On April 22, 2026 Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company developing targeted protein degradation therapies, reported new preclinical data from multiple oncology programs at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026.

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The presentations highlight continued progress across Nurix’s oncology pipeline, including programs targeting pan-mutant BRAF, CBL-B and Aurora Kinase A (AURKA), as well as a featured AACR (Free AACR Whitepaper) Advances session presentation highlighting the broader scientific progress and clinical translation of targeted protein degradation. Collectively, these data provide additional mechanistic validation of Nurix’s approach to CBL-B, Aurora kinase A (AURKA) and mutant BRAF to address key limitations of traditional approaches, including resistance, incomplete pathway suppression, and inability to target non-enzymatic protein functions.

"These data, together with our participation in the AACR (Free AACR Whitepaper) Advances session, highlight the growing clinical and scientific validation of targeted protein degradation as a new therapeutic modality," said Arthur T. Sands, M.D., Ph.D., president and chief executive officer. "Across multiple programs, we are seeing consistent evidence that these therapies can drive deeper and more durable biological responses, supporting their potential to deliver meaningful benefit for patients."

AACR Advances Session
Later today, April 22, 2026, Gwenn Hansen, Ph.D., chief scientific officer of Nurix, will present "Designing Effective Degrader Therapeutics: What Early Clinical Experience Has Taught Us" as part of the AACR (Free AACR Whitepaper) Advances session "Induced Proximity Pharmacology: Degraders and Beyond." Dr. Hansen’s remarks will provide a broad perspective on recent advances in targeted protein degradation, including insights from early clinical experience and the evolving potential of induced proximity approaches to expand the druggable target space and improve therapeutic outcomes.

Pan-Mutant BRAF Degrader Program
In a poster presentation titled "NRX-0305, an orally bioavailable, CNS penetrant pan-mutant BRAF degrader demonstrates robust efficacy in intracranial models of melanoma brain metastasis and primary glioma," Nurix reported that NRX-0305 achieves dose-proportional pharmacokinetics across plasma, tumor, and brain, enabling robust degradation of mutant BRAF and downstream pathway inhibition. These properties translate into potent antitumor activity in intracranial glioma and melanoma models while selectively sparing wildtype BRAF and avoiding paradoxical MAPK pathway activation. In a clinically relevant BRAF inhibitor–resistant melanoma brain metastasis patient-derived xenograft (PDX) model, NRX-0305 significantly extended survival versus both vehicle and dabrafenib, delivering a 142% increase in lifespan, compared with approximately 12% for the approved BRAF inhibitor.

Additional data were presented in a poster titled "NRX-0305 is an orally bioavailable, pan-mutant BRAF degrader that exhibits single-agent and combination efficacy with MEKi or anti-EGFR across Class 1/2/3 BRAF-mutant cancers." In preclinical tumor models, NRX-0305 demonstrates broad activity across mutant BRAF classes, including activity across 14 PDX models spanning Class 1 treatment-resistant, Class 2, and Class 3 BRAF mutations. Combination of NRX-0305 with MEK inhibitors or anti-EGFR therapy enhanced tumor regressions in Class 2 and drove complete responses in Class 1 and 3 models. Notably, the complete regressions are achieved at lower MEK inhibitor dose levels, supporting the potential for an improved therapeutic window relative to current treatment approaches.

CBL-B Program
In an oral presentation titled "Discovery and characterization of CBL-B intramolecular glue inhibitors that increase T cell activation and suppress tumor growth," Nurix reported the discovery and characterization of novel intramolecular glue inhibitors targeting CBL-B, an E3 ubiquitin ligase that negatively regulates T, B, and NK cell activation. Using mechanism-agnostic screening assays guided by CBL-B biology, Nurix identified a novel series of intramolecular glue inhibitors that stabilize the closed, inactive conformation of CBL-B, representing a first-in-class mechanism of action. Through structure-guided optimization, this series was advanced to NX-1607, a potent and selective CBL-B inhibitor with sub-nanomolar binding affinity. In preclinical studies, NX-1607 enhanced T cell activation, as evidenced by increased IL-2 and IFN-γ secretion in response to TCR stimulation, and demonstrated single-agent anti-tumor activity across multiple syngeneic tumor models, including colorectal, triple-negative breast cancer, and B cell lymphoma. NX-1607 also synergized with anti-PD-1 therapy to significantly enhance survival across multiple models. Early clinical data demonstrated dose-dependent pharmacokinetics and modulation of the proximal pharmacodynamic biomarker pHS1 in CD8 T cells, providing initial evidence of target engagement in patients.

