Shattuck Labs (NASDAQ: STTK) extends cash runway to 2029 on $54.9M warrant inflow and SL-325 data
Rhea-AI Filing Summary
Shattuck Labs reported encouraging Phase 1 results for SL-325, its lead DR3 blocking antibody, and a major cash influx from warrant exercises. The first-in-human trial in 72 healthy volunteers showed SL-325 was well tolerated across single and multiple ascending doses, with durable DR3 receptor occupancy, no evidence of agonist activity, and a low anti-drug antibody rate of 3.7%.
The company plans to start the RECEPTIVE-CD1 randomized Phase 2b trial of SL-325 in moderate-to-severe Crohn’s disease in the third quarter of 2026 and target 12-week induction data in the first half of 2028. Shattuck also highlighted SL-846, a DR3 x IL-23R bispecific antibody now in IND-enabling toxicology studies, with Phase 1 initiation expected in the first half of 2027.
Financially, Shattuck has received or expects to receive aggregate gross proceeds of approximately $54.9 million from the exercise of about 50.6 million common stock warrants, representing roughly 96% of warrants issued in an August 4, 2025 private placement. Combined with approximately $90.4 million in cash, cash equivalents and short-term investments as of March 31, 2026, the company now expects to fund operations into 2029 based on current plans.
Positive
- Substantial cash inflow from warrant exercises: Notices to exercise approximately 50.6 million common stock warrants, or about 96% of those issued in the August 4, 2025 private placement, are expected to generate aggregate gross proceeds of roughly $54.9 million, materially bolstering Shattuck’s balance sheet.
- Extended cash runway into 2029: Together with about $90.4 million in cash, cash equivalents and short-term investments as of March 31, 2026, the added warrant proceeds support management’s guidance that current capital should fund operations into 2029 under existing plans.
- Encouraging SL-325 Phase 1 profile: The first-in-human trial in 72 healthy participants showed SL-325 was well tolerated over single and multiple ascending doses, with durable DR3 occupancy, no evidence of residual DR3 agonism, and a low 3.7% anti-drug antibody rate.
- Clear clinical development path: A randomized, double-blind, placebo-controlled Phase 2b trial of SL-325 in moderate-to-severe Crohn’s disease is planned to start in the third quarter of 2026, with 12-week induction data targeted in the first half of 2028, providing defined upcoming value inflection points.
Negative
- None.
Insights
Early SL-325 data de-risk the DR3 program and support Phase 2b IBD plans.
Shattuck reports first-in-human data for SL-325 showing good tolerability across a wide dose range and prolonged DR3 receptor occupancy in 72 healthy volunteers. The low 3.7% ADA rate, measured with a drug-tolerant assay, contrasts with higher immunogenicity seen historically with TL1A antibodies.
The durable inhibition of TL1A binding at doses as low as 1 mg/kg supports a planned quarterly maintenance schedule in Crohn’s disease. A randomized, double-blind Phase 2b trial in moderate-to-severe Crohn’s, with a 12-week induction and 40-week maintenance, is expected to start in Q3 2026, with 12-week induction data targeted for 1H 2028.
Preclinical and Phase 1 data also underpin SL-846, a DR3 x IL-23R bispecific now in GLP toxicology, with Phase 1 initiation anticipated in 1H 2027. Future outcomes in these planned trials will determine whether the DR3-targeted strategy can improve on existing TL1A and IL‑23 therapies in inflammatory bowel disease.
Large warrant exercises extend Shattuck’s cash runway into 2029.
The company has received notices to exercise about 50.6 million common stock warrants, roughly 96% of those issued in an August 2025 private placement. These exercises are expected to generate aggregate gross proceeds of about $54.9 million.
As of March 31, 2026, Shattuck had already collected $5.6 million from 5,147,773 warrants and expects an additional $49.3 million from 45,438,709 warrants. Combined with approximately $90.4 million in cash, cash equivalents and short-term investments at that date, management now anticipates funding operations into 2029 under current plans.
This significantly strengthens liquidity ahead of capital-intensive Phase 2b and Phase 1 programs. Actual cash needs will depend on trial execution, any business development activity, and potential changes to clinical scope disclosed in future filings.
8-K Event Classification
Key Figures
Key Terms
DR3 blocking antibody medical
anti-drug antibody (ADA) medical
bispecific antibody medical
Phase 2b clinical trial medical
Crohn’s disease medical
IND-enabling GLP toxicology study technical
UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, DC 20549
FORM
CURRENT REPORT
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| Item 7.01 | Regulation FD Disclosure. |
On June 8, 2026, Shattuck Labs, Inc. (the “Company” or “Shattuck”) issued a press release announcing data from its Phase 1 clinical trial of SL-325, its lead DR3 blocking antibody. The Company hosted an investor call and webcast, during which it described additional expected data readouts and milestones for 2026, including (i) initiation of RECEPTIVE-CD1 Phase 2b trial of SL-325 in Crohn’s disease, expected in the third quarter of 2026 and (ii) IND filing for SL-846 (DR3xIL-23R bispecific), which is expected in the first half of 2027.
A copy of the press release is furnished as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated by reference herein. The exhibit furnished under Item 7.01 of this Current Report on Form 8-K shall not be deemed to be “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall they be deemed incorporated by reference in any filing under the Exchange Act or the Securities Act of 1933, as amended, regardless of any general incorporation language in such filing.
| Item 8.01 | Other Events. |
Data Release
On June 8, 2026, the Company released its presentation on data from its Phase 1 clinical trial of SL-325.
