RegulationPriority Review (United States), Breakthrough Therapy (United States), Fast Track (United States), Accelerated Approval (United States), Orphan Drug (United States), Priority Review (China), Breakthrough Therapy (China), Priority Review (Australia), Accelerated assessment (European Union), Special Review Project (China)

Structure/Sequence

Molecular FormulaC29H37N7O5S

InChIKeyFUKSNUHSJBTCFJ-UHFFFAOYSA-N

CAS Registry1421373-66-1

387

Clinical Trials associated with Osimertinib mesylate

NCT07680790

/ Not yet recruitingPhase 3

A Phase III, Randomized, Open-label Study of Izalontamab Brengitecan (BMS-986507) in Combination With Osimertinib Versus Osimertinib Monotherapy or Osimertinib in Combination With Platinum-based Chemotherapy as First-Line Therapy in Patients With EGFR-Mutant Locally Advanced or Metastatic Non-small Cell Lung Cancer

The purpose of this study is to evaluate izalontamab brengitecan (iza-bren) combined with osimertinib in participants with previously untreated, locally advanced or metastatic EGFR-mutant NSCLC, compared to osimertinib alone or osimertinib combined with platinum-based chemotherapy

Start Date30 Sep 2026

Sponsor / Collaborator

Bristol Myers Squibb Co.

NCT07738172

/ RecruitingPhase 3IIT

A Multicenter, Randomized Controlled Phase III Clinical Trial of Primary Tumor Resection in Patients With Oligometastatic EGFR-Mutant Non-Small Cell Lung Cancer After EGFR-Targeted Therapy

Osimertinib is a standard first-line treatment for patients with metastatic non-small cell lung cancer harboring an epidermal growth factor receptor exon 19 deletion or exon 21 L858R mutation. Although osimertinib can provide effective disease control, most patients eventually experience disease progression, and the primary lung tumor may remain an important site of treatment resistance.
This multicenter, randomized, open-label phase III trial will evaluate whether surgical removal of the primary lung tumor, in addition to continued osimertinib treatment, prolongs progression-free survival in patients with EGFR-mutated oligometastatic non-small cell lung cancer.
All participants will initially receive osimertinib 80 mg orally once daily for 12 weeks. Participants who have a partial response or stable disease according to RECIST version 1.1 and remain suitable for surgery will be randomly assigned in a 1:1 ratio to continue osimertinib alone or to undergo primary lung tumor resection followed by resumption of osimertinib. The study will also evaluate overall survival, safety, pathologic response, quality of life, patterns of disease progression, and changes in molecular biomarkers.

Start Date08 Sep 2026

Sponsor / Collaborator

National Taiwan University Hospital

NCT07710612

/ Not yet recruitingPhase 2

A Phase 2, Open-Label Study to Evaluate the Efficacy and Safety of ABSK043 Combined With Osimertinib in Participants With EGFR-Mutated Locally Advanced or Metastatic Non-Small Cell Lung Cancer

This is a phase 2, open-Label study to evaluate the efficacy and safety of ABSK043 Combined with Osimertinib in participants with EGFR-Mutated locally advanced or metastatic Non-Small Cell Lung Cancer

Start Date31 Aug 2026

Sponsor / Collaborator

Abbisko Therapeutics Co., Ltd.

[+1]

100 Clinical Results associated with Osimertinib mesylate

100 Translational Medicine associated with Osimertinib mesylate

100 Patents (Medical) associated with Osimertinib mesylate

4,407

Literatures (Medical) associated with Osimertinib mesylate

31 Dec 2026·JOURNAL OF MEDICAL ECONOMICS

Cost comparison of osimertinib plus platinum-pemetrexed versus amivantamab plus lazertinib for the first-line treatment of patients with locally advanced or metastatic epidermal growth factor receptor-mutated non-small cell lung cancer

Article

Author: Hearmon, Natalie ; Upton, Elysia ; Procter, Emily ; Nieva, Jorge J. ; Rattigan-Brown, Yanique ; Freeman, Harry ; Karia, Pritesh ; Lopes, Gilberto de Lima

OBJECTIVES:

Novel first-line (1L) combination regimens offer improved efficacy for patients with epidermal growth factor receptor-mutated (EGFRm) locally advanced or metastatic non-small cell lung cancer (NSCLC) versus the standard of care, but their costs have not been comprehensively evaluated. Total and differential costs of 1L osimertinib plus platinum-pemetrexed, intravenous (IV) amivantamab plus lazertinib, and subcutaneous (SC) amivantamab plus lazertinib were estimated from a United States (US) payer perspective.

METHODS:

A cost of care model was developed to assess treatment acquisition, administration, disease management, and adverse event (AE) management costs for osimertinib plus platinum-pemetrexed versus IV and SC amivantamab plus lazertinib for patients with EGFRm NSCLC. A one-year time horizon was chosen to allow for direct treatment comparison; a one-year treatment duration was assumed for treat-to-progression regimen components.

