HUTCHMED Licenses KRAS-EGFR-Antibody to GSK

• Exclusive License for HMPL-A830, a first-in-class KRAS-EGFR Antibody-Targeted Therapy Conjugate ("ATTC"), which is expected to enter clinical trials in H2 2026 -
• HUTCHMED webcasts today at 4:30 p.m. HKT in Chinese (Putonghua) and at 7:30 a.m. EDT / 12:30 p.m. BST / 7:30 p.m. HKT in English -

Hong Kong, Shanghai & Florham Park, NJ - Thursday, September 3, 2026: HUTCHMED (China) Limited ("HUTCHMED") (Nasdaq/AIM: HCM; HKEX: 13) today announces that its subsidiary, HUTCHMED Limited, has 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. Clinical development will initially focus on colorectal, pancreatic and lung cancer indications. The agreement includes a US$110 million upfront payment and potential development, regulatory and commercial milestone payments, for up to a total of US$1.295 billion, and royalties on net sales. This first-in-class drug candidate, an Antibody-Targeted Therapy Conjugate ("ATTC"), comprises a highly selective and potent Kirsten rat sarcoma ("KRAS") small molecule inhibitor payload conjugated to an anti-epidermal growth factor receptor ("EGFR") antibody. An ATTC enables tumor-selective activity of potent, cell-killing payloads by leveraging antibody-guided therapy.

Colorectal, lung, and pancreatic 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.

Under the terms of the agreement, HUTCHMED Limited will be responsible for the global phase I development program, which is expected to start in the second half of 2026 (clinicaltrials.gov identifier NCT07718581). The GSK subsidiary will be responsible for all subsequent clinical development and commercialization activities outside of Mainland China, Hong Kong, Macau and Taiwan.

"We are proud to work with GSK, a globally leading biopharmaceutical company that, like HUTCHMED, is committed to developing innovative new cancer medicines to address significant unmet medical needs worldwide," said Mr Johnny Cheng, Acting Chief Executive Officer and Chief Financial Officer of HUTCHMED. "Our ATTCs combine antibodies with our proprietary small-molecule inhibitor payloads to deliver dual mechanisms of action. HMPL-A830 is our third drug candidate from these novel payload platforms and the first from our platform to be licensed to a global partner, following two candidates that have entered clinical development. This collaboration marks a significant step in maximizing its potential as a treatment for patients, unlocking an entirely new class of precision oncology medicines."

Dr Hesham Abdullah, Senior Vice President, Global Head Oncology, R&D, GSK said, "This agreement reflects GSK's growing leadership across oncology and our commitment to advance the latest innovation for patients living with cancer. The dual KRAS-EGFR mechanism of HMPL-A830 has the potential to significantly improve upon current standard of care. We look forward to working with HUTCHMED to progress this innovative asset through development."

License Terms

Under the agreement, HUTCHMED Limited will receive an upfront payment of US$110 million and may receive additional development, regulatory and commercial milestone payments of up to a total of US$1.185 billion. The GSK subsidiary GlaxoSmithKline Intellectual Property (No. 4) Limited will also pay tiered royalties on its annual net sales. HUTCHMED Limited will retain full development and commercialization rights in Mainland China, Hong Kong, Macau and Taiwan. In addition, the GSK subsidiary has a right of first negotiation on one earlier stage ATTC drug candidate. The upfront payment is payable at closing, which is subject to customary closing conditions, including completion of any antitrust regulatory reviews.

HUTCHMED will host webcasts today on Thursday September 3, 2026 at 4:30 p.m. HKT in Chinese (Putonghua) and at 7:30 a.m. EDT / 12:30 p.m. BST / 7:30 p.m. HKT in English. After registration, investors may access the live webcast at www.hutch-med.com/event.

BofA Securities is acting as exclusive financial advisor to HUTCHMED.

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.

About GSK plc

GSK plc is a global biopharma company with a purpose to unite science, technology, and talent to get ahead of disease together. Find out more at www.gsk.com.

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