Key Phase 1 Findings
The Phase 1 trial is a first-in-human, randomized, placebo-controlled trial evaluating the safety, tolerability, pharmacokinetics (“PK”), receptor occupancy (“RO”), pharmacodynamics (“PD”), and immunogenicity of SL-325 in healthy volunteers. The study enrolled 72 participants, across six single-ascending dose cohorts, with doses ranging from 0.1 mg/kg to 30.0 mg/kg, and three multiple-ascending dose cohorts, with doses ranging from 1 mg/kg to 10 mg/kg.
| • | Immunogenicity: Antidrug antibodies (“ADA”) to SL-325 were detected in 3.7% [2/54] of participants who received SL-325. |
| • | In these two participants, ADA were low titer (≤16), and no impact to PK or receptor occupancy was observed. |
| • | The ADA assay used to detect ADA to SL-325 has a sensitivity of 5.0 ng/ml and drug tolerance of up to SL-325 concentrations of 160.0 µg/ml in the serum. For each participant in this Phase 1 trial, samples were analyzed over a time course, ensuring that samples from each participant fell within the dynamic range of the assay across the full dose range, and thus limiting the possibility of false negative results. |
| • | Published and emerging data suggest that ADA to anti-TL1A antibodies impact efficacy. SL-325’s potentially best-in-mechanism immunogenicity profile is expected to lead to improved efficacy at both the induction and maintenance timepoints compared to anti-TL1A antibodies. |
| • | Pharmacokinetics and Receptor Occupancy: |
| • | Complete DR3 occupancy, as measured by blockade of TL1A binding, was observed at doses of 0.1 mg/kg and higher in all participants. |
| • | Complete inhibition of TL1A binding was durable for more than 10 weeks, and extended PK modeling suggests that complete inhibition of TL1A binding may be sustained for greater than 3 months at doses of greater than1 mg/kg of SL-325. |
| • | The PK profile of SL-325 demonstrated proportional increases in Cmax and AUClast across all dose levels. |
| • | Repeated dosing demonstrated an accumulation ratio of 1.64-1.75. |
| • | A subcutaneous formulation of SL-325 has been developed. These Phase 1 results indicate the potential for quarterly dosing at a volume compatible with an autoinjector pen. |
| • | Pharmacodynamics: Clinical data now corroborate our previous preclinical findings that SL-325 is a pure DR3 blocking antibody. |
| • | No evidence of DR3 agonism was observed. |
| • | No evidence of SL-325 mediated lymphocyte proliferation or changes in serum cytokines was observed in any participant at any dose level. |
| • | No increases in serum levels of TL1A from baseline were observed. |
| • | Safety: SL-325 was well tolerated at all dose levels and upon repeat dosing, with a favorable safety profile consistent with the TL1A inhibitor class. |
| • | There were no serious treatment-emergent adverse events (“TEAEs”) or serious adverse events. |
| • | All treatment-related adverse events (“TRAEs”) were Grade 1. TRAEs were observed in 12 participants. |
RECEPTIVE-CD1 Phase 2b Trial of SL-325 in Crohn’s Disease
The RECEPTIVE-CD1 clinical trial is designed as a randomized, double-blind, placebo-controlled Phase 2b clinical trial to evaluate the safety and efficacy of two dose levels of SL-325 as monotherapy versus placebo in moderate-to-severe Crohn’s disease. SL-325 will be administered intravenously, and the trial will include a 12-week induction period, followed by a 40-week maintenance period, for a total of 52 weeks of treatment for each patient enrolled.
| • | RECEPTIVE-CD1 is expected to enroll approximately 174 patients, randomized 1:1:1, with patients receiving either low dose SL-325, high dose SL-325, or placebo. RECEPTIVE-CD1 will enroll patients at clinical sites in the United States, Canada, and Europe. |
| • | RECEPTIVE-CD1 is expected to enroll patients with moderate-to-severe Crohn’s disease, as defined with a Crohn’s Disease Activity Index (“CDAI”) score of between 220 and 450. |
| • | The primary endpoint is expected to be endoscopic response at Week 12, and the key secondary endpoint will be clinical remission at Week 12. |
| • | Patients randomized to the placebo arm will be eligible to receive SL-325 after the 12-week induction period. |
| • | The primary endpoint, endoscopic response at 12 weeks, is expected to be disclosed in the first half of 2028. |
SL-846: A Dual DR3 and IL-23 Receptor Blocking Antibody
SL-846 is Shattuck’s lead bispecific product candidate and is designed to simultaneously bind to DR3 and to IL-23 receptor, blocking the interaction with TL1A and IL-23, respectively, while avoiding the risk of immune complex formation and resulting ADA challenges of the TL1A-based bispecifics.
| • | SL-846 is an Fc-silenced, half-life extended, IgG1 bispecific antibody. |
| • | Preclinical data demonstrated that SL-846 was equipotent, or more potent, than sequence equivalents of risankizumab and icotrokinra controls in multiple in vitro and cell-based potency assays. |
| • | SL-846 is currently being evaluated in an ongoing IND-enabling GLP toxicology study in non-human primates. Safety and immunogenicity data are expected in the second half of 2026. |
| • | Shattuck expects to submit an IND for SL-846 in the first half of 2027. |
The Company also released its data presentation, which supersedes prior content of the same nature in previously published presentations and which is attached hereto as Exhibit 99.3 and is incorporated by reference in this Item 8.01.