RESULTS:

The total first-year cost per-patient for osimertinib plus platinum-pemetrexed (all-payer perspective: $172,600; private perspective: $253,529; Medicare perspective: $84,926) was over twofold lower than for IV amivantamab plus lazertinib (all-payer perspective: $418,176; private perspective: $618,240; Medicare perspective: $201,441) and for SC amivantamab plus lazertinib (all-payer perspective: $419,718; private perspective: $621,166; Medicare perspective: $201,482). This translated to per-patient cost savings of $245,577; $364,711; and $116,514 for osimertinib plus platinum-pemetrexed versus IV amivantamab plus lazertinib and $247,118; $367,637; and $116,555 versus SC amivantamab plus lazertinib for the all-payer, private, and Medicare perspectives, respectively.

LIMITATIONS:

Limited data availability necessitated cost conversions across payer perspectives and assumptions for select inputs, including specific concomitant medication durations. Additionally, as any payer-negotiated discounts for treatment are confidential, model treatment acquisition costs reflected list prices. These data limitations contributed to uncertainty surrounding model inputs.

CONCLUSIONS:

From a US payer perspective, osimertinib plus platinum-pemetrexed was associated with substantially lower overall costs compared with IV and SC amivantamab plus lazertinib for the 1L treatment of patients with EGFRm locally advanced or metastatic NSCLC.

31 Dec 2026·RENAL FAILURE

A tri-scale in silico framework integrating pharmacovigilance and mechanistic modeling suggests tepotinib-associated acute kidney injury risk

Article

Author: Bai, Zhixun ; Wang, Qin ; Zheng, Rubin ; Han, Jinfen ; Lyu, Jiayi ; Lu, Jing ; Deng, Miao ; Chen, Jiaxi

Proactive safety evaluation of molecularly targeted therapies requires generalizable frameworks that integrate real-world evidence with mechanistic insights. As a case in point, tepotinib, a mesenchymal-epithelial transition (MET) inhibitor for non-small cell lung cancer, has a known pulmonary toxicity profile, but its link to acute kidney injury (AKI) and underlying mechanism remain unclear. We devised a tri-scale in silico strategy encompassing population-scale pharmacovigilance signal extraction from the FDA Adverse Event Reporting System (FAERS) (2020-2025) via disproportionality analysis (Reporting Odds Ratio, ROR, and Proportional Reporting Ratio, PRR), network toxicology-based multi-target exploration for shared target and hub gene identification, and mechanistic docking-based molecular plausibility assessment using the Cavity-detection guided Blind Docking (CB-Dock2) platform. Pharmacovigilance analysis identified a significant renal impairment signal (ROR = 20.60). Network toxicology suggested potential nephrotoxicity and revealed 173 shared targets and prioritizing six hub genes (HSP90AA1, AKT1, EGFR, CASP3, TNF, SRC). These genes were shown to be critically involved in PI3K-Akt and MAPK pathways. Molecular docking revealed high-affinity binding between tepotiniband all six hub targets (Vina scores: -8.0 to -10.6 kcal/mol), providing a structural basis for the postulated mechanistic link to AKI. These findings not only highlight the necessity for enhanced renal monitoring in tepotinib-treated patients but, more broadly, establish the FAERS-NetDock Pipeline as a reusable, generalizable and hypothesis-generating framework for evaluating tyrosine kinase inhibitors (TKIs)-induced nephrotoxicity; this framework is immediately applicable to profiling the safety of other TKIs (e.g. crizotinib, capmatinib, savolitinib, afatinib and osimertinib) and is readily adaptable for de-risking a wider spectrum of targeted therapies.

01 Oct 2026·Translational Research

Dynamic 3D imaging system detects vasculogenic mimicry and screens inhibitors in EGFR-mutant lung cancer

Article

Author: Su, Wu-Chou ; Chen, Helen H W ; Chiu, Wen-Tai ; Yeh, Yu-Min ; Hong, Tse-Ming ; Chung, Wei-Pang ; Wang, Hsueh-Chun ; Wu, Shang-Yin ; Lee, Chun-Hui

Vasculogenic mimicry (VM), wherein tumor cells form vessel-like structures independent of endothelial cells, drives metastasis and therapeutic resistance. Current in vitro VM research relies on conventional two-dimensional imaging, which fails to capture complex three-dimensional VM architecture, limiting anti-VM therapeutic development. We established a novel dynamic 3D imaging platform utilizing light sheet fluorescence microscopy for real-time visualization of physiologically relevant VM structures. Non-small cell lung cancer cell lines with different EGFR mutation statuses were cultured in three-dimensional matrices and monitored continuously. Structural characteristics including tubule diameter, lumen formation, and network complexity were quantified. Following validation of physiological 3D VM formation, we developed a high-content screening platform to assess anti-VM therapeutics, including foslinanib and osimertinib, individually and in combination. Our 3D VM platform revealed patent tubules and hollow lumens (25-50 μm diameter) approximating physiological 3D VM architecture, fundamentally distinct from planar network patterns seen with conventional 2D images. EGFR-mutant cells consistently formed complex 3D VM structures with functional lumens, whereas wild-type cell lines examined did not develop comparable three-dimensional architecture. In an EGFR L858R model, the foslinanib-osimertinib combination produced synergistic disruption of 3D VM structures; in other EGFR-mutant lines, the combination showed additive rather than synergistic effects. These findings indicate that combination activity is context-dependent and linked to specific EGFR genotypes. This 3D imaging platform provides a physiologically relevant, quantitative method for studying VM and screening anti-VM therapeutics, addressing a key limitation of conventional 2D assays. The association between EGFR mutation status and 3D VM formation offers insight into resistance mechanisms and identifies candidate combination strategies for further investigation, including the potential contribution of co-occurring genetic alterations. As a preclinical, hypothesis-generating study, these findings warrant validation in vivo and in clinical settings.

