Myocardial ILD Joints Cutaneous trajectory PAH GISRC Joints Pericarditis Late-stageEarly-stage (0–3 years) Internal organ involvement Internal organ involvement Internal organ involvement
34 Polymyalgia Rheumatica (PMR)
35 PMR: inflammatory disease that leads to reduced mobility, loss of independence, and significant quality-of-life burden Hot-spots of pain and stiffness Chronic inflammatory disease • Causes bilateral aching and stiffness in the shoulders, hip girdle, neck, and torso1,2 • Systemic inflammation is 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+ years4,7 Sources: 1. Dasgupta et al. Ann Rheum Dis. 2012; 2. Dejaco et al. Lancet. 2017; 3. Weyand et al. N Engl J Med. 2014; 4. Flor is et a l. 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.
36 PMR represents a 700K+ US patient population with significant headroom for advanced therapy adoption Today, only 1 FDA-approved biologic2 PMR is an underserved and underpenetrated disease Need for more effective therapies3,4,5 Even with use of on- and off-label therapies, complete and sustained 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.
37 Current reliance on steroids provides short-term relief but leads to long-term dependence, relapse, and toxicity Steroid-associated toxicities are common (e.g., insomnia, weight gain, hyperglycemia, osteoporosis, and infections) and can be problematic in the PMR age demographic due to high rates 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 B io. Data on file. 2026. Over 6 Yrs2 Approx.
38 Targeting BAFF and IL-17 may help address both immune dysregulation and inflammation in PMR Sources: 1. van der Geest et al. Arthritis Rheumatol. 2014; 2. van der Geest et al. Rheumatology (Oxford). 2015; 3. Reitsema et al. Front Immunol. 2022; 4. Ramiro et al. Rheumatol Ther. 2025. B-cell homeostasis and trafficking are dysregulated1,2 Circulating B cells: Traffic out of blood during active disease and return in remission1,2 May co-stimulate T cells or produce cytokines (including TNF and IL-6) in sites of inflammation1,2 BAFF levels correlate with disease activity1,2 Serum BAFF is: Elevated in newly diagnosed PMR1,2 Decreased during remission1,2 Highly correlated with ESR, CRP, and IL-62 ↓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 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
39 IL-17 and B-cell-targeted therapies have shown positive glucocorticoid-sparing effects in PMR * Sustained remission defined as remission that occurred by Week 12 and was sustained until Week 52, without recurrence of PM R and no new diagnosis of GCA; complete sustained remission defined as sustained remission plus no ESR/CRP elevation at Week 52 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) P e rc e n ta g e o f p a tie n ts 41% 28% 41% 25% 20% 5% 0 20 40 60 80 100 Sustained remission Complete sustained remission 89% 43% 52% 86% 43% 54% 78% 24% 34% 0 20 40 60 80 100 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 (21 weeks) and Phase 3 REDUCE- PMR-1 (52 weeks) IITs G lu co c o rt ic o id -f re e r e m is si o n (P M R -A S < 1 0 , n o c u rr e n t G C u se ) 48% 21% 48% 35% 0 20 40 60 80 100 Rituximab Phase 2 Placebo (BRIDGE- PMR) Rituximab Phase 3 Placebo (REDUCE- PMR-1) Anti-CD20 – new/relapsing PMR (Phase 2) and new- only PMR (Phase 3) Rituximab • Anti-CD20 provides clinical evidence that B cells contribute to 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)
40 Despite IL-17 advances, the unmet need for PMR remains significant Source: Stone et a l. N Engl J Med. 2026 (REPLENISH). • Glucocorticoids control PMR but cannot be withdrawn: three in four patients on taper alone needed escape or rescue therapy by Week 52 • IL-17 inhibition provides meaningful but only partial benefit: more than half of participants in secukinumab arms do not achieve sustained remission
41 Proposed PMR Phase 2 study to be initiated by year-end 2026 Key Inclusion Criteria • Diagnosis of PMR according to the 2012 provisional ACR/EULAR classification criteria • History of treatment for ≥8 weeks for PMR with prednisone ≥10 mg/day • ≥1 episode of PMR relapse at a prednisone dose ≥5 mg/day Key Efficacy Endpoints Primary endpoint • Sustained remission at Week 52 defined as: – Clinical remission at Week 12 and 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 R steroid taper placebo Study timeline (weeks) 0 5224 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 28 36 4420 24 32 40 48 56 60 64 68 8072 76 OLE Period (28 weeks) tibulizumab
42 Summary & Milestones
43 Executive Team and Board of Directors Amit Munshi Chairman Sandeep Kulkarni, MD Co-Founder, CEO & Director Dan Becker, MD, PhD Director Mark Eisner, MD, MPH Director Jennifer Jarrett Director Ajay Nirula, MD, PhD Director Steve Schoch Director Parvinder Thiara Director Kim Davis, JD Chief 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 Board of DirectorsExecutive Team
44 Multiple potential near-term clinical milestones and strong pipeline for the future TARGET DISCOVERY PHASE 1 PHASE 2 PHASE 3 Tibulizumab (ZB-106) Anti-BAFF and IL-17 Anti-BAFF and IL-17 Anti-BAFF and IL-17 Crebankitug (ZB-168) Anti-IL-7Rα Torudokimab (ZB-880) Anti-IL-33 Hidradenitis Suppurativa Systemic Sclerosis Polymyalgia Rheumatica TibuSURE Readout H1 2027 TibuSHIELD Readout Q4 2026 Anticipated Study Initiation YE 2026 Phase 2-ready Phase 2-ready
45 Crebankitug: Phase 2-ready multi-functional antibody with potential in dermatology and beyond TSLP binds to its specific receptor, TSLPR, initiating a signaling process that is optimized when IL-7Rα integrates into the complex • TSLP activates signaling pathways primarily associated with type 2 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 JAK1 JAK2JAK1JAK3 IL-7Rα Dendritic cell TSLPIL-7 TSLPIL-7 Crebankitug inhibits two distinct cytokine pathways, IL-7 and TSLP, through a single target Source: Markovic et al. Front Immunol. 2020.