Aurora Kinase A (AURKA) Degrader Program
In a poster presentation titled "NRX-4972, a selective, oral, Aurora kinase A degrader, demonstrates increased efficacy in an SCLC tumor model, and greater in vitro synergy than an AURKA inhibitor," Nurix reported new data demonstrating that targeted degradation of AURKA enables more complete biological modulation compared to inhibition alone. NRX-4972 exhibits central nervous system penetration and a favorable pharmacokinetic and pharmacodynamic profile, translating into superior antitumor activity in aggressive small cell lung cancer models, particularly with an optimized twice-daily dosing regimen. In the H82 SCLC model, twice-daily administration of NRX-4972 resulted in 60% of mice surviving to the end of the study, whereas none of the mice treated with AURKA inhibitors alisertib or LY3295668 survived. Mechanistically, degradation of AURKA results in downregulation of MYC and enhanced induction of DNA damage, apoptosis, and G2/M arrest. NRX-4972 also demonstrated broader and more potent synergy than an AURKA inhibitor in an in vitro screen of combination agents across triple-negative breast cancer, SCLC, and NSCLC cell lines, further supporting its therapeutic potential.

About NRX-0305
NRX-0305 is a potent, selective, and orally bioavailable central nervous system (CNS)-penetrant pan-mutant BRAF degrader that Nurix is exploring for use in oncology. Nurix has reported preclinical data demonstrating potent anti-tumor activity in multiple cell line-derived and patient-derived xenograft disease models representing Class 1, Class 2, and Class 3 B-RAF mutations. Anti-tumor activity was also observed in the setting of CNS disease and treatment-resistance, suggesting the potential for utility across a broad range of solid tumor types.

About NX-1607
NX-1607 is an investigational first-in-class oral inhibitor of the E3 ligase Casitas B-lineage lymphoma proto-oncogene B (CBL-B) being developed for immuno-oncology indications, including a range of solid tumor types. CBL-B is a cytoplasmic E3 ubiquitin ligase that negatively regulates T cell activation, making it an attractive target for immuno-oncology and offering a novel therapeutic approach to treat solid tumors. Inhibition of CBL-B in preclinical studies reverses T cell exhaustion, alleviates tumor induced immunosuppression, and may also exert direct antitumor effects. Nurix is evaluating NX-1607 in an ongoing Phase 1 trial in adults in a range of oncology indications. This study includes a thorough investigation of both dose and schedule in the Phase 1a portion. Additional information on the NX-1607 clinical trial can be accessed at www.clinicaltrials.gov (NCT05107674).

About NRX-4972
NRX-4972 is a CNS-penetrant, orally bioavailable and highly selective degrader of Aurora A kinase (AURKA). AURKA is an oncogene frequently overexpressed in adult solid tumors, hematologic malignancies, and pediatric cancers. Several AURKA inhibitors are effective in preclinical tumor models, but this activity has failed to translate into clinical efficacy. To address the limitations of inhibitors, Nurix has designed bifunctional targeted protein degraders of AURKA that enable removal of both enzymatic and scaffolding functions.

(Press release, Nurix Therapeutics, APR 22, 2026, View Source [SID1234664694])

On April 22, 2026 SEED Therapeutics, Inc. ("SEED"), a clinical-stage biotechnology company pioneering rationally designed molecular glue degraders, reported new data demonstrating potent anticancer activity of its RBM39 degrader program in neuroblastoma, a pediatric cancer with high unmet medical need. SEED’s scientific work also identified potential biomarkers predictive of anticancer response that will be further examined in the clinic, with Phase 1 dose escalation projected to be completed by Q1 2027. The findings are being presented at the 2026 Annual Meeting of the American Association for Cancer Research (AACR) (Free AACR Whitepaper), which convenes more than 22,000 scientists, clinicians, and investors this week in San Diego.