1,020

News (Medical) associated with Osimertinib mesylate

23 Sep 2026

·www.biospace.com

HUTCHMED Highlights Clinical Data to be Presented at the ESMO Congress 2026

HONG KONG and SHANGHAI and FLORHAM PARK, N.J., Sept. 23, 2026 (GLOBE NEWSWIRE) -- HUTCHMED (China) Limited (“ HUTCHMED ”) (Nasdaq/AIM:HCM; HKEX:13) today announces that new and updated data from several studies of compounds discovered by HUTCHMED will be presented at the European Society for Medical Oncology (“ESMO”) Congress 2026, taking place on October 23-27, 2026, in Madrid, Spain. Notably, results from two positive Phase III studies evaluating the savolitinib and osimertinib combination have been selected for oral presentations. Results from the global SAFFRON study will be featured in the Presidential Symposium session, while results from the SANOVO study in China will be presented in a Proffered Paper session, both highlighting important new clinical data. Having two Phase III studies featured as late-breaking abstracts underscores the potential of this all-oral, chemo-free combination to deliver meaningful advancements for patients with non-small cell lung cancer (“NSCLC”). The SAFFRON Global Phase III Study has been selected for a Presidential Symposium oral presentation. The study evaluated the combination in patients with epidermal growth factor receptor (EGFR)-mutated NSCLC with MET overexpression or amplification following disease progression on osimertinib. The trial reported positive high-level results on August 17, 2026, demonstrating a statistically significant and clinically meaningful improvement in progression-free survival (“PFS”) and overall survival (“OS”) compared to doublet platinum-based chemotherapy. The SANOVO China Phase III Study has been selected for a Proffered Paper oral presentation. The study evaluated the combination in previously untreated patients with locally advanced or metastatic NSCLC harboring activating EGFR mutations and MET overexpression. The trial reported positive high-level results on August 31, 2026, demonstrating a statistically significant and clinically meaningful improvement in PFS and a clinically meaningful benefit in OS versus osimertinib monotherapy. Details of the presentations are as follows: Abstract title Presenter / Lead author Presentation details SPONSORED STUDIES Osimertinib (osi) + savolitinib (savo) vs platinum–pemetrexed (plat–pem) in EGFRm MET-overexpressed (OE) and/or -amplified (AMP) advanced NSCLC post-osi: SAFFRON Phase (Ph) 3 primary results Shun Lu (Shanghai, China) LBA6 Presidential Symposium II Alicante Auditorium - Hall 6 Sunday, October 25, 2026 16:30 - 18:15 CEST Savolitinib or Placebo Combined with Osimertinib in Treatment-Naïve Advanced NSCLC with EGFR Mutation and MET Overexpression: Results from the Phase 3 SANOVO Study Yi-Long Wu (Guangzhou, China) LBA69 Proffered paper 2: NSCLC, metastatic Alicante Auditorium - Hall 6 Monday, October 26, 2026 08:30 - 10:00 CEST Updated results from a fruquintinib Expanded Access Program for patients with previously treated metastatic colorectal cancer Stefan Kasper (Essen, Germany) 848P Poster Session: Colon cancer Association between dose adjustment and treatment outcomes in patients with advanced renal cell carcinoma receiving fruquintinib plus sintilimab: A post-hoc analysis of the FRUSICA-2 trial Yuanyuan Qu (Shanghai, China) 3655eP E-poster Session: Renal cancer Efficacy of fruquintinib plus sintilimab in special populations with advanced renal cell carcinoma: A subgroup analysis of FRUSICA-2 study Kaiwei Yang (Beijing, China) 3667eP E-poster Session: Renal cancer Final phase 2 analysis of surufatinib plus camrelizumab, nab-paclitaxel and gemcitabine in first-line metastatic pancreatic cancer Shukui Qin (Nanjing, China) 3156P Poster Session: Pancreatic cancer INVESTIGATOR-INITIATED STUDIES Fruquintinib plus capecitabine maintenance after first-line anti-EGFR antibody plus chemotherapy in RAS/BRAF wild-type metastatic colorectal cancer: A phase Ib/II study Lin Yang/ Letian Zhang (Beijing, China) 877eP E-poster Session: Colon cancer Real-world effectiveness and safety of fruquintinib in patients with metastatic colorectal cancer in Spain: The FrESP study Ana Fernandez Montes (Ourense, Spain) 880eP E-poster Session: Colon cancer CONCEPT (COmbinatioN of CEtuximab Plus fruquintinib Treatment ± immunotherapy): A multicenter, randomized, open-label phase II trial in first-line pMMR RAS/BRAF wild-type unresectable metastatic colorectal cancer Kefeng Ding (Hangzhou, China) 890eP E-poster Session: Colon cancer A real-world study of low-dose fruquintinib combined with trifluridine/tipiracil hydrochloride (TAS-102) in the third-line and beyond treatment of metastatic colorectal cancer Yuehong Cui/ Li Liang (Shanghai, China) 903eP E-poster Session: Colon cancer Real-world outcomes with fruquintinib in heavily pretreated metastatic colorectal cancer: Impact of patient and disease characteristics Maria Maddalena Laterza (Pozzuoli, Italy) 964eP E-poster Session: