Oral, Selective RBM39Degrader Under Evaluation in Phase 1 Trial; Preclinical Data Support ExpansionPotential Across Ewing Sarcoma, Hepatocellular Carcinoma, KRAS-Mutant Cancers,Neuroblastoma, and Other RBM39-Dependent Tumors

KING OF PRUSSIA, PA, June2, 2026 — SEED Therapeutics, Inc. (“SEED”), a clinical-stage biotechnology companypioneering rationally designed molecular glue degraders, today announced thepresentation of a trial-in-progress poster at the 2026 American Society of Clinical Oncology(ASCO) Annual Meeting highlightingthe first-in-human Phase 1 study of ST-01156, SEED’s oral,  selective RBM39 molecular glue degrader. Thepresentation underscores SEED’s transition from platform validation to clinicalexecution, with ST-01156 advancing across multiple RBM39-dependent cancers,with development informed by mechanism-based preclinical data and real-time pharmacokineticand pharmacodynamic assessments.

ST-01156 is designed to degradeRNA-binding motif protein 39 (RBM39), a regulator of RNA splicing programs thatgovern oncogenes essential for tumor survival. The ASCO poster outlines thescientific rationale, Phase 1 dose-escalation design, and planned expansionstrategy for ST-01156which is currently being evaluated in a first-in-humanPhase 1 dose-escalation study (NCT07197554)in patients with advanced solidmalignancies.

Highlights At A Glance

·      Clinical-stagelead asset: ST-01156 is currently being evaluatedin an open-label Phase 1 study in patients with advanced solid malignancies.

·      Oral,brain-penetrant molecular glue degrader: ST-01156 was rationally optimized for selective RBM39 degradation,potency, metabolic stability, and drug-like properties.

·      Integratedbiomarker and dose-selection strategy: The study incorporates real-time RBM39 target engagement in peripheralblood mononuclear cells (PBMCs), together with safety and pharmacokinetics, tosupport recommended Phase 2 dose (RP2D) selection.

·      Broadoncology expansion potential: Planned expansion cohorts include Ewing sarcoma, advancedhepatocellular carcinoma, KRAS-mutant cancers, and other RBM39-dependenttumors, including biliary tract carcinoma, endometrial carcinoma, and DNAdamage repair–aberrant cancers.

·      Preclinical proof-of-conceptacross multiple models: SEED hasdemonstrated preclinical antitumor activity in response to RBM39 degradation,including tumor regression, with complete regression observed in Ewing sarcoma,neuroblastoma, and KRAS-mutant colorectal cancer models.

Together, these findings support SEED’sstrategy to advance ST-01156 from dose escalation into patient-enrichedexpansion cohorts where emerging RBM39 biology informs indication selection andclinical proof-of-concept.

Scientific Rationale and ASCO Poster Takeaways

RBM39 is an RNA-binding protein thatregulates cancer-relevant RNA splicing programs, including pathways involved intumor proliferation, survival, DNA damage response, and oncogenic fusionproteins. ST-01156 is designed to act as a molecular glue degrader byrecruiting RBM39 to DCAF15, an E3 ligase adapter, leading to RBM39 degradationthrough the ubiquitin-proteasome system. By eliminating RBM39, ST-01156 has thepotential to disrupt multiple cancer-driving pathways that are difficult toaddress with conventional targeted therapies.

The ASCO poster highlights preclinicaland clinical-development findings supporting SEED’s strategy:

·      Ewingsarcoma rationale: ST-01156 demonstrated tumor regressionin an A673 Ewing sarcoma xenograft model, with complete regression at higherdose levels. Separately, treatment with ST-00937, a non-deuterated precursor ofST-01156, showed complete elimination of RBM39 and the EWS-FLI1 fusion proteinin tumor lysates.

·      Neuroblastomaand KRAS-mutant cancer activity: ST-01156 produced complete tumor regression in an SH-SY5Y neuroblastomaxenograft model, while ST-00937 demonstrated complete regression in an HCT-116KRAS G13D-mutant colorectal cancer xenograft model.

·      Mechanism-basedexpansion strategy: The clinical development plan includesexpansion cohorts in Ewing sarcoma, advanced hepatocellular carcinoma,KRAS-mutant cancers, and other RBM39-dependent tumors, including biliary tractcarcinoma, endometrial carcinoma, and tumors with DNA damage repairaberrations.

·      Integrateddose-selection approach: The Phase 1study is designed to determine the optimal dose and recommended Phase 2 doseusing safety, pharmacokinetic, and pharmacodynamic data, including real-timemeasurement of RBM39 target engagement in PBMCs.