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ST-01156, SEED’s clinical-stage RBM39 molecular glue degrader, is currently being evaluated in a Phase 1 dose escalation study (NCT07197554) at six leading U.S. oncology centers.

Highlights At A Glance

Tumor eradication in a rigorous in vivo model: ST-01156 achieved complete tumor regression in neuroblastoma model using a differentiated dosing regimen — a demanding efficacy benchmark in solid tumor oncology.
Active Phase 1 clinical trial: Dose escalation is underway (NCT07197554) at six leading U.S. oncology centers, with clinical sites in additional geographies in preparation.
Biomarker strategy: MYC overexpression (sensitivity) and CDKN2A/B deletion (resistance) were identified as part of SEED’s biomarker program, potentially enabling precision patient enrollment as the trial advances.
Rare Pediatric and Orphan disease opportunity: Neuroblastoma is a high-unmet-need rare pediatric cancer representing a Rare Pediatric Disease and Orphan Disease designation-eligible indication, with potential for expedited regulatory pathways including Priority Review Voucher eligibility.

Scientific Rationale: Why RBM39 Matters

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

Molecular glue degraders achieve this by redirecting the cell’s own quality-control machinery — the ubiquitin-proteasome system — to tag and destroy the target protein. SEED’s proprietary RITE3 platform was designed from inception to identify, validate, and optimize molecular glues with a defined therapeutic window, bringing rational drug design to protein targets previously considered undruggable.

Key Data Highlights — AACR (Free AACR Whitepaper) 2026 Poster #5785

Tumor eradication in an in vivo model: ST-01156 achieved complete tumor regression in a neuroblastoma xenograft model — meaning tumors disappeared entirely — using the same dosing schedule now deployed in the Phase 1 trial. This direct correspondence between preclinical and clinical dosing strengthens confidence in the translational path forward.
Consistent potency across a biologically diverse disease: ST-01156 demonstrated potent anticancer activity across ten neuroblastoma models — six established cell lines and four patient-derived models — with IC50 values (the concentration required to kill half of cancer cells) in the low-to-sub-micromolar range. Neuroblastoma is genetically heterogeneous; this breadth of coverage matters.
A clear mechanism of action: Treatment with ST-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 MYC overexpression as a marker of sensitivity to ST-01156, and CDKN2A/B deletion as a marker of resistance. These biomarkers — identifiable through standard tumor profiling — may provide a practical framework for selecting patients most likely to benefit as the Phase 1 trial progresses toward expansion cohorts.

"ST-01156’s advancement into clinical testing in 2026 marks a pivotal milestone for SEED and for patients with RBM39 dependent cancers, including neuroblastoma — a pediatric cancer with very limited effective treatment options. The identification of MYC and CDKN2A/B status as potential biomarkers is the product of SEED’s focus on identifying the patients who will significantly benefit from ST-01156."

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

"The RBM39 data we are presenting at AACR (Free AACR Whitepaper) 2026 reflect what SEED’s RITE3 platform was designed to do — not just degrade a difficult target, but understand which patients are most likely to benefit. Seeing ST-01156 achieve complete tumor regression in a neuroblastoma model, at the same dosing schedule now in the clinic, is deeply gratifying and scientifically meaningful. Our focus at SEED is on ensuring that the molecular insight behind this program translates into real outcomes for patients with very few options."

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

Clinical Development Status

ST-01156 is being evaluated in an ongoing Phase 1 dose escalation study (NCT07197554) designed to establish safety, pharmacokinetics, and target engagement. The study enrolls patients enriched for cancer types with demonstrated RBM39 dependency in preclinical research. The trial is currently active at six leading U.S. oncology centers, with additional clinical sites in preparation. Phase 1 dose escalation is projected to be completed by Q1 2027. The dosing schedule employed is consistent with that used in IND-enabling studies and in the in vivo efficacy program reported at AACR (Free AACR Whitepaper) 2026 — providing a robust translational foundation.

AACR 2026 Poster Presentation Details

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

(Press release, Seed Therapeutics, APR 22, 2026, View Source [SID1234664710])

On April 21, 2026 AulosTM Bioscience, an immuno-oncology company working to revolutionize cancer care through development of its lead immune-activating antibody therapeutic imneskibart (AU-007), reported that new Phase 1/2 data from its ongoing study of imneskibart will be presented at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) 2026 Annual Meeting. The presentation will focus on promising results for imneskibart with and without nivolumab in checkpoint inhibitor (CPI)-refractory cutaneous melanoma. The ASCO (Free ASCO Whitepaper) Annual Meeting is being held online and in Chicago, Illinois, from May 29–June 2, 2026.