Colon cancer A phase II, open-label, randomized study of doublet chemotherapy (FOLFOX or FOLFIRI) plus fruquintinib compared with doublet chemotherapy (FOLFOX or FOLFIRI) plus bevacizumab in second line setting for a metastatic colorectal cancer: ULYSSE- FFCD2406 - PRODIGE115 (trials in progress) Jean Marc Phelip (Saint-Étienne, France) 991eTiP E-poster Session: Colon cancer Phase II study of fruquintinib plus utidelone in platinum-resistant recurrent ovarian cancer (FRUTD Trial) Zheng Feng (Shanghai, China) 1283P Poster Session: Gynaecological cancers Fruquintinib plus eribulin in patients with metastatic HR+, HER2 - breast cancer after progression on endocrine therapy plus CDK4/6 inhibitor: Updated results from a phase II study Yuan Yuan (Nanjing, China) 1896eP E-poster Session: HR+ breast cancer Fruquintinib plus sintilimab and XELOX as first-line treatment for advanced gastric or gastroesophageal junction adenocarcinoma: A single-arm, open-label, multicenter phase II study Hua Wang (Nanchang, China) 2980eP E-poster Session: Oesophagogastric cancer Fruquintinib plus cadonilimab and S-1 in previously treated unresectable locally advanced or metastatic esophageal squamous cell carcinoma: preliminary efficacy and safety results from a phase Ib/II study Huiyan Luo (Guangzhou, China) 2981eP E-poster Session: Oesophagogastric cancer Nanoliposomal irinotecan (nal-IRI) combined with fruquintinib as second-line treatment for advanced gastric cancer: A single-arm, open-label, dose-escalation and expansion phase I/II trial Jieer Ying/ Qi Xu (Hangzhou, China) 2986eP E-poster Session: Oesophagogastric cancer FRUQUITAS trial: ENGIC intergroup randomized phase III of trifluridine/tipiracil +/- fruquintinib in pre-treated metastatic gastro-oesophageal adenocarcinoma David Tougeron (Poitiers, France) 3079eTiP E-poster Session: Oesophagogastric cancer CHOICE III: short-course preoperative radiotherapy followed by fruquintinib plus anti–PD-1 antibody (serplulimab) for neoadjuvant treatment of pMMR/MSS mid-to-low locally advanced rectal cancer: A single-arm, single-center, prospective phase II study Wei Zhang (Shanghai, China) 3582eTiP E-poster Session: Rectal and anal cancer First-line fruquintinib plus serplulimab for metastatic non-clear cell renal cell carcinoma: Updated results from the phase II FRONTIER study Jiwei Huang (Shanghai, China) 3614P Poster Session: Renal cancer Latest efficacy and safety analysis of surufatinib combined with EP regimen and serplulimab as first-line treatment for extrapulmonary neuroendocrine carcinoma Tao Zhang/ Zhenyu Lin (Wuhan, China) 2394RO Rapid Oral Session: NETs and endocrine tumours Pamplona Auditorium - Hall 5 Friday, October 23, 2026 16:15 - 17:45 CEST Surufatinib combined with toripalimab and nab-paclitaxel/ gemcitabine chemotherapy as first-line treatment for advanced pancreatobiliary-type ampullary carcinoma: A prospective phase II Clinical Trial Juan Du (Nanjing, China) 507eP E-poster Session: Biliary tract cancer, incl. cholangiocarcinoma Efficacy and safety of surufatinib in combination with CAPTEM in advanced G2/G3 Neuroendocrine Tumors: Results from a single-arm, phase II Trial Wei Wang (Guangzhou, China) 2403P Poster Session: Neuroendocrine tumours Surufatinib plus S-1/temozolomide as first-line therapy in MGMT-low advanced pancreatic neuroendocrine tumours (SUSTEM-p): An open-label, single-centre phase Ib/II trial Yihebali Chi (Beijing, China) 2411P Poster Session: Neuroendocrine tumours Updated results of a prospective, open-label study of surufatinib plus CAPTEM as conversion therapy for unresectable pancreatic neuroendocrine tumors Ziyao Wang (Chengdu, China) 2412P Poster Session: Neuroendocrine tumours Matching-adjusted indirect comparison of surufatinib versus high-dose OCT-LAR in patients with advanced GEP-NETs who progressed on prior SSA Therapy Jianming Xu (Beijing, China) 2415P Poster Session: Neuroendocrine tumours Surufatinib combined with octreotide LAR for the treatment of G1/G2 GEP-NETs: A single-arm, prospective, open-label phase II study Xiaofeng Sun (Nanjing, China) 2439eP E-poster Session: Neuroendocrine tumours Six weeks of induction gemcitabine plus nab paclitaxel (AG) followed by sequential surufatinib plus AG or AG alone as first line therapy for locally advanced or metastatic pancreatic ductal adenocarcinoma (mPDAC): A single center, two cohort, phase II study Jin Xu/ Jialin Li (Shanghai, China) 3168P Poster Session: Pancreatic cancer A phase Ib/II study of radiotherapy combined with surufatinib and sintilimab for localized high-risk limb and trunk soft tissue sarcomas: A prospective single-center trial Yan Wang (Shanghai, China) 3739P Poster Session: Sarcoma Surufatinib plus serplulimab, etoposide, and carboplatin as first-line treatment for extensive-stage small cell lung cancer (ES-SCLC): Updated results from a single-arm, phase Ia/Ib trial Haipeng Xu/ Longfeng Zhang (Fuzhou, China) 3831P Poster Session: Small cell lung cancer About Fruquintinib Fruquintinib is a selective