Warrant Exercises
On June 9, 2026, the Company announced that it had received notices to exercise an aggregate of approximately 50.6 million outstanding common stock warrants, representing approximately 96% of the warrants issued in the Company’s August 4, 2025 private placement. As of March 31, 2026, the Company had received aggregate gross proceeds of approximately $5.6 million from the exercise of 5,147,773 warrants and expects to receive additional aggregate gross proceeds of approximately $49.3 million from the exercise of an additional 45,438,709 warrants. A copy of the press release announcing the warrant exercises is attached as Exhibit 99.2 to this Current Report on Form 8-K and is incorporated herein by reference.
| Item 9.01 | Financial Statements and Exhibits. |
(d) Exhibits. The following exhibits are being furnished herewith:
EXHIBIT INDEX
| Exhibit No. |
Description | |
| 99.1 | Press Release, dated June 8, 2026 | |
| 99.2 | Press Release, dated June 9, 2026 | |
| 99.3 | Data Presentation, dated June 8, 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.
| Shattuck Labs, Inc. | ||||||
| Date: June 9, 2026 | By: | /s/ Taylor Schreiber | ||||
| Dr. Taylor Schreiber | ||||||
| Chief Executive Officer | ||||||
| (principal executive officer) | ||||||
Exhibit 99.1
Shattuck Labs Announces Phase 1 Results for SL-325
| • | Potentially best-in-mechanism immunogenicity profile, with only 3.7% of participants developing antidrug antibodies |
| • | Complete blockade of TL1A binding to DR3 for over 3 months expected at doses of 1 mg/kg and higher |
| • | Well tolerated with a favorable safety profile consistent with the TL1A inhibitor class |
| • | No evidence of DR3 agonism |
| • | RECEPTIVE-CD1 Phase 2b clinical trial in patients with Crohn’s disease expected to initiate in the third quarter of 2026 |
| • | Lead bispecific product candidate, SL-846 (DR3xIL-23R), currently being evaluated in IND-enabling toxicology studies; Phase 1 initiation expected in the first half of 2027 |
AUSTIN, TX and DURHAM, NC, June 8, 2026 – Shattuck Labs, Inc. (Shattuck or the Company) (NASDAQ: STTK), a clinical-stage biotechnology company pioneering the development of potential first-in-class monoclonal and bispecific DR3 blocking antibodies for the treatment of patients with inflammatory and immune-mediated diseases, today announced data from its Phase 1 clinical trial of SL-325, Shattuck’s lead DR3 blocking antibody candidate.
“SL-325 is now the first antibody that blocks the receptor for TL1A, known as DR3, to generate human clinical data. The profile of SL-325 is highly encouraging, including a potentially best-in-mechanism immunogenicity profile, saturation of DR3 at low doses of SL-325, and durable inhibition of TL1A binding for months after a single dose.” said Taylor Schreiber, M.D., Ph.D., Chief Executive Officer of Shattuck. “These data indicate that blocking DR3 with SL-325, or with our DR3 by IL-23 receptor blocking bispecific antibody candidate, SL-846, may substantially improve upon the efficacy shown to date with the TL1A inhibitor class, providing an opportunity to maximize potential efficacy for TL1A blockade in IBD and beyond.”
Key Phase 1 Findings
The Phase 1 trial is a first-in-human, randomized, placebo-controlled trial evaluating the safety, tolerability, pharmacokinetics (“PK”), receptor occupancy (“RO”), pharmacodynamics (“PD”), and immunogenicity of SL-325 in healthy volunteers. The study enrolled 72 participants, across six single-ascending dose cohorts, with doses ranging from 0.1 mg/kg to 30.0 mg/kg, and three multiple-ascending dose cohorts, with doses ranging from 1 mg/kg to 10 mg/kg.
| • | Immunogenicity: Antidrug antibodies (“ADA”) to SL-325 were detected in 3.7% [2/54] of participants who received SL-325. |
| • | In these two participants, ADA were low titer (≤16), and no impact to PK or receptor occupancy was observed. |
| • | The ADA assay used to detect ADA to SL-325 has a sensitivity of 5.0 ng/ml and drug tolerance of up to SL-325 concentrations of 160.0 µg/ml in the serum. For each participant in this Phase 1 trial, samples were analyzed over a time course, ensuring that samples from each participant fell within the dynamic range of the assay across the full dose range, and thus limiting the possibility of false negative results. |
| • | Published and emerging data suggest that ADA to anti-TL1A antibodies impact efficacy. SL-325’s potentially best-in-mechanism immunogenicity profile is expected to lead to improved efficacy at both the induction and maintenance timepoints compared to anti-TL1A antibodies. |
| • | Pharmacokinetics and Receptor Occupancy: |
| • | Complete DR3 occupancy, as measured by blockade of TL1A binding, was observed at doses of 0.1 mg/kg and higher in all participants. |
| • | Complete inhibition of TL1A binding was durable for more than 10 weeks, and extended PK modeling suggests that complete inhibition of TL1A binding may be sustained for greater than 3 months at doses of greater than1 mg/kg of SL-325. |
| • | The PK profile of SL-325 demonstrated proportional increases in Cmax and AUClast across all dose levels. |
| • | Repeated dosing demonstrated an accumulation ratio of 1.64-1.75. |
| • | A subcutaneous formulation of SL-325 has been developed. These Phase 1 results indicate the potential for quarterly dosing at a volume compatible with an autoinjector pen. |
| • | Pharmacodynamics: Clinical data now corroborate our previous preclinical findings that SL-325 is a pure DR3 blocking antibody. |
| • | No evidence of DR3 agonism was observed. |
| • | No evidence of SL-325 mediated lymphocyte proliferation or changes in serum cytokines was observed in any participant at any dose level. |
| • | No increases in serum levels of TL1A from baseline were observed. |
| • | Safety: SL-325 was well tolerated at all dose levels and upon repeat dosing, with a favorable safety profile consistent with the TL1A inhibitor class. |
| • | There were no serious treatment-emergent adverse events (“TEAEs”) or serious adverse events. |
| • | All treatment-related adverse events (“TRAEs”) were Grade 1. TRAEs were observed in 12 participants. |
RECEPTIVE-CD1 Phase 2b Trial of SL-325 in Crohn’s Disease
The RECEPTIVE-CD1 clinical trial is designed as a randomized, double-blind, placebo-controlled Phase 2b clinical trial to evaluate the safety and efficacy of two dose levels of SL-325 as monotherapy versus placebo in moderate-to-severe Crohn’s disease. SL-325 will be administered intravenously, and the trial will include a 12-week induction period, followed by a 40-week maintenance period, for a total of 52 weeks of treatment for each patient enrolled.
