SHANGHAI, Sep 14, 2026— Hansoh Pharmaceutical Group Co., Ltd. (“Hansoh Pharma,” 03692.HK) today announced that HS-10370 combination regimen has yielded encouraging results in patients with untreated advanced KRAS G12C-mutated NSCLC.The results were delivered as an oral presentation at the 2026 World Conference on Lung Cancer (WCLC 2026), held in Seoul, South Korea, from September 12 to 15.

HS-10370 is a selective, covalent and orally bioavailable KRAS G12C inhibitor under clinical development for the treatment of patients with advanced KRAS G12C-mutated NSCLC. Preliminary results of the HS-10370-102 study (NCT06594874), which evaluated HS-10370 combined with adebrelimab plus platinum‑based chemotherapy, were disclosed at WCLC 2026. HS-10370-102 is an open‑label, multicenter, phase Ib study for untreated advanced KRAS G12C-mutated NSCLC patients. Eligible patients received HS-10370 at 400 mg or 800 mg once daily orally , combined with adebrelimab plus platinum chemotherapy every 3 weeks intravenously. Treatment continued until disease progression or intolerable toxicity. Key study endpoints included safety, tolerability, ORR and PFS assessed by the investigator per RECIST v1.1 criteria.

The study results showed:

Robust Anti-tumor Activity: With median follow-up of 13.6 months, The confirmed ORR was 81.5% and the disease control rate (DCR) was 98.1%. Median PFS has not yet reached, and the 12‑month PFS rate was 78.7%. The combination regimen demonstrated consistent antitumor activity across different PD‑L1 expression subgroups. Notably, patients with PD‑L1 TPS ≥ 50% achieved a confirmed ORR of 93.8% and12‑month PFS rate of 100%.

Manageable safety profile: Grade ≥3 treatment-related adverse event (TRAEs) occurred in 80.0% of subjects and there were no treatment-related deaths. The permanent discontinuation rate of full study treatments due to TRAEs was only 5.5%, suggesting that most toxicities could be managed with supportive care and dose adjustments without long‑term treatment interruption. The most common TRAEs were hematologic toxicities and liver enzyme elevations, consistent with the known safety characteristics of each individual agent; no unexpected new safety risks were observed with this combination regimen.

These compelling efficacy and safety results support advancing this combination into a phase 3 trial to further investigate its value as first-line therapy for patients with KRAS G12C-mutated NSCLC.

Details of the oral presentation are as follows:

Title: Efficacy and Safety of HS-10370 Combined with Adebrelimab and Chemotherapy in First-Line Advanced KRAS G12C-Mutated NSCLC

Session:OA12. Beyond KRAS: Emerging Targets, Smarter Therapies

Abstract No.: 436

Date/Time: Monday, September 14, 2026, 5:00-6:15 PM KST (5:22 PM -5:32 PM)

Presenter: Fan Tong, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology

About HS-10370

HS-10370 is a highly selective small-molecule inhibitor of the KRAS G12C mutant. Through irreversible targeted covalent binding to the cysteine residue of the KRAS G12C mutant, it locks KRAS G12C in an inactive GDP-bound conformation, thereby blocking downstream signal transduction and inhibiting tumor cell proliferation.

About KRAS G12C-mutated NSCLC

Lung cancer is among the malignancies with the highest incidence and mortality worldwide; in the Chinese population, both its incidence and mortality rank first among all malignant tumors. ^[1]. Non‑small cell lung cancer (NSCLC) represents the major pathological subtype of lung cancer, accounting for 85%‑90% of all lung cancer cases ^[2]. According to histopathology, NSCLC is further divided into lung adenocarcinoma and lung squamous cell carcinoma; lung adenocarcinoma accounts for 55%‑60% of all NSCLC ^[3]. Due to the high invasiveness of NSCLC and the fact that early‑stage NSCLC is often asymptomatic, most patients are diagnosed at an advanced stage ^[2]. For these advanced‑stage patients, the disease has spread beyond local anatomical boundaries, accompanied by regional lymph node metastasis or distant organ metastasis, and is associated with a short natural disease course with rapid disease progression, which seriously endangers their lives.

KRAS gene mutation is one of the most critical oncogenic drivers in NSCLC and is particularly prevalent in lung adenocarcinoma. Among these mutations, the G12C point mutation accounts for approximately 3‑4% of all NSCLC cases and 8‑10% of lung adenocarcinomas. According to data released by the World Health Organization (WHO) in 2020, an estimated 35 000 patients in China were diagnosed with KRAS G12C‑mutated newly‑onset lung cancer in 2020. ^[4]

According to the 2026 NCCN Guidelines and CSCO Guidelines,first-line treatment options for NSCLC with KRAS G12C mutation are identical to those for NSCLC patients without actionable driver mutations, namely immune checkpoint inhibitor combined with platinum‑based doublet chemotherapy.There remains a lack of effective targeted therapeutic agents for first‑line therapy. Although this regimen has achieved remarkable progress, the majority of patients with metastatic NSCLC without actionable gene alterations experience disease progression within 1 year of diagnosis and die from the disease within 3 years ^[5]. Therefore, there remains an unmet medical need for novel therapies that can further improve treatment response and survival in patients with metastatic NSCLC.

References

[1]Bray F, Laversanne M, Sung H, Ferlay J, Siegel RL, Soerjomataram I, Jemal A., et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries [J]. CA Cancer J Clin, 2024, 74 (3): 229-263.

[2]中国抗癌协会肿瘤精准治疗专业委员会 中华医学会杂志社肺癌研究协作组. 驱动基因阳性晚期非小细胞肺癌免疫治疗专家共识（2023版）. 中华肿瘤杂志2023, 45(9): 717-740.

[3]Chen et al. Non-small cell lung cancer in China. Cancer Commun (Lond). 2022 Oct;42(10):937-970.

[4]Zheng RS, Chen R, Han BF, et al. Cancer incidence and mortality in China, 2022. Zhonghua Zhong Liu Za Zhi. 2024 Mar 23;46(3):221-231. 

[5]Pantsar T. The current understanding of KRAS protein structure and dynamics. Comput Struct Biotechnol J. 2020;18:189-98