oral inhibitor of all three vascular endothelial growth factor receptors (“VEGFR”) -1, -2 and -3. Fruquintinib is co-developed and co-commercialized in China by HUTCHMED and Eli Lilly and Company under the brand name ELUNATE ® . Takeda holds the exclusive worldwide license to further develop, commercialize, and manufacture fruquintinib outside mainland China, Hong Kong and Macau, marketing it under the brand name FRUZAQLA ® . About Savolitinib Savolitinib is an oral, potent and highly selective MET tyrosine kinase inhibitor that has demonstrated clinical activity in advanced solid tumors. It blocks atypical activation of the MET receptor tyrosine kinase pathway that occurs because of mutations (such as exon 14 skipping alterations or other point mutations), gene amplification or protein overexpression. Savolitinib is being jointly developed by AstraZeneca and HUTCHMED, and commercialized by AstraZeneca under the brand name ORPATHYS ® . About Surufatinib Surufatinib is a novel, oral angio-immuno kinase inhibitor that selectively inhibits the tyrosine kinase activity associated with VEGFRs and fibroblast growth factor receptor (FGFR), which both inhibit angiogenesis, and colony stimulating factor-1 receptor (CSF-1R), which regulates tumor-associated macrophages, promoting the body’s immune response against tumor cells. Surufatinib is marketed in China by HUTCHMED under the brand name SULANDA ® . HUTCHMED currently retains all rights to surufatinib worldwide. About HUTCHMED HUTCHMED (Nasdaq/AIM:HCM; HKEX:13) is an innovative, commercial-stage, biopharmaceutical company. It is committed to the discovery and global development and commercialization of targeted therapies and immunotherapies for the treatment of cancer and immunological diseases. Since inception it has focused on bringing drug candidates from in-house discovery to patients around the world, with its first four medicines marketed in China, the first of which is also approved around the world including in the US, Europe and Japan. For more information, please visit: or follow us on LinkedIn . Forward-Looking Statements This press release contains forward-looking statements within the meaning of the “safe harbor” provisions of the US Private Securities Litigation Reform Act of 1995. These forward-looking statements reflect HUTCHMED’s current expectations regarding future events, including but not limited to its expectations regarding the therapeutic potential of fruquintinib, surufatinib and savolitinib, the further clinical development for fruquintinib, surufatinib and savolitinib, its expectations as to whether any studies on fruquintinib, surufatinib and savolitinib would meet their primary or secondary endpoints, and its expectations as to the timing of the completion and the release of results from such studies. Such risks and uncertainties include, among other things, assumptions regarding enrollment rates and the timing and availability of subjects meeting a study’s inclusion and exclusion criteria; changes to clinical protocols or regulatory requirements; unexpected adverse events or safety issues; the ability of fruquintinib, surufatinib and savolitinib, including as combination therapies, to meet the primary or secondary endpoint of a study, to obtain regulatory approval in different jurisdictions and to gain commercial acceptance after obtaining regulatory approval; the potential markets of fruquintinib, surufatinib and savolitinib for a targeted indication, and the sufficiency of funding. In addition, as certain studies rely on the use of other drug products such as sintilimab and toripalimab as combination therapeutics, such risks and uncertainties include assumptions regarding their safety, efficacy, supply and continued regulatory approval. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. For further discussion of these and other risks, see HUTCHMED’s filings with the US Securities and Exchange Commission, The Stock Exchange of Hong Kong Limited and on AIM. HUTCHMED undertakes no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise. Medical Information This press release contains information about products that may not be available in all countries, or may be available under different trademarks, for different indications, in different dosages, or in different strengths. Nothing contained herein should be considered a solicitation, promotion or advertisement for any prescription drugs including the ones under development. CONTACTS Investor Enquiries +852 2121 8200 / ir@hutch-med.com Media Enquiries FTI Consulting – +44 20 3727 1030 / HUTCHMED@fticonsulting.com Ben Atwell / Tim Stamper +44 7771 913 902 (Mobile) / +44 7779 436 698 (Mobile) Brunswick – Zhou Yi +852 9783 6894 (Mobile) / HUTCHMED@brunswickgroup.com Panmure Liberum Nominated Advisor and Joint Broker Atholl Tweedie / Emma Earl / Rupert Dearden +44 20 7886 2500 Cavendish Joint Broker Geoff Nash / Nigel Birks +44 20 7220 0500 Deutsche Numis Joint Broker Duncan Monteith / Ramin Naji +44 20 7545 8000