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Details of the poster presentation are as follows:

Poster Title: Imneskibart + low-dose subcutaneous IL-2 ± nivolumab in patients with CPI-refractory cutaneous melanoma: Promising results from an ongoing phase 1/2 study
Abstract: 9526
Session Type/Title: Poster Session – Melanoma/Skin Cancers
Session Date and Time: Sunday, May 31, 2026, 9:00 a.m.-12:00 p.m. CDT

The poster will be presented in the Exhibit Hall at McCormick Place. An electronic version will also be available on the ASCO (Free ASCO Whitepaper) 2026 online meeting platform.

About Imneskibart
Imneskibart (AU-007) is a human IgG1 monoclonal antibody designed by leveraging artificial intelligence that is highly selective to the CD25-binding portion of IL-2. With a mechanism of action unlike any other IL-2 therapeutic in development, imneskibart redirects IL-2 to reinforce anti-tumor immune effects. This is achieved by preventing IL-2, either exogenous or secreted by effector T cells, from binding to trimeric receptors on regulatory T cells while still allowing IL-2 to bind and expand effector T cells and NK cells. This prevents the negative feedback loop caused by other IL-2-based treatments and biases the immune system toward activation over suppression. Imneskibart also prevents IL-2 from binding to CD25-containing receptors on eosinophils, as well as vasculature and pulmonary endothelium, which may significantly reduce the vascular leak syndrome and pulmonary edema associated with high-dose IL-2 therapy.

To learn more about the imneskibart Phase 1/2 clinical trial program, including study locations in the United States and Australia, please visit ClinicalTrials.gov (identifier: NCT05267626), www.solidtumorstudy.com (U.S.) and www.solidtumourstudy.com (Australia).

(Press release, Aulos Bioscience, APR 21, 2026, View Source [SID1234664598])

On April 21, 2026 Karyopharm Therapeutics Inc. (Nasdaq: KPTI), a commercial-stage pharmaceutical company pioneering novel cancer therapies, reported that its late-breaking abstract was accepted for an oral presentation at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting, taking place May 29 to June 2 in Chicago. The oral presentation will feature results from the Phase 3 SENTRY trial, a randomized, double-blind, placebo-controlled trial of 60 mg selinexor in combination with ruxolitinib in myelofibrosis.

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Presentation Details:

Title: Selinexor plus ruxolitinib in JAK inhibitor–naïve myelofibrosis: Phase 3 SENTRY trial

Abstract Number: LBA6500

Session Title: Oral Abstract Session – Hematologic Malignancies—Leukemia, Myelodysplastic Syndromes, and Allotransplant

Presentation Time: June 2, 2026, 9:45 a.m. to 12:45 p.m. Central Time

Presenter: Dr. John Mascarenhas, Professor of Medicine at the Icahn School of Medicine at Mount Sinai and Director of the Center of Excellence for Blood Cancers and Myeloid Disorders
Late-breaking abstracts for presentations being held on June 2, 2026 will be released by ASCO (Free ASCO Whitepaper) on Tuesday, June 2, 2026 at 8:00 a.m. Eastern Time / 7:00 a.m. Central Time. A copy of the SENTRY presentation being delivered at ASCO (Free ASCO Whitepaper) on June 2, 2026 will be available following the event under "Publications and Presentations" in the Investor section of the Company’s website.

About the Phase 3 SENTRY Trial

SENTRY (XPORT-MF-034; NCT04562389) is a Phase 3 clinical trial evaluating a once-weekly dose of 60 mg of selinexor in combination with ruxolitinib compared to placebo plus ruxolitinib in JAKi-naïve myelofibrosis patients with platelet counts >100 x 109/L. Patients were randomized 2-to-1 to the selinexor arm. The co-primary endpoints for this trial are spleen volume reduction ≥ 35% (SVR35) at week 24 and the average change in absolute total symptom score (Abs-TSS) over 24 weeks relative to baseline.