46 About IL-33 and torudokimab Growing clinical validation of IL-33-targeting in respiratory: • Potential for first-in-class opportunities • Validated pathways in COPD and asthma6 Torudokimab: Phase 2-ready IL-33 targeting antibody with potential in respiratory disease and beyond Sources: 1. Cohen 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. N Engl 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
47 Key Takeaways Clear differentiation Tibulizumab is a potential first and currently only in-class bispecific antibody in development designed to simultaneously target IL-17– mediated signaling and BAFF, addressing immune complexity beyond single- pathway approaches Defined, anticipated clinical 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
48 Appendix
49 Cash and Shares Outstanding Cash and cash equivalents balance $187.7M (as of 9/30/26) Number of shares (M) Common stock 96.3 Prefunded warrants 29.3 Total Outstanding 125.6
50 Glossary Ab antibody ACA anti-centromere antibodies ACR American College of Rheumatology ADA anti-drug ant ibody AN abscess and inflammatory nodule A-RNA Pol-III anti-RNA polymerase 3 antibodies ATA anti-topoisomerase antibodies BAFF B-cell activat ing factor BAFF-R B-cell activat ing factor receptor BTK Bruton’s tyrosine kinase BTKi Bruton’s tyrosine kinase inhibitor CCL2/3/5/17/24 C-C motif chemokine ligand 2/3/5/17/24 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 CXCL2 C-X-C motif chemokine ligand 2 CyTOF cytometry by time-of-flight dcSSc dif fuse cutaneous systemic sclerosis DLCO dif fusing capacity of the lung for carbon monoxide DLQI Dermatology Life Quality Index EOS end of study ESR erythrocyte sedimentation rate EULAR European Alliance of Associations for Rheumatology FDA Food and Drug Administration FVC forced vital capacity GC glucocorticoid GCA giant cell arterit is GI gastrointest inal HAQ-DI Health Assessment Questionnaire Disability Index HCP healthcare professional HiSCR50 Hidradenitis Suppurat iva Clinical Response ≥50% HiSCR75 Hidradenitis Suppurat iva Clinical Response ≥75% HRCT high-resolution computed tomography HS hidradenit is suppurativa I&D incision and drainage 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-3 interleukin 3 IL-5 interleukin 5 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 lcSSc limited cutaneous systemic sclerosis LPA1 lysophosphat idic acid receptor 1 LTB4 leukotriene B4 mAb monoclonal antibody MMF mycophenolate mofetil MoA mechanism of action mRNA messenger RNA mRSS Modified Rodnan Skin Score N number of subjects NETosis neutrophil extracellular t rap 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 PEA primary endpoint assessment PGD2 prostaglandin D2 PK pharmacokinetics pM picomolar PMR polymyalgia rheumatica PMR-AS Polymyalgia Rheumatica Activity Score 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 Quest ionnaire 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 interst it ial lung disease ST2 suppression of tumorigenicity 2 T2D type 2 diabetes TARC thymus and activation-regulated chemokine TGF-β transforming growth factor beta Th17 T helper 17 cells TLS tert iary lymphoid structure TNF tumor necrosis factor TNF-α tumor necrosis factor alpha TNFi tumor necrosis factor inhibitor TSLP thymic stromal lymphopoietin TSLPR thymic stromal lymphopoietin receptor VAS visual analog scale
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