Clinical ResultPhase 2Phase 3ImmunotherapyLicense out/in

22 Sep 2026

·www.sciencedaily.com

This new drug could break cancer’s resistance to treatment

A new experimental drug called CS18 may help break through cancer drug resistance by disabling several of the defenses tumors use to survive treatment. It strengthened existing therapies, restored drug sensitivity in resistant lung cancer cells, and slowed tumor growth in animal models.Researchers at Baylor College of Medicine have developed an experimental drug called CS18 that may help cancer treatments work against tumors that have become resistant to therapy. The study, published in Science Advances, provides early evidence supporting further investigation of CS18 as a possible future cancer treatment. "Therapeutic resistance is a main obstacle to achieve effective and durable cancer treatments," said corresponding author Dr. Weei-Chin Lin, professor of medicine - hematology and oncology and of molecular and cellular biology at Baylor. "While some therapies are effective at the beginning, many patients eventually relapse because cancer cells can activate compensatory and convergent biological pathways that allow them to overcome the toxic effects of therapy, promoting survival." Targeting Cancer's Survival Network Rather than focusing on a single cancer pathway, the researchers set out to develop a drug that could interfere with a broader control center involved in several cancer-promoting processes at once. Their target was topoisomerase IIß-binding protein 1 (TopBP1), which the team describes as a 'biological switchboard' because it helps regulate multiple pathways associated with cancer growth and survival. The researchers wanted to determine whether disrupting this central control point could produce longer-lasting treatment responses and help overcome resistance. "Of all the 'biological switches' on TopBP1, switch BRCT7/8 interacts with several key regulators of cancer growth, including MIZ1, a suppressor of cancer driver MYC; mutant p53, which can acquire cancer-promoting functions; and PLK1 and CIP2A, proteins that help cancer cells survive and divide," said Lin, a member of Baylor's Dan L Duncan Comprehensive Cancer Center. "All together, these diverse roles position TopBP1-BRCT7/8 as a promising target for intervention." Developing CS18 To find a compound capable of blocking BRCT7/8, the researchers screened thousands of chemicals with a combination of computer modeling and laboratory experiments. This search identified a compound known as 3B6. The team then modified 3B6 and tested numerous versions of the molecule, eventually identifying CS18 as the most effective candidate. "When CS18 binds to BRCT7/8, the cancer-promoting activities of MYC and mutant p53 decreased, proteins involved in DNA repair became less active and cancer cells were more likely to die," Lin said. "In addition, CS18 increased the activity of genes that stop uncontrolled cancer growth. Altogether, CS18 appears to reduce several of the defenses that help cancer cells survive therapy." Testing CS18 Across Multiple Cancers The researchers saw these effects across several types of cancer cells, including triple-negative breast cancer, ovarian cancer, lung adenocarcinoma, lung squamous cell carcinoma and acute myeloid leukemia. CS18 was also less toxic to non-cancerous cells. The results became particularly notable when CS18 was paired with cancer drugs that are already in use. Combining CS18 with treatments such as PARP inhibitors or osimertinib killed cancer cells more effectively than either treatment used on its own. "In the case of lung cancer cells that were already resistant to osimertinib, adding CS18 restored the cells' sensitivity to osimertinib, increasing cancer cell death," Lin said. "We observed a significant reduction of tumor growth in animal models with no major weight loss or other signs of toxicity." A Potential Strategy Against Drug Resistance Based on these findings, the researchers suggest that CS18 warrants further development as a possible component of combination cancer therapies. Such treatments could potentially help prevent resistance from emerging or make resistant cancers responsive to therapy again. Other contributors to this work include Fang-Tsyr Lin, Kang Liu, Yang Xiao, Lidija A. Wilhelms Garan and Helena Folly-Kossi, all at Baylor College of Medicine. Shwu-Jiuan Lin is at Taipei Medical University. This work was supported by the National Institutes of Health grants (R01CA203824, R01CA269971, T32CA174647 and T32GM136560) and Department of Defense grants (W81XWH-18-1-0329, W81XWH-19-1-0369, W81XWH-22-1-0226, W81XWH-22-1-0534 and HT9425-24-1-0045). Further support was provided by a Rivkin Center for Ovarian Cancer Pilot Award and a Taiwan Ministry of Science and Technology grant (MOST 107-2635-B-038-001).