| • | RECEPTIVE-CD1 is expected to enroll approximately 174 patients, randomized 1:1:1, with patients receiving either low dose SL-325, high dose SL-325, or placebo. RECEPTIVE-CD1 will enroll patients at clinical sites in the United States, Canada, and Europe. |
| • | RECEPTIVE-CD1 is expected to enroll patients with moderate-to-severe Crohn’s disease, as defined with a Crohn’s Disease Activity Index (“CDAI”) score of between 220 and 450. |
| • | The primary endpoint is expected to be endoscopic response at Week 12, and the key secondary endpoint will be clinical remission at Week 12. |
| • | Patients randomized to the placebo arm will be eligible to receive SL-325 after the 12-week induction period. |
| • | The primary endpoint, endoscopic response at 12 weeks, is expected to be disclosed in the first half of 2028. |
SL-846: A Dual DR3 and IL-23 Receptor Blocking Antibody
SL-846 is Shattuck’s lead bispecific product candidate and is designed to simultaneously bind to DR3 and to IL-23 receptor, blocking the interaction with TL1A and IL-23, respectively, while avoiding the risk of immune complex formation and resulting ADA challenges of the TL1A-based bispecifics.
| • | SL-846 is an Fc-silenced, half-life extended, IgG1 bispecific antibody. |
| • | Preclinical data demonstrated that SL-846 was equipotent, or more potent, than sequence equivalents of risankizumab and icotrokinra controls in multiple in vitro and cell-based potency assays. |
| • | SL-846 is currently being evaluated in an ongoing IND-enabling GLP toxicology study in non-human primates. Safety and immunogenicity data are expected in the second half of 2026. |
| • | Shattuck expects to submit an IND for SL-846 in the first half of 2027. |
About SL-325
SL-325 is a potentially first-in-class Death Receptor 3 (DR3) blocking antibody designed to achieve a complete and durable blockade of the clinically validated DR3/TL1A pathway. Shattuck’s preclinical studies demonstrate high affinity binding and superior activity over TL1A antibodies, and offer a data-driven rationale for targeting the TNF receptor, DR3, versus its ligand, TL1A. SL-325 is a fully Fc-silenced, fully human immunoglobulin G monoclonal antibody with a favorable safety profile, potentially best-in-mechanism immunogenicity profile, no evidence of residual DR3 agonism capable of providing durable blockade of TL1A binding to DR3 at low doses in a recently completed Phase 1 clinical trial. SL-325 is expected to be evaluated in a Phase 2b clinical trial in Crohn’s Disease patients initiating in the third quarter of 2026.
About SL-846
SL-846 is a potentially first-in-class Death Receptor 3 (DR3) by IL-23 receptor (IL-23R) blocking bispecific antibody designed to achieve complete and durable blockade of the clinically validated DR3/TL1A and IL-23/IL-23R pathways. Shattuck’s preclinical studies demonstrate high affinity binding to both DR3 and IL-23R, with equivalent or superior in vitro potency in comparison to benchmark IL-23 controls (sequence equivalents of risankizumab and icotrokinra) in a variety of preclinical assays. SL-846 is an Fc-silenced, half-life extended, fully human immunoglobulin G bispecific antibody currently being evaluated for safety, tolerability, immunogenicity, and pharmacodynamics in an IND-enabling GLP toxicology study in non-human primates.
About Shattuck Labs, Inc.
Shattuck Labs, Inc. is a clinical-stage biotechnology company pioneering the development of potentially first-in-class monoclonal and bispecific DR3 blocking antibodies for the treatment of patients with inflammatory and immune-mediated diseases. Shattuck’s expertise in protein engineering and the development of novel TNF receptor therapeutics come together in its lead program, SL-325, a potentially first-in-class DR3 antagonist antibody designed to achieve a more complete blockade of the clinically validated DR3/TL1A pathway. The Company has offices in both Austin, Texas and Durham, North Carolina. For more information, please visit: www.ShattuckLabs.com.
Forward-Looking Statements
Certain statements in this press release may constitute “forward-looking statements” within the meaning of the federal securities laws, including, but not limited to, Shattuck’s expectations regarding: plans for its preclinical studies, clinical trials and research and development programs, particularly with respect to SL-325; the anticipated timing of release of data from the Company’s ongoing Phase 1 clinical trial of SL-325; the anticipated timing of initiation of a Phase 2 clinical trial of SL-325 in patients with Crohn’s disease; the clinical benefit, safety and tolerability of SL-325; anticipated development of additional preclinical pipeline candidates; the timing of nomination, release of preclinical data and development timelines of a lead bispecific antibody candidate; and expectations regarding the time period over which the Company’s capital resources will be sufficient to fund its anticipated operations. Words such as “may,” “might,” “will,” “objective,” “intend,” “should,” “could,” “can,” “would,” “expect,” “believe,” “design,” “estimate,” “predict,” “potential,” “develop,” “plan” or the negative of these terms, and similar expressions, or statements regarding intent, belief, or current expectations, are forward-looking statements. While the Company believes these forward-looking statements are reasonable, undue reliance should not be placed on any such forward-looking statements, which are based on information available to it on the date of this release. These forward-looking statements are based upon current estimates and assumptions and are subject to various risks and uncertainties (including, without limitation, those set forth in Shattuck’s filings with the U.S. Securities and Exchange Commission (SEC)), many of which are beyond its control and subject to change. Actual results could be materially different. Risks and uncertainties include: global macroeconomic conditions and related volatility; expectations regarding the initiation, progress, and expected results of the Company’s preclinical studies, clinical trials and research and development programs; expectations regarding the timing, completion and outcome of the Company’s preclinical studies and clinical trials; the unpredictable relationship between preclinical study results and clinical study results; the timing or likelihood of regulatory filings and approvals; liquidity and capital resources, including the time period over which current capital resources are expected to the fund the Company’s operations; and other risks and uncertainties identified in Shattuck’s Annual Report on Form 10-K for the year ended December 31, 2025, and subsequent disclosure documents filed with the SEC. Shattuck claims the protection of the Safe Harbor contained in the Private Securities Litigation Reform Act of 1995 for forward-looking statements. The Company expressly disclaims any obligation to update or alter any statements whether as a result of new information, future events or otherwise, except as required by law.