About Myelofibrosis

Myelofibrosis is a rare blood cancer that affects approximately 20,000 patients in the United States and 17,000 patients in the European Union1. The disease causes bone marrow fibrosis (scarring in the bone marrow), which makes it difficult for the bone marrow to make healthy blood cells, splenomegaly (enlarged spleen), progressive anemia which often leads to symptoms like fatigue and weakness, and other disease associated symptoms including abdominal discomfort, pain under the left ribs, early satiety, night sweats and bone pain. The only approved class of therapies to treat myelofibrosis are JAK inhibitors, including ruxolitinib.

1. Clarivate/DRG (2023)

About XPOVIO (selinexor)

XPOVIO is a first-in-class, oral exportin 1 (XPO1) inhibitor compound for the treatment of cancer. XPOVIO functions by selectively binding to and inhibiting the nuclear export protein XPO1. XPOVIO is approved in the U.S. and marketed by Karyopharm in multiple oncology indications, including: (i) in combination with VELCADE (bortezomib) and dexamethasone (XVd) in adult patients with multiple myeloma after at least one prior therapy; (ii) in combination with dexamethasone in adult patients with heavily pre-treated multiple myeloma; and (iii) under accelerated approval in adult patients with diffuse large B-cell lymphoma (DLBCL), including DLBCL arising from follicular lymphoma, after at least two lines of systemic therapy. XPOVIO (also known as NEXPOVIO in certain countries) has received regulatory approvals in various indications in a growing number of ex-U.S. territories and countries, including but not limited to the European Union, the United Kingdom, Mainland China, Taiwan, Hong Kong, Australia, South Korea, Singapore, Israel, and Canada. XPOVIO/NEXPOVIO is marketed in these respective ex-U.S. territories by Karyopharm’s partners: Antengene, Menarini, Neopharm, and FORUS. Selinexor is also being investigated in several other mid- and late-stage clinical trials across multiple high unmet need cancer indications, including in myelofibrosis and endometrial cancer.

For more information about Karyopharm’s products or clinical trials, please contact the Medical Information department at: Tel: +1 (888) 209-9326; Email: [email protected]

XPOVIO (selinexor) is a prescription medicine approved:

In combination with bortezomib and dexamethasone for the treatment of adult patients with multiple myeloma who have received at least one prior therapy (XVd).

In combination with dexamethasone for the treatment of adult patients with relapsed or refractory multiple myeloma who have received at least four prior therapies and whose disease is refractory to at least two proteasome inhibitors, at least two immunomodulatory agents, and an anti‐CD38 monoclonal antibody (Xd).

For the treatment of adult patients with relapsed or refractory diffuse large B‐cell lymphoma (DLBCL), not otherwise specified, including DLBCL arising from follicular lymphoma, after at least two lines of systemic therapy. This indication is approved under accelerated approval based on response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trial(s).
SELECT IMPORTANT SAFETY INFORMATION

Warnings and Precautions

Thrombocytopenia: Monitor platelet counts throughout treatment. Manage with dose interruption and/or reduction and supportive care.

Neutropenia: Monitor neutrophil counts throughout treatment. Manage with dose interruption and/or reduction and granulocyte colony‐stimulating factors.

Gastrointestinal Toxicity: Nausea, vomiting, diarrhea, anorexia, and weight loss may occur. Provide antiemetic prophylaxis. Manage with dose interruption and/or reduction, antiemetics, and supportive care.

Hyponatremia: Monitor serum sodium levels throughout treatment. Correct for concurrent hyperglycemia and high serum paraprotein levels. Manage with dose interruption, reduction, or discontinuation, and supportive care.

Serious Infection: Monitor for infection and treat promptly.

Neurological Toxicity: Advise patients to refrain from driving and engaging in hazardous occupations or activities until neurological toxicity resolves. Optimize hydration status and concomitant medications to avoid dizziness or mental status changes.

Embryo‐Fetal Toxicity: Can cause fetal harm. Advise females of reproductive potential and males with a female partner of reproductive potential, of the potential risk to a fetus and use of effective contraception.