17 Sep 2026

·www.fiercebiotech.com

Rare EGFR mutation increases lung cancer risk 62 times in never smokers

A new study published on Sept. 17 in Science reported that a rare inherited germline mutation can increase lung cancer risk 62 times in never-smokers and 25 times in smokers. Smoking on its own increases the risk of developing lung cancer 4 times in the general population. To look for the T790M mutation in the epidermal growth factor receptor (EGFR), researchers evaluated 23andMe genotyping data across 3.37 million individuals and found its prevalence to be 1 in 15,850. Out of the 17 cancers and non-pulmonary conditions screened, this mutation showed a strong association only with lung cancer. The study also traced the origination of the mutation to southern Appalachian populations in the U.S. “At the moment, screening for lung cancer is based, essentially, solely on tobacco exposure,” said Pasi Jänne, M.D., Ph.D., lung cancer specialist at Dana-Farber Cancer Institute and corresponding author, told Fierce. “Here we've identified a genetic component that is also a risk factor, and maybe these are individuals that would benefit from screening and early detection to identify cancers at an earlier early stage when they're still potentially curable.” Lung cancer is the second most common cancer in the U.S. and the leading cause of cancer death in both men and women. EGFR is a protein that regulates how cells grow and divide, and when it is mutated, it can cause cancer cells to grow and spread. EGFR mutation-positive lung cancer makes up around 10-15% of lung cancers in the U.S., with a higher incidence in Asian populations. Tobacco smoking is the leading cause of lung cancer. Interestingly, patients who have an EGFR mutation and develop lung cancer are typically individuals who have never smoked. Jänne acknowledged that this study does not give the full picture of the lifetime risk of developing lung cancer in someone who has this mutation. “There may be more nuances to the genetics of those individuals that modify the risk," he said. "Even in the presence of this mutation or environmental exposures that modify the risk.” Therapies targeting EGFR-mutated lung cancer have long been in development, with AstraZeneca’s Tagrisso and Johnson & Johnson’s Rybrevant . Back in 2015, AstraZeneca announced that its therapy showed positive median progression free survival data of 13.5 months in patients harboring the EGFR T790M mutation, data that eventually led to its FDA approval. In August, BlossomHill announced a macrocyclic EGFR-targeting molecule called BH-30643 to challenge Tagrisso. Other such therapies, however, have hit roadblocks. In 2015, Boehringer Ingelheim handed over as much as $730 million to South Korean drugmaker Hanmi Pharmaceutical in exchange for the rights to olmutinib (BI 1482694), an oral tyrosine kinase inhibitor for EGFR, but the drug caused a life-threatening skin condition. Ingelheim backed out of the deal after a year, and Hamni eventually put olmutinib to bed .

License out/inAcquisition

100 Deals associated with Osimertinib mesylate

External Link

KEGG	Wiki	ATC	Drug Bank
D10766	Osimertinib mesylate	L01XE	DB09330

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Non-Small Cell Lung Cancer	Canada	AstraZeneca Canada, Inc.	05 Jul 2016
EGFR positive non-small cell lung cancer	Japan	AstraZeneca Pharmaceuticals Co. Ltd.	28 Mar 2016
EGFR exon 19 Deletions Mutant Non-small Cell Lung Cancer	European Union	AstraZeneca AB	01 Feb 2016
EGFR exon 19 Deletions Mutant Non-small Cell Lung Cancer	Iceland	AstraZeneca AB	01 Feb 2016
EGFR exon 19 Deletions Mutant Non-small Cell Lung Cancer	Liechtenstein	AstraZeneca AB	01 Feb 2016
EGFR exon 19 Deletions Mutant Non-small Cell Lung Cancer	Norway	AstraZeneca AB	01 Feb 2016
EGFR exon 21 Substitution Mutant Non-small Cell Lung Cancer	European Union	AstraZeneca AB	01 Feb 2016
EGFR exon 21 Substitution Mutant Non-small Cell Lung Cancer	Iceland	AstraZeneca AB	01 Feb 2016
EGFR exon 21 Substitution Mutant Non-small Cell Lung Cancer	Liechtenstein	AstraZeneca AB	01 Feb 2016
EGFR exon 21 Substitution Mutant Non-small Cell Lung Cancer	Norway	AstraZeneca AB	01 Feb 2016
EGFR-mutated non-small Cell Lung Cancer	European Union	AstraZeneca AB	01 Feb 2016
EGFR-mutated non-small Cell Lung Cancer	Iceland	AstraZeneca AB	01 Feb 2016
EGFR-mutated non-small Cell Lung Cancer	Liechtenstein	AstraZeneca AB	01 Feb 2016
EGFR-mutated non-small Cell Lung Cancer	Norway	AstraZeneca AB	01 Feb 2016
metastatic non-small cell lung cancer	European Union	AstraZeneca AB	01 Feb 2016
metastatic non-small cell lung cancer	Iceland	AstraZeneca AB	01 Feb 2016
metastatic non-small cell lung cancer	Liechtenstein	AstraZeneca AB	01 Feb 2016
metastatic non-small cell lung cancer	Norway	AstraZeneca AB	01 Feb 2016
EGFR T790M Mutation Positive Non-Small Cell Lung Carcinoma	United States	AstraZeneca Pharmaceuticals LP	13 Nov 2015