The Company intends to use the investor relations portion of its website as a means of disclosing material non-public information and for complying with disclosure obligations under Regulation FD.
Investor & Media Contact:
Andrew R. Neill
Chief Financial Officer
Shattuck Labs, Inc.
InvestorRelations@shattucklabs.com
Exhibit 99.2
Shattuck Labs Announces Exercise of Outstanding Common Stock Warrants and Provides Financial Update
AUSTIN, Texas and DURHAM, N.C., June 9, 2026 (GLOBE NEWSWIRE) — Shattuck Labs, Inc. (Shattuck) (NASDAQ: STTK), a clinical-stage biotechnology company pioneering the development of potentially first-in-class monoclonal and bispecific DR3-blocking antibodies for the treatment of patients with inflammatory and immune-mediated diseases, today announced it has received notices to exercise totaling approximately 50.6 million common stock warrants to date, representing approximately 96% of the warrants issued in the Company’s August 4, 2025 private placement. The exercise of these warrants is expected to result in aggregate gross proceeds of approximately $54.9 million. As of March 31, 2026, the Company had received aggregate gross proceeds of approximately $5.6 million pursuant to the exercise of 5,147,773 warrants. The Company expects to receive additional aggregate gross proceeds totaling approximately $49.3 million from the exercise of 45,438,709 common stock warrants since March 31, 2026. Together with existing cash and cash equivalents and short term investments of approximately $90.4 million as of March 31, 2026, Shattuck expects to be able to fund operations into 2029. This cash runway guidance is based on the Company’s current operational plans and excludes any additional capital that may be received (other than from the exercise of these common stock warrants), proceeds from business development transactions, and/or additional costs associated with clinical development activities that may be undertaken.
About Shattuck Labs, Inc.
Shattuck Labs, Inc. is a clinical-stage biotechnology company pioneering the development of potentially first-in-class monoclonal and bispecific DR3 blocking antibodies for the treatment of patients with inflammatory and immune-mediated diseases. Shattuck’s expertise in protein engineering and the development of novel TNF receptor therapeutics come together in its lead program, SL-325, a potentially first-in-class DR3 antagonist antibody designed to achieve a more complete blockade of the clinically validated DR3/TL1A pathway. The Company has offices in both Austin, Texas and Durham, North Carolina. For more information, please visit: www.ShattuckLabs.com.
Forward-Looking Statements
Certain statements in this press release may constitute “forward-looking statements” within the meaning of the federal securities laws, including, but not limited to, Shattuck’s expectations regarding: plans for its preclinical studies, clinical trials and research and development programs, particularly with respect to SL-325; the anticipated timing of initiation of a Phase 2 clinical trial of SL-325 in patients with Crohn’s disease; the clinical benefit, safety and tolerability of SL-325; anticipated development of additional preclinical pipeline candidates; the timing of nomination, release of preclinical data and development timelines of a lead bispecific antibody candidate; and expectations regarding the time period over which the Company’s capital resources will be sufficient to fund its anticipated operations. Words such as “may,” “might,” “will,” “objective,” “intend,” “should,” “could,” “can,” “would,” “expect,” “believe,” “design,” “estimate,” “predict,” “potential,” “develop,” “plan” or the negative of these terms, and similar expressions, or statements regarding intent, belief, or current expectations, are forward-looking statements. While the Company believes these forward-looking statements are reasonable, undue reliance should not be placed on any such forward-looking statements, which are based on information available to it on the date of this release. These forward-looking statements are based upon current estimates and assumptions and are subject to various risks and uncertainties (including, without limitation, those set forth in Shattuck’s filings with the U.S. Securities and Exchange Commission (SEC)), many of which are beyond its control and subject to change. Actual results could be materially different. Risks and uncertainties include: global macroeconomic conditions and related volatility; expectations regarding the initiation, progress, and expected results of the Company’s preclinical studies, clinical trials and research and development programs; expectations regarding the timing, completion and outcome
of the Company’s preclinical studies and clinical trials; the unpredictable relationship between preclinical study results and clinical study results; the timing or likelihood of regulatory filings and approvals; liquidity and capital resources, including the time period over which current capital resources are expected to the fund the Company’s operations; and other risks and uncertainties identified in Shattuck’s Annual Report on Form 10-K for the year ended December 31, 2025, and subsequent disclosure documents filed with the SEC. Shattuck claims the protection of the Safe Harbor contained in the Private Securities Litigation Reform Act of 1995 for forward-looking statements. The Company expressly disclaims any intention to update or alter any statements whether as a result of new information, future events or otherwise, except as required by law.
The Company intends to use the investor relations portion of its website as a means of disclosing material non-public information and for complying with disclosure obligations under Regulation FD.
Investor & Media Contact:
Andrew R. Neill
Chief Financial Officer
Shattuck Labs, Inc.
