on February 28, 2019 Amgen (NASDAQ:AMGN) reported that new data from its early-stage oncology pipeline will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in Atlanta, March 29 – April 3, 2019 (Press release, Amgen, FEB 28, 2019, View Source;p=RssLanding&cat=news&id=2389545 [SID1234533864]).
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"At Amgen, we are searching for and finding answers to incredibly complex questions to advance care and improve lives for cancer patients," said David M. Reese, M.D., executive vice president of Research and Development at Amgen. "In a significant milestone in the oncology community, we will share the latest preclinical data from our KRASG12C inhibitor, AMG 510. KRAS has eluded targeting despite more than 30 years of industry and academic research. Our program is the first to reach the clinical stage, which will evaluate its potential against a target that is easily identifiable and present in a wide range of solid tumors."
For the first time, preclinical data will be presented on AMG 510, a first-in-class investigational KRASG12C inhibitor being evaluated for the treatment of solid tumors. Data at the meeting will also showcase Amgen’s novel bispecific T cell engager (BiTE) platform, including preclinical data evaluating the use of AMG 757, a DLL3-targeted BiTE molecule, in resistant subtypes of melanoma. Additional research to be presented will include preclinical data evaluating the use of Amgen’s intravenous investigational MCL-1 inhibitor, AMG 176, in combination with standard of care therapies in acute myeloid leukemia.
A complete listing of abstracts can be found on the AACR (Free AACR Whitepaper) website. Notable abstracts of interest include:
Discovery of AMG 510: A Noval Covalent Inhibitor of KRASG12C, Now in a Phase 1 Clinical Trial for Patients with Solid Tumors Harboring the KRAS P.G12C Allele
Oral Presentation, Sunday, March 31 from 4:28-4:52 p.m. ET in Georgia World Congress Center, Building A, Level 3, Room A305
Discovery and In Vitro Characterization of AMG 510, a Potent and Selective Covalent Small Molecule Inhibitor of KRASG12C
Abstract #4484, Oral Presentation, Tuesday, April 2 from 3-5 p.m. ET in Georgia World Congress Center, Building C, Level 3, Georgia Ballroom 3
Discovery of AMG 510, a First-In-Human Covalent Inhibitor of KRASG12C for the Treatment of Solid Tumors
Abstract #4455, Oral Presentation, Tuesday, April 2 from 3-5 p.m. ET in Georgia World Congress Center, Building B, Level 2, Room B206
In Vivo Characterization of AMG 510, A Potent and Selective KRASG12C Covalent Small Molecule Inhibitor in Preclinical KRASG12C Cancer Models
Abstract #3090/24, Poster Presentation, Tuesday, April 2 from 8 a.m.-noon ET in Georgia World Congress Center, Exhibit Hall B, Section 14
BiTE Antibody Construct:
Melanoma Subtypes that Emerge During Adaptive Resistance to Therapy are Targets for Bispecific T Cell Engager (BiTE) Antibody Constructs Directed to CDH19 And DLL3
Abstract #553/17, Poster Presentation, Sunday, March 31 from 1-5 p.m. ET in Georgia World Congress Center, Exhibit Hall B, Section 23
Evaluation of Mesothelin BiTE Antibody Constructs in Models of Pancreatic Ductal Adenocarcinoma
Abstract #1561/30, Poster Presentation, Monday, April 1 from 8 a.m.-noon ET in Georgia World Congress Center, Exhibit Hall B, Section 25
Additional Preclinical Data:
AMG 176 Exhibits Robust Antitumor Activity in Combination with Standard of Care Agents in Models of Acute Myeloid Leukemia
Abstract #2180/2, Poster Presentation, Monday, April 1 from 1-5 p.m. ET in Georgia World Congress Center, Exhibit Hall B, Section 14
CSF-1 Receptor-Mediated Macrophage Depletion Can Induce Immunomodulatory Resistance Mechanisms in Murine Tumor Models
Abstract #2803/19, Poster Presentation, Tuesday, April 2 from 8 a.m.-noon ET in Georgia World Congress Center, Exhibit Hall B, Section 3
The subject of more than three decades of research, RAS proteins make up the most frequently mutated gene family 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 KRASG12C accounts for approximately 12 percent of all KRAS mutations across tumor types.3 Amgen is exploring the potential of KRASG12C inhibition across a broad variety of tumor types.
About BiTE Technology
Bispecific T cell engager (BiTE) antibody construct is an innovative technology that can be engineered to target any tumor antigen expressed by any type of cancer. The protein molecules are designed to kill malignant cells using the patient’s own immune system by bridging T cells to tumor cells. BiTE antibody construct helps connect the T cells to the targeted cell, with the intent of causing T cells to inject toxins which trigger cancer cell death (apoptosis). Amgen is developing BiTE antibody constructs to uniquely (or specifically) target numerous hematologic malignancies and solid tumors.
About Amgen’s Commitment to Oncology
Amgen is committed to helping patients take on some of the toughest cancers, such as those that have been resistant to drugs, those that progress rapidly through the body and those where limited treatment options exist. Amgen’s supportive care treatments help patients combat certain side effects of strong chemotherapy, and our targeted medicines and immunotherapies focus on more than a dozen different malignancies, ranging from blood cancers to solid tumors. With decades of experience providing therapies for cancer patients, Amgen continues to grow its portfolio of innovative and biosimilar oncology medicines.