HUTCHMED Initiates Global Trial of HMPL-A830

HUTCHMED Initiates Global Trial of KRAS-EGFR-Antibody Conjugate Therapy HMPL-A830 in Patients with Solid Tumors

— First-in-class KRAS-payload leveraging synchronized EGFR inhibition —

Hong Kong, Shanghai & Florham Park, NJ — Monday, September 28, 2026: HUTCHMED (China) Limited (“HUTCHMED” or the “Company”) (Nasdaq/AIM:HCM; HKEX:13) today announces that it has initiated the Phase Ia part of a global clinical trial of HMPL-A830 in patients with unresectable, advanced or metastatic solid tumors. The first patient received the first dose in China on September 24, 2026.

An Antibody-Targeted Therapy Conjugate (“ATTC”) enables tumor-specific activity of potent, cell-killing, targeted therapy payloads by leveraging antibody-guided delivery. This first-in-class ATTC drug candidate comprises a highly selective and potent Kirsten rat sarcoma (“KRAS”) small molecule inhibitor payload conjugated to an anti‑epidermal growth factor receptor (“EGFR”) antibody. Colorectal, pancreatic and lung cancers have the highest incidence of patients with KRAS-altered tumors, who often lack a safe and durable KRAS therapy. HMPL‑A830 is designed to address this need by delivering a KRAS inhibitor directly to EGFR‑expressing tumors, while simultaneously blocking EGFR and KRAS signaling to enhance efficacy, durability, and tolerability.

This first-in-human, multicenter, open-label Phase I clinical study evaluates the safety, tolerability, pharmacokinetics, immunogenicity and preliminary efficacy of HMPL-A830. The current study consists of a Phase Ia dose escalation part to determine the maximum tolerated dose and recommended dose for expansion. The subsequent dose expansion/​optimization part is to further characterize its safety, tolerability and preliminary anti-tumor activity in selected solid tumors. Additional details may be found at clinicaltrials.gov, using identifier NCT07718581.

On September 3, 2026, HUTCHMED Limited (a subsidiary of the Company) entered into an exclusive development and license agreement with a subsidiary of GSK plc (“GSK”), granting the GSK subsidiary worldwide rights excluding Mainland China, Hong Kong, Macau and Taiwan to develop and commercialize HMPL-A830. HUTCHMED Limited is responsible for the global Phase I development program of HMPL‑A830. The GSK subsidiary will be responsible for all subsequent clinical development and commercialization activities outside of Mainland China, Hong Kong, Macau and Taiwan. The agreement is subject to customary closing conditions, including completion of any antitrust regulatory reviews.

About KRAS

Rat sarcoma (“RAS”) mutations represent one of the most prevalent and well-established drivers in human oncology, driving the progression and aggressive pathology of multiple solid tumors. KRAS, the most dominant RAS isoform, is mutated in approximately 44% of colorectal cancer (“CRC”), 34% of lung adenocarcinoma and up to 89% of pancreatic ductal adenocarcinoma (“PDAC”) patients.[1] KRAS regulates key downstream pathways, including RAS/MAPK and PI3K/AKT/mTOR, to drive cell differentiation, proliferation, and survival.

While recent targeted therapies have validated KRAS as a viable therapeutic target, significant clinical gaps persist, particularly for patients with non-G12C mutations. Most patients eventually experience disease progression driven by acquired resistance, largely fueled by upstream receptor tyrosine kinase upregulation and secondary KRAS alterations. Beyond mutation coverage, systemic delivery of pan-KRAS and pan-RAS inhibitors is associated with on-target toxicities, such as dermatological toxicity reflecting RAS pathway inhibition in normal tissue. These present challenges for dosing, long-term tolerability, and combination with cytotoxic chemotherapy or immunotherapy backbones that constitute frontline standard-of-care.

About EGFR

EGFR is a widely expressed receptor tyrosine kinase and established driver of tumor cell proliferation, survival, and disease progression across multiple solid tumors, including CRC, PDAC, and non-small cell lung cancer (“NSCLC”). Signaling through EGFR activates the downstream RAS/MAPK and PI3K/AKT/mTOR pathways, positioning the receptor immediately upstream of KRAS. EGFR has also emerged as a key mediator of resistance to KRAS-targeted therapies, particularly in CRC, where adaptive feedback and increased upstream EGFR signaling reactivate the MAPK pathway and limit the depth and durability of KRAS inhibition. Together, these provide a strong rationale for the dual targeting of EGFR and KRAS, not only in CRC but also additional indications such as PDAC and NSCLC.

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