InvestorRelations@shattucklabs.com
Phase 1 Clinical Data of SL-325, a Potentially First-In-Class DR3 Blocking Antibody & Pipeline Update SHATTUCK LABS, INC. NASDAQ: STTK Exhibit 99.3
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Call Agenda and Participants SL-325 Phase 2b Study in Crohn’s Disease RECEPTIVE-CD1 Taylor Schreiber, MD, PhD Chief Executive Officer Lini Pandite, MD, MBA Chief Medical Officer Suresh De Silva, PhD Chief Scientific Officer Michael Choi, MD VP Clinical Development Andrew Neill, MBA Chief Financial Officer All Closing and Q&A SL-846, A Potentially First-In-Class DR3 x IL-23R Bispecific Antibody SL-325 Phase 1 Results TL1A/DR3 Biology Potential Advantages of DR3 Blockade Introduction
Introduction SL-325 DR3 SL-325 is a fully human, Fc-silenced, IgG1 monoclonal antibody (mAb) that selectively binds to DR3 and blocks its interaction with TL1A* DR3 blockade has the potential to provide superior efficacy in comparison to TL1A blockade because: DR3 is a more abundant and stable target than TL1A Immunogenicity due to immune complex formation is not expected for SL-325 Phase 1 first-in-human trial evaluated the safety, tolerability, pharmacokinetics (PK), immunogenicity, and pharmacodynamic (PD) effects of SL-325 in healthy participants (NCT07158437) Key Findings Well tolerated across all dose levels, with a safety profile similar to those reported for anti-TL1A mAbs Prolonged blockade of TL1A binding at low doses may support quarterly maintenance dosing intervals No evidence of DR3 agonism, confirming SL-325 is a pure DR3 blocking antibody Potentially best-in-mechanism immunogenicity profile with ADA rate of 3.7% *Hussain M et al. IBD Journal 2026. In Press
Bamias G. Gut 2025;74:652-668 Hussain M et al. IBD Journal 2026. In Press SL-325 Is a High-Affinity, Highly Specific, DR3 Blocking Antibody TL1A Is Primarily Expressed by Tissue-Resident APCs TL1A is the sole known signaling ligand for DR3 and does not signal through any other receptors SL-325 potently inhibits TL1A binding to DR3 SL-325 does not bind DcR3, allowing TL1A clearance by DcR3 to remain intact SL-325 binds DR3 with very high affinity (1.3 pM) Highly durable blockade of TL1A binding is expected to extend dosing intervals By targeting membrane-bound DR3 rather than soluble TL1A, SL-325 is designed to avoid circulating TL1A immune complex formation which leads to high ADA rates DR3 Is Primarily Expressed by Lymphoid Cells In Blood and Tissue
Potentially First-in-Class Pipeline Targeting DR3 IBD = Inflammatory Bowel Disease; RA = rheumatoid arthritis; PsA = psoriatic arthritis; HS = hidradenitis suppurativa, I&I = inflammatory and immune-mediated diseases Developing potentially first-in-class DR3 monospecific and bispecific antibodies LEAD TARGET(S) INDICATIONS IND-ENABLING PHASE 1 PHASE 2 EXPECTED MILESTONES SL-325 DR3 IBD Potentially RA, PsA, HS, other I&I Phase 2b in Crohn’s disease Initiation in Q3 2026 Phase 2b in CD 12W Induction Data in 1H 2028 SL-425 EXTENDED HALF-LIFE DR3 Potentially RA, PsA, HS, other I&I SL-846 EXTENDED HALF-LIFE DR3 X IL-23R Potentially IBD, PsA, other I&I Phase 1 Initiation in 1H 2027 DR3 blockade with SL-325 provides potentially best-in-mechanism immunogenicity compared to TL1A blocking antibodies Blocking DR3 may provide more potent inhibition of the TL1A/DR3 axis than TL1A blockade due to more durable inhibition of TL1A signaling
*Danese S et al. Lancet Gastroenterol and Hepatol. 2025;10:882-895; SYRE Corp Update 6/17/2025; Balyan R et al. J Crohn‘s and Colitis 2024;18:1206-1207; RXDX Corp Update 12/7/2021; XNCR Corp Update 5/4/2026. **Emery P et al. Scand J Rheumatol 2020;49:361-370 Created in https://BioRender.com Immune Complex Mediated Immunogenicity Limits Efficacy of TL1A Blocking Antibodies Anti-TL1A antibody binding to soluble TL1A in blood is an undesired site of action that causes immune complex formation This leads to anti-drug antibody (ADA) rates for anti-TL1A antibodies of 48-100% in Phase 1 trials* Both total ADA and neutralizing ADA cause similar reduction in efficacy** ADA can accelerate clearance of TL1A blocking antibodies, which correlates with reduced efficacy*
*Combined 450 mg and 900 mg dose levels **50à50, 150à150 and 450à450 mg dose levels combined ***AT-IR patients Data in the figure are presented as a proportion of the total number of patients in remission at the maintenance timepoint relative to the induction timepoint. Example for upadacitinib: 90 patients in remission in maintenance divided by 55 patients in remission at induction equates to an increase in the number of patients in remission from induction to maintenance of 38% High ADA May Limit Durability of Clinical Benefit in IBD The mechanism of immune complex formation is similar for anti-TL1A and anti-TNF antibodies, leading to high rates of ADA to both classes ADA rates to IL-23 inhibitors are significantly lower than TL1A or TNF inhibitors The number of patients in clinical remission improves over time for IBD drugs with low rates of ADA Placebo Adjusted Clinical Remission at Induction No. Patients in Remission Induction Maintenance Infliximab UC FDA Label 19.5% 161 160 Adalimumab UC Sandborn Gastro 2012, FDA Label 8.25% 41 43 Tulisokibart UC Ma C UEGW 2024 25% 18 19 Duvakitug UC* Teva Corp Updates 2/24/2025 & 2/19/2026 27% 39 37 Afimkibart UC Danese S, Lancet Gastro 2025** 20% 33 33 Upadacitinib UC Danese, Lancet 2022 29% 58 80 Tofacitinib UC Sandborn, NEJM 2017, FDA Label 13% 55 90 Ustekinumab UC Sands, NEJM 2019, FDA Label 12% 41 79 Risankizumab UC Panaccione, J Crohn’s & Colitis 2025***, FDA Label 16% 38 90
