On October 21, 2026 HUTCHMED (China) Limited ("HUTCHMED" or the "Company") (Nasdaq/AIM:HCM; HKEX:13) reported that further to its announcement on September 3, 2026 and following the completion of customary closing conditions including antitrust regulatory reviews, the exclusive development and license agreement between HUTCHMED Limited (a subsidiary of the Company) and a subsidiary of GSK plc ("GSK") has closed. The agreement grants the GSK subsidiary worldwide rights excluding Mainland China, Hong Kong, Macau and Taiwan to develop and commercialize HMPL-A830.
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This first-in-class Antibody-Targeted Therapy Conjugate ("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 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. The Phase Ia part of a global clinical trial of HMPL-A830 in patients with unresectable, advanced or metastatic solid tumors in China and the US was initiated in September 2026 (clinicaltrials.gov identifier NCT07718581).
Under the terms of the agreement, HUTCHMED Limited is responsible for the global Phase I development program. The GSK subsidiary will be responsible for all subsequent clinical development and commercialization activities in its territory. Following the closing of the exclusive license agreement, HUTCHMED Limited expects to receive US$110 million upfront payment shortly, and may receive additional development, regulatory and commercial milestone payments of up to a total of US$1.185 billion, as well as tiered royalties on annual net sales.
About HUTCHMED ATTCs
HUTCHMED’s ATTCs represent a next-generation approach to precision oncology, combining monoclonal antibodies with proprietary small-molecule inhibitor payload platforms to deliver dual mechanisms of action. Unlike traditional cytotoxin-based antibody-drug conjugates, ATTCs combine targeted therapies to achieve synergistic anti-tumor activity and durable responses in preclinical models, outperforming standalone antibody or small-molecule inhibitor components in both efficacy and safety.
Built on over 20 years of targeted therapy expertise, the ATTC platforms enable development of drug candidates across diverse cancer types. By leveraging antibody-guided delivery and tumor-specific payload release, ATTCs improve accessibility to tumors and reduce off-tumor toxicity. This may overcome the on-target, off-tumor toxicity limitations of systemically-delivered small molecule inhibitors, which in turn could ensure safer long-term use and support combinations with chemotherapy and immunotherapy in earlier-line treatments.
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.
(Press release, HUTCHMED, OCT 21, 2026, View Source [SID1234673637])