“ST-01156 is designed to address abiologically important and difficult-to-drug target through selective RBM39degradation. The ASCO presentation highlights a disciplined clinical strategythat integrates safety, pharmacokinetics, and real-time target engagement toguide dose selection and expansion into cancers with strong mechanisticrationale. We believe this approach positions ST-01156 to generate early meaningfulclinical proof-of-concept across multiple RBM39-dependent tumor types,” said Dr.James Tonra, PhD, President, and Chief Scientific Officer of SEED.

“The advancement of ST-01156 intofirst-in-human clinical evaluation is an important milestone for SEED and avalidation of our RITE3™ technology. Our goal is not only to discover molecularglues, but to rationally design degraders with clear target biology,translational biomarkers, and a defined clinical development path. ST-01156reflects that strategy and represents a meaningful step toward unlockingdisease drivers that have historically been considered undruggable,” said Dr. LanHuang, PhD, Co-Founder, Chairman, and Chief Executive Officer of SEED.

Clinical DevelopmentStatus

ST-01156 is being evaluated in anongoing, open-label Phase 1 multiple ascending dose (MAD) study in patientswith advanced solid malignancies. The study is designed to enroll approximately30 to 50 patients, with ST-01156 administered orally once daily for five daysevery seven days, with the option to adapt to a continuous once-daily schedulebased on emerging data.

The primary objectives are tocharacterize safety and tolerability and determine the optimal dose andrecommended Phase 2 dose. Secondary objectives include pharmacokinetics, RBM39target engagement in PBMCs, and preliminary antitumor activity. Per protocol,SEED plans to evaluate ST-01156 in mechanism-based back-fill cohorts withinthis MAD study, including Ewing sarcoma, advanced hepatocellular carcinoma,KRAS-mutant cancers, and other RBM39-dependent tumors. Data from these cohortsare intended to inform the design of the protocol’s subsequent Phase 1expansion phase.

ASCO 2026 PosterPresentation Details:

·       Title: First-in-Human Clinical Evaluation of ST-01156, anOptimized and Selective Degrader of RNA-Binding Motif 39 (RBM39): A Phase 1Study in Advanced Solid Malignancies with a Focus on RBM39-Dependent Cancers

·       Presenter/Authors: Eric K. Rowinsky, Gregory M. Cote, George D.Demetri, Robert G.Maki, Suzanne George, Daneng Li, AlainC. Mita, Monica M. Mita, Jordi Rodon Ahnert, Dan Lu, Dong Liu, Lan Huang, JamesTonra

·       Session: DevelopmentalTherapeutics—Molecularly Targeted Agents and Tumor Biology

·       Abstract Number: TPS3164

About SEED Therapeutics

SEED Therapeutics is a clinical-stagebiotechnology company developing rationally designed molecular glue degradersto treat diseases driven by proteins previously considered undruggable. Itsproprietary RITE3™ technology enables selective targeted protein degradationwith a defined therapeutic window, supporting a pipeline of six molecular glueprograms across oncology, neurodegeneration, and immunology.

SEED was co-founded by four preeminent scientists:

•  NobelLaureate Prof. Avram Hershko, co-discoverer of the ubiquitin-proteasome system, the cellularmachinery that SEED’s molecular glue degraders harness to eliminatedisease-causing proteins.

•  Dr. LanHuang, a pioneering structural biochemistwho determined the first high-resolution structure of an E3 ligasesubstrate-binding domain, providing foundational insight into how targetedprotein degradation can be rationally designed.

•  Prof. NingZheng (University of Washington, HHMIInvestigator), structural biologist and pioneer of RING-finger E3 ligasemechanisms, and the scientist who coined the term “molecular glue” to describesmall molecules that redirect E3 ligases to degrade neo-substrates.

•  Prof. Michele Pagano (NYU Grossman School of Medicine, HHMIInvestigator), one of the world’s foremost authorities on ubiquitin-mediatedproteolysis and its role in cell cycle control and cancer, whose work hasdefined how E3 ligase dysregulation drives tumor development.

Additional information is available at www.seedtherapeutics.com.

Forward-LookingStatements

This press release contains forward-looking statements regarding SEEDTherapeutics, including statements about the design and progress of itsclinical and preclinical programs. Actual results may differ materially due tovarious risks, including those inherent to drug development. SEED undertakes noobligation to update these statements except as required by law.

Media & InvestorContact

Investor Relations: IR@seedtherapeutics.com

Media Relations: PR@seedtherapeutics.com

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