Developing

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Indication	Highest Phase	Country/Location	Organization	Date
Neoplasms	Phase 3	China	AstraZeneca PLC	08 May 2023
Neoplasms	Phase 3	Japan	AstraZeneca PLC	08 May 2023
Neoplasms	Phase 3	France	AstraZeneca PLC	08 May 2023
Neoplasms	Phase 3	Malaysia	AstraZeneca PLC	08 May 2023
Neoplasms	Phase 3	Poland	AstraZeneca PLC	08 May 2023
Neoplasms	Phase 3	South Korea	AstraZeneca PLC	08 May 2023
Neoplasms	Phase 3	Taiwan Province	AstraZeneca PLC	08 May 2023
Neoplasms	Phase 3	United Kingdom	AstraZeneca PLC	08 May 2023
Carcinoma	Phase 3	United States	AstraZeneca PLC	03 Aug 2022
Carcinoma	Phase 3	China	AstraZeneca PLC	03 Aug 2022

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


WCLC2026	Not Applicable	EGFR-mutated non-small Cell Lung Cancer First line EGFR-mutant	64	Osimertinib	mqyjbimelo(wsyoeeldzp) = 1.6% developed interstitial lung disease lxswrfgrpi (okljhovldq ) View more	Positive	12 Sep 2026
				Osimertinib (exon 19 deletion)
WCLC2026	Phase 2	Adjuvant EGFR-sensitive mutations	70	Osimertinib 80 mg	bisbzpgzpk(ntglyaghss) = aavbmjlmcy pnzijdrwgz (wubggwshbo ) View more	Positive	12 Sep 2026
WCLC2026	Not Applicable	Lung Cancer First line	79	Osimertinib	cvfpvqnuzj(dkohgnrcgr) = gusrryyoir bvfzwjcuwn (sfglgvsmcw ) View more	Positive	12 Sep 2026
WCLC2026	Not Applicable	EGFR-mutated non-small Cell Lung Cancer First line EGFR alterations	93	Osimertinib	heymzzexnk(duopuxtklm) = xlazqyltwj zhaianiqqz (wijspwysla ) View more	Negative	12 Sep 2026
NCT03969823 (WCLC2026)	Phase 2	Non-Small Cell Lung Cancer First line EGFR mutation	119	Osimertinib 80 mg	eolxjhenuk(jtzidyckep) = lbdqkklkbq dejyjpjain (ozylbukduy, 67.1 - 89.7) View more	Positive	12 Sep 2026
WCLC2026	Not Applicable	RIT1-A77G \| ARID1A \| RIT1-M90I ... View more	3	pembrolizumab	jjnbwobdzq(idjjzxyile) = vtrrxwxlei dsdbudlzrt (jdcpnwotvy )	Negative	12 Sep 2026
				Lazertinib/placebo and osimertinib/placebo (RIT1 amplified LUAD with bone metastasis)	jjnbwobdzq(idjjzxyile) = qbgqomdcdw dsdbudlzrt (jdcpnwotvy )
NCT04743505 (WCLC2026)	Phase 1/2	EGFR-mutated non-small Cell Lung Cancer First line EGFR mutations	22	Vebreltinib (APL-101) + Osimertinib	noordycxqk(muivsmdosy) = veveawfaoq utozkgziye (jbeyefmprr ) View more	Positive	12 Sep 2026
WCLC2026	Not Applicable	Non-Small Cell Lung Cancer First line	1,198	Second-generation EGFR-TKIs (afatinib or dacomitinib)	isgtdsyjfp(gjitccydkj): HR = 1.107 (95.0% CI, 0.86 - 1.426), P-Value = 0.431 View more	Positive	12 Sep 2026
				Third-generation EGFR-TKIs (osimertinib or lazertinib)
WCLC2026	Not Applicable	EGFR-mutated non-small Cell Lung Cancer First line EGFR mutation	123	Osimertinib	fjlqjreshp(xwwetcdyrz) = jlckrvioio jbmxcxvbbc (ebdgigjagg )	Positive	12 Sep 2026
				Lazertinib	fjlqjreshp(xwwetcdyrz) = shmavrauvz jbmxcxvbbc (ebdgigjagg )
WCLC2026	Not Applicable	metastatic non-small cell lung cancer Second line EGFR exon 19 deletion \| L858R mutations	185	Osimertinib	hwdlfzxfyv(sbmpyozgiz) = rwwqyajczb pllgfztjag (cljkhmtwfk, 6.5 - 25.2) View more	Positive	12 Sep 2026
				Lazertinib	hwdlfzxfyv(sbmpyozgiz) = kwyoryzmow pllgfztjag (cljkhmtwfk, 7.3 - 12.6) View more

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