Cataract: Cataracts may develop or progress. Treatment of cataracts usually requires surgical removal of the cataract.
Adverse Reactions

The most common adverse reactions (≥20%) in patients with multiple myeloma who receive XVd are fatigue, nausea, decreased appetite, diarrhea, peripheral neuropathy, upper respiratory tract infection, decreased weight, cataract and vomiting. Grade 3‐4 laboratory abnormalities (≥10%) are thrombocytopenia, lymphopenia, hypophosphatemia, anemia, hyponatremia and neutropenia. In the BOSTON trial, fatal adverse reactions occurred in 6% of patients within 30 days of last treatment. Serious adverse reactions occurred in 52% of patients. Treatment discontinuation rate due to adverse reactions was 19%.

The most common adverse reactions (≥20%) in patients with multiple myeloma who receive Xd are thrombocytopenia, fatigue, nausea, anemia, decreased appetite, decreased weight, diarrhea, vomiting, hyponatremia, neutropenia, leukopenia, constipation, dyspnea and upper respiratory tract infection. In the STORM trial, fatal adverse reactions occurred in 9% of patients. Serious adverse reactions occurred in 58% of patients. Treatment discontinuation rate due to adverse reactions was 27%.

The most common adverse reactions (incidence ≥20%) in patients with DLBCL, excluding laboratory abnormalities, are fatigue, nausea, diarrhea, appetite decrease, weight decrease, constipation, vomiting, and pyrexia. Grade 3‐4 laboratory abnormalities (≥15%) are thrombocytopenia, lymphopenia, neutropenia, anemia, and hyponatremia. In the SADAL trial, fatal adverse reactions occurred in 3.7% of patients within 30 days, and 5% of patients within 60 days of last treatment; the most frequent fatal adverse reactions was infection (4.5% of patients). Serious adverse reactions occurred in 46% of patients; the most frequent serious adverse reaction was infection (21% of patients). Discontinuation due to adverse reactions occurred in 17% of patients.
Use In Specific Populations

Lactation: Advise not to breastfeed.

For additional product information, including full prescribing information, please visit www.XPOVIO.com.

To report SUSPECTED ADVERSE REACTIONS, contact Karyopharm Therapeutics Inc. at 1‐888‐209‐9326 or FDA at 1‐800‐FDA‐1088 or www.fda.gov/medwatch.

(Press release, Karyopharm, APR 21, 2026, View Source [SID1234664614])

On April 21, 2026 Sichuan Kelun-Biotech Biopharmaceutical Co., Ltd. (6990.HK) reported it will present results from three clinical studies, including data from its TROP2 ADC sacituzumab tirumotecan (sac-TMT, 佳泰莱), next-generation selective RET inhibitor lunbotinib fumarate (A400/EP0031, 宁泰莱[1]) and novel ADC SKB500. The abstracts for these studies will be published on the ASCO (Free ASCO Whitepaper) official website on May 21, 2026, local time.

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Detailed information on the studies selected for 2026 ASCO (Free ASCO Whitepaper) is as follows:

Title: Sacituzumab tirumotecan (sac-TMT) plus pembrolizumab (P) versus pembrolizumab (P) as first-line treatment for PD-L1-positive advanced non-small cell lung cancer (NSCLC): Results from the randomized, controlled phase III OptiTROP-Lung05 study
Presentation Type: Oral
Abstract Number: 8506
Session Date and Time: May 29, 3:12 PM-3:24 PM CDT | Lung Cancer-Non-Small Cell Metastatic

Title: Efficacy and safety of lunbotinib (A400/EP0031), a next-generation selective RET inhibitor (SRI), from a pivotal phase Ⅱ study in patients with advanced RET fusion-positive non-small cell lung cancer (NSCLC)
Presentation Type: Oral
Abstract Number: 8505
Session Date and Time: May 29, 2:36 PM-2:48 PM CDT | Lung Cancer-Non-Small Cell Metastatic

Title: An open-label, first-in-human study of SKB500 in patients with locally advanced or metastatic solid tumors
Presentation Type: Rapid oral
Abstract Number: 3011
Session Date and Time: June 2, 9:57 AM-10:03 AM CDT | Molecularly Targeted Agents and Tumor Biology