Immune Complexes Between TL1A and Anti-TL1A Antibodies Directly Increase TL1A Expression *Meylan et al. Immunity 2008; 29:79-89 **Data demonstrate fold increase in TL1A mRNA expression from human monocytes following exposure to the indicated test articles in vitro. Study conducted by Shattuck. Study utilized a sequence-equivalent of tulisokibart. Created in https://BioRender.com Tulisokibart/TL1A immune complex (IC) triggers >75-fold increase in TL1A production by human monocytes in vitro** A feedback loop of TL1A immune complexes increasing TL1A expression may: Further increase immunogenicity risk Increase the amount of antibody needed to neutralize free TL1A, potentially contributing to high dose requirements for TL1A antibodies
Phase 1 Clinical Trial of SL-325 in Healthy Participants 0.1 mg/kg 1 mg/kg 0.3 mg/kg 3 mg/kg 1 mg/kg 10 mg/kg 3 mg/kg 10 mg/kg 30 mg/kg Single Ascending Dose PART B Multiple Ascending Dose (3 doses, q2w) Single ascending dose (SAD) and multiple ascending dose (MAD) study in healthy participants Dosing is complete for all 72 participants Phase 1 Clinical Trial Design Key Questions Evaluated in Phase 1 Is SL-325 as well tolerated as anti-TL1A antibodies? Does human data confirm that SL-325 is a pure DR3 blocking antibody? How durable is DR3 occupancy, and what does that translate to with regard to expected maintenance dosing intervals? Is SL-325 less immunogenic than TL1A blocking antibodies? INCREASING DOSE PART A 6 SL-325 : 2 Placebo Participants Per Cohort 6 SL-325 : 2 Placebo Participants Per Cohort Placebo SL-325 N 18 54 Median Age (years, range) 31 (21, 53) 35 (22, 54) Sex, % Female 56 69 Participant Demographics
TEAE = treatment emergent adverse events; TRAE = treatment related or possibly related adverse events; IRR = infusion-related reaction *The participant experienced a mild IRR during the second infusion. The symptoms resolved without therapeutic intervention and within 10 minutes. ADA remained negative. The participant was diagnosed with severe Strep throat the following day. The underlying medical condition may have contributed to the reaction. The third dose was not given. SL-325 Was Safe and Well Tolerated Across a Wide Dosing Range Data are inclusive of all participants in all SAD and MAD cohorts TEAE observed in ≥2 participants included: headache, nasal congestion, nausea, venipuncture site pain, cough, diarrhea, feeling hot, hyperhidrosis, dizziness, urinary tract infection, arthropod bite, and elective termination of pregnancy Mild TRAE (all Grade 1) observed in ≥2 participants included: headache (n=8), hyperhidrosis (n=2), dizziness (n=2), feeling hot (n=2) SL-325 was discontinued in one participant who experienced a mild IRR (Grade 1)* SL-325 DOSE LEVEL (mg/kg) Placebo 0.1 0.3 1.0 3.0 10 30 N 18 6 6 12 12 12 6 ≥ 1 TEAE 5 2 2 6 7 4 2 ≥ 1 TRAE Mild (SAD) 1 0 0 1 2 0 1 Mild (MAD) 0 - - 2 3 3 - Moderate 0 0 0 0 0 0 0 Severe 0 0 0 0 0 0 0 Serious AE 0 0 0 0 0 0 0 Discontinued Due to TRAE 0 0 0 0 0 1* 0
*Cytokine panel evaluated: IFNγ, TNFα, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12 and IL-13 No Evidence of Residual DR3 Agonism in Phase 1 in Healthy Human Participants The risk of agonism must be discharged for receptor targeted antibodies No SL-325 mediated changes in serum cytokines were observed (IFNγ shown as example below)* No change from baseline in the serum concentration of TL1A was observed These data corroborate our preclinical findings that SL-325 is a pure DR3 blocking antibody Dose Level No changes from pre-dose in proportions of cells (upper panels), nor the proportion of proliferating cells (lower panels) at any dose level
PK Profile of SL-325 from Phase 1 in Healthy Human Participants Dose proportional increase in Cmax and AUClast across all dose levels from 0.1 to 30 mg/kg Clearance consistent across all dose levels Estimated half-life of 16 days Figure shows participant-level PK profiles from all SAD cohorts Accumulation ratio of between 1.64-1.75 with repeated dosing
A Single Dose of SL-325 Blocked TL1A Binding in a Dose-Dependent Manner for Months DR3 occupancy was measured by inhibition of TL1A binding Full DR3 occupancy was achieved even at the lowest dose of 0.1 mg/kg Dose-dependent extension in the duration of TL1A blockade was observed, lasting months at ≥1 mg/kg Durable inhibition of TL1A binding could enable quarterly dosing intervals in the maintenance phase of therapy for SL-325 Shattuck has developed a subcutaneous formulation of SL-325, and these data also potentially indicate feasibility of administration with an autoinjector pen
*Wang Y et al. Pharm Res 2012;29:3384-3392, Wang Y ASCPT 2017 Anti-Drug Antibody (ADA) Assay Performance and Data Interpretability Inadequate assay tolerance contributes to a commonly held belief that higher doses of drug lead to lower incidence of ADA Sponsors commonly report ADA qualitatively, or simply report an ADA percentage ADA assay results are only valid if the serum concentration of the therapeutic antibody is below the assay’s drug tolerance threshold (Assay Tolerance) at the time of sample analysis FDA has reported that only 25% of antibodies have sufficient drug tolerance in the ADA assay at the time of BLA submission* This may be a source of high rates of false-negative results in reported ADA percentages, especially in high-dose cohorts.
