Phase 1 Dose Escalation Underway at Six Leading U.S. Oncology Centers;MYC Overexpression and CDKN2A/B Deletion Identified as PotentialPatient-Selection Biomarkers — Data Presented at AACR Annual Meeting 2026

KING OF PRUSSIA, PA — April 22,2026 — SEED Therapeutics, Inc. (“SEED”), a clinical-stagebiotechnology company pioneering rationally designed molecular glue degraders,today announced new data demonstrating potent anticancer activity of its RBM39degrader program in neuroblastoma, a pediatric cancer with high unmet medicalneed. SEED’s scientific work also identified potential biomarkers predictive ofanticancer response that will be further examined in the clinic, with Phase 1dose escalation projected to be completed by Q1 2027. The findings are beingpresented at the 2026 Annual Meetingof the American Association for Cancer Research (AACR), which convenes more than 22,000 scientists, clinicians,and investors this week in San Diego.

ST-01156, SEED’s clinical-stageRBM39 molecular glue degrader, is currently being evaluated in a Phase 1 doseescalation study (NCT07197554) at six leading U.S. oncology centers.

Highlights At AGlance

•  Tumoreradication in a rigorous in vivo model: ST-01156achieved complete tumor regression in neuroblastoma model using adifferentiated dosing regimen — a demanding efficacy benchmark in solid tumoroncology.

•  ActivePhase 1 clinical trial: Dose escalationis underway (NCT07197554) at six leading U.S. oncology centers, with clinicalsites in additional geographies in preparation.

•  Biomarkerstrategy: MYC overexpression (sensitivity)and CDKN2A/B deletion (resistance) were identified as part of SEED’s biomarkerprogram, potentially enabling precision patient enrollment as the trialadvances.

•  RarePediatric and Orphan disease opportunity: Neuroblastomais a high-unmet-need rare pediatric cancer representing a Rare PediatricDisease and Orphan Disease designation-eligible indication, with potential forexpedited regulatory pathways including Priority Review Voucher eligibility.

Scientific Rationale: Why RBM39Matters

RBM39is an RNA-binding protein that governs pre-mRNA splicing — a process cancercells exploit to fuel uncontrolled growth, evade cell death, and repair DNAdamage. By degrading RBM39 entirely, rather than merely inhibiting it, SEED’sapproach disrupts multiple oncogenic pathways simultaneously: cell cycleprogression, metabolic reprogramming, DNA damage response, and programmed celldeath (apoptosis — the process by which damaged or cancerous cells areeliminated by the body). This breadth of effect is a key differentiator fromconventional targeted therapies.

Molecularglue degraders achieve this by redirecting the cell’s own quality-controlmachinery — the ubiquitin-proteasome system — to tag and destroy the targetprotein. SEED’s proprietary RITE3™ platform was designed from inception toidentify, validate, and optimize molecular glues with a defined therapeuticwindow, bringing rational drug design to protein targets previously consideredundruggable.

Key Data Highlights — AACR 2026Poster #5785

•  Tumoreradication in an in vivo model: ST-01156achieved complete tumor regression in a neuroblastoma xenograft model — meaningtumors disappeared entirely — using the same dosing schedule now deployed inthe Phase 1 trial. This direct correspondence between preclinical and clinicaldosing strengthens confidence in the translational path forward.

•  Consistentpotency across a biologically diverse disease: ST-01156 demonstrated potent anticancer activity acrossten neuroblastoma models — six established cell lines and four patient-derivedmodels — with IC50 values (the concentration required to kill half of cancercells) in the low-to-sub-micromolar range. Neuroblastoma is geneticallyheterogeneous; this breadth of coverage matters.

•  Aclear mechanism of action: Treatment withST-01156 induced DNA damage, switched on the tumor-suppressing p53/p21 pathway,and reduced the levels of known cancer-driving proteins cMYC and EZH2 —confirming a coherent, multi-pronged path to programmed cancer cell death(apoptosis).

•  Biomarker roadmap for precision enrollment: SEED’s translational research identified MYCoverexpression as a marker of sensitivity to ST-01156, and CDKN2A/B deletion asa marker of resistance. These biomarkers — identifiable through standard tumorprofiling — may provide a practical framework for selecting patients mostlikely to benefit as the Phase 1 trial progresses toward expansion cohorts.

“ST-01156’s advancement into clinical testing in 2026marks a pivotal milestone for SEED and for patients with RBM39 dependentcancers, including neuroblastoma — a pediatric cancer with very limitedeffective treatment options. The identification of MYC and CDKN2A/B status as potential biomarkers is the product of SEED’sfocus on identifying the patients who will significantly benefit fromST-01156.”

— James Tonra,PhD, President & Chief Scientific Officer, SEED Therapeutics

“The RBM39 datawe are presenting at AACR 2026 reflect what SEED’s RITE3™ platform was designedto do — not just degrade a difficult target, but understand which patients aremost likely to benefit. Seeing ST-01156 achieve complete tumor regression in a neuroblastomamodel, at the same dosing schedule now in the clinic, is deeply gratifying andscientifically meaningful. Our focus at SEED is on ensuring that the molecularinsight behind this program translates into real outcomes for patients withvery few options.”

— Lan Huang, PhD,Co-Founder, SEED Therapeutics

Clinical Development Status

ST-01156is being evaluated in an ongoing Phase 1 dose escalation study (NCT07197554)designed to establish safety, pharmacokinetics, and target engagement. Thestudy enrolls patients enriched for cancer types with demonstrated RBM39dependency in preclinical research. The trial is currently active at sixleading U.S. oncology centers, with additional clinical sites in preparation.Phase 1 dose escalation is projected to be completed by Q1 2027. The dosingschedule employed is consistent with that used in IND-enabling studies and inthe in vivo efficacy program reported at AACR 2026 — providing a robusttranslational foundation.

AACR 2026 Poster PresentationDetails

Title: RBM39 Degrader Anticancer Activity Against Neuroblastoma;MYC and CDKN2A/B as Potential Response Biomarkers

Poster Number: 5785

Session: Proximity-Induced Drug Discovery 2 (Experimental andMolecular Therapeutics)

Authors: James Finn, Imad Salhab, Haihong Jin, Fei Liu, Dong Liu,Yunkai Zhang, Xing Liu, James Tonra, Lan Huang, Dan Lu

About SEED Therapeutics

SEED Therapeutics is aclinical-stage biotechnology company pioneering rationally designed molecularglue degraders to treat diseases driven by proteins previously consideredundruggable. Its proprietary RITE3™ platform enables impactful targeted proteindegradation with a defined therapeutic window, supporting a pipeline of sixmolecular glue programs across oncology, neurodegeneration, and immunology.

SEEDwas co-founded by four preeminent scientists:

•  Nobel Laureate Prof. Avram Hershko,discoverer of the ubiquitin-proteasome system — the cellular machinery thatSEED’s molecular glue degraders harness to eliminate disease-causing proteins.

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

•  Prof. Ning Zheng (University of Washington,HHMI Investigator), 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. MichelePagano (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.

Eli Lilly and Company and EisaiCo., Ltd. serve as cornerstone investors and cornerstone researchcollaborators, providing both capital validation and deep scientificpartnership in support of SEED’s mission to unlock undruggable disease targets.Additional information is available at www.seedtherapeutics.com.

Forward-Looking Statements

This press release containsforward-looking statements, including statements regarding ongoing clinicaltrials, the potential of ST-01156, the utility of identified biomarkers, andSEED’s business strategy. These statements involve known and unknown risks anduncertainties that may cause actual results to differ materially. SEEDundertakes no obligation to update forward-looking statements.

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