About sac-TMT

Sac-TMT, a core product of the Company, is a novel human TROP2 ADC in which the Company has proprietary intellectual property rights, targeting advanced solid tumors such as NSCLC, breast cancer (BC), gastric cancer (GC), gynecological tumors and genitourinary tumors, among others. Sac-TMT is developed with a unique, bifunctional linker that maximizes payload delivery to tumor cells both through its irreversible connection with the anti-TROP2 monoclonal antibody sacituzumab and its pH-sensitive cleavage from a belotecan-derivative topoisomerase I inhibitor payload in the lysosome, with a drug-to-antibody-ratio (DAR) of 7.4. Sac-TMT specifically recognizes TROP2 on the surface of tumor cells by recombinant anti-TROP2 humanized monoclonal antibodies, which is then endocytosed by tumor cells and releases the payload KL610023 intracellularly. KL610023, as a topoisomerase I inhibitor, induces DNA damage to tumor cells, which in turn leads to cell-cycle arrest and apoptosis. In addition, it also releases KL610023 in the tumor microenvironment. Given that KL610023 is membrane permeable, it can enable a bystander effect, or in other words kill adjacent tumor cells.

In May 2022, the Company licensed the exclusive rights to MSD (the tradename of Merck & Co., Inc, Rahway, NJ, USA) to develop, use, manufacture and commercialize sac-TMT in all territories outside of Greater China (which includes Mainland China, Hong Kong, Macao and Taiwan).

To date, four indications for sac-TMT have been approved and marketed in China for: 1) unresectable locally advanced or metastatic TNBC who have received at least two prior systemic therapies (at least one of them for advanced or metastatic setting);2) EGFR mutant-positive locally advanced or metastatic non-squamous NSCLC following progression on EGFR-TKI therapy and platinum-based chemotherapy; 3) EGFR mutant-positive locally advanced or metastatic non-squamous NSCLC who progressed after treatment with EGFR-TKI therapy; 4) unresectable or metastatic HR+/HER2- (IHC 0, IHC 1+ or IHC 2+/ISH-) BC who have received prior ET and at least one line of chemotherapy in advanced setting. The first two indications above have been included in China’s National Reimbursement Drug List (NRDL). This inclusion is expected to bring clinically meaningful benefits to a greater number of patients with BC and NSCLC. Additionally, sac-TMT has been granted six Breakthrough Therapy Designations (BTDs) by the NMPA.

Sac-TMT is the world’s first TROP2 ADC drug approved for marketing in lung cancer. As of today, Kelun-Biotech has initiated 9 registrational clinical studies in China. MSD is evaluating 17 ongoing global Phase III clinical studies of sac-TMT as a monotherapy or in combination with pembrolizumab or other anti-cancer agents for several types of cancer. These studies are sponsored and led by MSD.

About A400/EP0031

A400/EP0031 novel next-generation selective RET inhibitor for NSCLC, medullary thyroid cancer (MTC) and other solid tumors with a high prevalence of RET alterations. The NDA of A400/EP0031 has been accepted for review by the Center for Drug Evaluation (CDE) of the National Medical Products Administration (NMPA) of China for the treatment of adult patients with RET-fusion positive locally advanced or metastatic NSCLC. The Company is also conducting a Phase Ib/II clinical study in China for the treatment of RET-positive solid tumors.

In March 2021, the Company granted Ellipses Pharma Limited, a U.K.-based international oncology drug development company, an exclusive license to develop, manufacture and commercialize this agent outside Greater China and certain Asian countries. In April 2024, A400/EP0031 was cleared by the Food and Drug Administration (FDA) to progress into a Phase II clinical trial (NCT05443126) which is currently recruiting in the United States, United Kingdom, Europe and United Arab Emirates, where it is being evaluated as a monotherapy and in combination with chemotherapy in RET fusion positive NSCLC.

About SKB500

SKB500, a novel, proprietary ADC developed via the OptiDC platform, is designed to leverage specific target biology through a validated target combined with a differentiated payload-linker strategy. In preclinical investigations, SKB500 demonstrated a favorable therapeutic window with robust efficacy and manageable safety profiles across multiple advanced solid tumors.

Currently, a Phase II exploratory study of SKB500 in combination with immunotherapy with or without chemotherapy as first-line treatment for extensive-stage small cell lung cancer (ES-SCLC) is ongoing in China.

(Press release, Kelun, APR 21, 2026, View Source [SID1234664630])