*ADA rates are provided as they were reported in the referenced publications/reports. These data were not generated in head-to-head clinical trials. Comparisons across trials have inherent limitations and caution should be exercised when comparing data from unrelated studies. **Data as of June 8, 2026. As of the cutoff date, ADA follow up complete for all SAD cohorts and the 1.0 mg/kg MAD cohort. For the 3.0 mg/kg and 10 mg/kg MAD cohorts, each participant has had at least three valid negative ADA assay results, including after the last dose, with continued confirmatory follow-up ongoing. SL-325 Demonstrated a Potentially Best-In-Mechanism Immunogenicity Profile with 3.7% ADA SL-325 ADA assay has a sensitivity of 5 ng/mL and assay tolerance up to SL-325 concentrations of 160 µg/mL in serum Data includes all participants from all SAD and MAD cohorts in all dose levels in the study** ADA were observed in 2/54 participants who received SL-325. In the two participants who developed ADA, titers remained low (8 and 16), without any impact on PK or RO Longitudinal sampling was performed to ensure that SL-325 concentrations fell within the dynamic range of the ADA assay for all study participants Reported ADA Rates from Phase 1 Trials* Afimkibart ADA titer of ≤60 was reported as ADA negative: Danese S et al. Lancet Gastroenterol and Hepatol. 2025;10:882-895 SL-325 ADA rate is 0% when analyzed using this cutoff.
Key Questions Answered in Phase 1 for SL-325 Is SL-325 as well-tolerated as anti-TL1A antibodies? Yes, SL-325 was well tolerated across a wide dosing range. Does human data confirm that SL-325 is a pure DR3 blocking antibody? Yes, SL-325 is a pure blocking antibody with no evidence of residual agonism. How durable is DR3 occupancy, and what does that translate to for expected maintenance dosing intervals? A single dose of SL-325 inhibits TL1A binding to DR3 for months, potentially enabling quarterly dosing intervals. Is SL-325 less immunogenic than TL1A blocking antibodies? Potentially best-in-mechanism immunogenicity profile with ADA rate of 3.7%
*Study design as currently contemplated, subject to change Study Design Elements Double-blind, placebo-controlled IV induction and maintenance Dose selection informed by Phase 1 PK/RO based QSP modeling with >95% TL1A signal inhibition throughout the dosing interval Population Moderate to severe CD (CDAI 220-450) All patients have opportunity to receive SL-325 N = 174, randomized 1:1:1 Key Endpoints Primary: Endoscopic response at 12 weeks Secondary: Clinical remission at 12 weeks HD = high dose, LD = low dose, LTE = long term extension SL-325 HD Placebo SL-325 HD SL-325 HD Blinded SL-325 LD SL-325 LD 12 Week Induction 40 Week Maintenance à LTE A Multi-Dose, Placebo-Controlled Planned Phase 2b Study of SL-325 in Crohn’s Disease
SL-846 A Potentially First-in-Class DR3 x IL-23R Bispecific Antibody
Strategies to Block TL1A/DR3 in Future Combination Therapy Created in https://BioRender.com
TL1A-Directed Bispecific Antibodies Are Hyper-Immunogenic Kroenke M et al. Frontiers Immunol 2021; Neelakantan S et al. Br J Clin Pharmacol 2026 Genovese M et al. Arth & Rheumatol 2018; Kroenke M et al. AAPS Journal 2021 Created in https://BioRender.com
SL-846 – A Potentially First-In-Class DR3 x IL-23R Half-Life Extended Bispecific Antibody DR3 Binding Arm IL-23R Binding Arm Same binding epitope as SL-325 Avoids risk of immune complex formation Enables binding in cis to IL-23R expressing cells Validated mechanism of action (icotrokinra) Similar in vitro potency when compared to icotrokinra and risankizumab Enables binding in cis to DR3 expressing cells Effector-Null Human IgG1 Fc Mutations to remove Fc gamma receptor binding potential Knob-In-Hole Recombination Clinically validated bispecific antibody format Half-Life Extended Substitutions to increase exposure and allow for extended dosing intervals
*Sequence equivalents of tulisokibart, risankizumab, and icotrokinra SL-846 Demonstrated Competitive In Vitro Potency to Icotrokinra and Risankizumab SL-846 was tested head-to-head against tulisokibart, risankizumab and icotrokinra* in a variety of in vitro binding and potency assays SL-846 performed similarly to, or slightly better than, each assay relative to the TL1A or IL-23 control Additional pre-clinical characterization of SL-846 versus controls will be provided at an upcoming medical meeting
Conclusions SL-325 Has the Profile of a Winning Antibody Phase 2 Initiation in CD Expected in Q3 2026 12W Induction Data Expected in 1H 2028 SL-846 is a Potentially First-In-Class DR3 x IL-23R Bispecific Antibody NHP Tox/Immunogenicity Data Expected in 2H 2026 Phase 1 Initiation Expected in 1H 2027 Potentially best-in-mechanism ADA rate from the completed Phase 1 study with a highly drug-tolerant assay and longitudinal sampling SL-325 was well-tolerated across a wide dose range, with a safety profile consistent with those reported for the TL1A class PK and RO results support the potential for extended dosing intervals during maintenance therapy while maintaining full blockade of TL1A binding Low dose levels required for durable RO potentially indicate feasibility of administration with a SC autoinjector pen SL-325 will soon enter a Phase 2b clinical proof of concept study in Crohn’s Disease Unlocks blockade of the TL1A/DR3 pathway in a bispecific without immune complex related ADA risk associated with TL1A antibodies Pre-clinical studies showed similar potency to icotrokinra and risankizumab Leverages the clinical data generated to date with SL-325 Combination in a single drug enables simpler clinical proof of concept study designs with two of the most promising target classes in I&I disease Opens portfolio expansion to target indications where IL-23 inhibition is clinically validated
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