54% of 13 Evaluable Non-Small Cell Lung Cancer Patients Experienced a Partial Response at the Target Dose of 960 mg in the Ongoing Phase 1 Study

46% of Patients had Stable Disease for a Disease Control Rate of 100% at the Target Dose

FDA Grants AMG 510 Fast Track Designation for Previously Treated Metastatic NSCLC With KRAS G12C Mutation

THOUSAND OAKS, CA, USA I September 8, 2019 I Amgen (NASDAQ:AMGN) today announced new data from the ongoing Phase 1 study evaluating AMG 510 in patients with previously treated KRAS G12C-mutated solid tumors. AMG 510 is a first-in-class investigational oral therapy that is designed to selectively and irreversibly target the KRASG12C protein. The additional follow-up in a larger group of patients with non-small cell lung cancer (NSCLC) continued to show anti-tumor activity with no dose-limiting toxicities. These data are being presented during an oral presentation at IASLC 2019 World Conference on Lung Cancer (WCLC) hosted by the International Association for the Study of Lung Cancer.

Initial data from the Phase 1 study were presented at the 55th Annual Meeting of the American Society of Clinical Oncology (ASCO) earlier this year. The additional follow-up in a larger group of patients being presented at WCLC includes a subset of 34 NSCLC patients enrolled, with 23 of the patients being evaluable for efficacy. Thirteen of the evaluable patients received the target dose of 960 mg once daily, of which seven (54%) achieved a partial response at one or more timepoints and six (46%) achieved stable disease, for a disease control rate of 100%.

“These new data reinforce the earlier positive response rate we shared at ASCO in more non-small cell lung cancer patients receiving AMG 510,” said David M. Reese, M.D., executive vice president of Research and Development at Amgen. “We remain enthusiastic about the promise of AMG 510 and continue to rapidly advance its development program both as monotherapy and in combination.”

Among the 34 NSCLC patients enrolled, there were no observed dose-limiting toxicities and no adverse events leading to discontinuation. Twenty-seven of these patients remain on treatment. Of the 34 patients, only nine (26.5%) reported treatment-related adverse events (TRAEs) of grade 1 or 2. Three patients reported grade 3 TRAEs (anemia and diarrhea). There were no grade 4 or higher TRAEs.

“There is a need for targeted treatments for specific driver mutations of cancer that do not have an approved therapy,” said Ramaswamy Govindan, M.D., principal investigator and professor at Washington University School of Medicine in St. Louis. “These data continue to show encouraging anti-tumor activity with AMG 510, underscoring the potential to close the treatment gap for non-small cell lung cancer patients with previously treated KRAS G12C-mutated NSCLC.”

Additional data on AMG 510 will be presented at the European Society for Medical Oncology (ESMO) 2019 Congress in Barcelona, Spain from Sept. 27-Oct. 1.

About the Phase 1 Study
The Phase 1, first-in-human, open-label multicenter study enrolled patients with KRAS G12C mutant solid tumors. Eligible patients were heavily pretreated with at least two or more prior lines of treatment, consistent with their tumor type and stage of disease. The primary endpoint is safety, and key secondary endpoints include pharmacokinetics, objective response rate (assessed every six weeks), duration of response and progression-free survival. Patients were enrolled in four dose cohorts: 180 mg, 360 mg, 720 mg and 960 mg, taken orally once a day.

About KRAS
The subject of more than three decades of research, the RAS gene family are the most frequently mutated oncogenes in human cancers.1,2 Within this family, KRAS is the most prevalent variant and is particularly common in solid tumors.2 A specific mutation known as KRAS G12C accounts for approximately 13% of non-small cell lung cancers, 3-5% of colorectal cancers and one to two percent of numerous other solid tumors.3 Approximately 30,000 patients are diagnosed each year in the United States with KRAS G12C-driven cancers.4 KRASG12C has been considered “undruggable” due to a lack of traditional small molecule binding pockets on the protein. Amgen is exploring the potential of KRASG12C inhibition across a broad variety of tumor types.

About Amgen Oncology
Amgen Oncology is searching for and finding answers to incredibly complex questions that will advance care and improve lives for cancer patients and their families. Our research drives us to understand the disease in the context of the patient’s life – not just their cancer journey – so they can take control of their lives.

For the last four decades, we have been dedicated to discovering the firsts that matter in oncology and to finding ways to reduce the burden of cancer. Building on our heritage, Amgen continues to advance the largest pipeline in the Company’s history, moving with great speed to advance those innovations for the patients who need them.

At Amgen, we are driven by our commitment to transform the lives of cancer patients and keep them at the center of everything we do.   

For more information, follow us on www.twitter.com/amgenoncology.

About Amgen
Amgen is committed to unlocking the potential of biology for patients suffering from serious illnesses by discovering, developing, manufacturing and delivering innovative human therapeutics. This approach begins by using tools like advanced human genetics to unravel the complexities of disease and understand the fundamentals of human biology.

Amgen focuses on areas of high unmet medical need and leverages its expertise to strive for solutions that improve health outcomes and dramatically improve people’s lives. A biotechnology pioneer since 1980, Amgen has grown to be one of the world’s leading independent biotechnology companies, has reached millions of patients around the world and is developing a pipeline of medicines with breakaway potential.

For more information, visit www.amgen.com and follow us on www.twitter.com/amgen.


  1. Cox A, et al. Drugging the undruggable RAS: Mission possible? Nat Rev Drug Discov. 2014 Nov;13(11):828-51.
  2. Fernandez-Medarde A, Santos E. RAS in cancer and developmental diseases. Genes Cancer. 2011 Mar;2(3):344-58.
  3. Lipford, JR. Pre-clinical development of AMG 510: the first inhibitor of KRASG12C in clinical testing. Oral presentation at AACR 2019, Atlanta, GA. March 29-April 3, 2019.
  4. Stephen AG, et al. Dragging RAS back in the ring. Cancer Cell. 2014 Mar 17;25(3):272-81.