BERKELEY, Calif .– (COMMERCIAL THREAD) – Carmot Therapeutics, Inc. (Berkeley, CA), a clinical-stage biotechnology company applying its proprietary therapeutic platform, Chemotype Evolution (CE), to discover and develop disease-modifying therapies in metabolic diseases and cancer, today announced that in connection with the recent United States Food and Drug Administration (FDA) approval and commercial launch of Amgen’s LUMAKRAS (sotorasib), Carmot is eligible to receive royalties on future sales.
The FDA recently approved LUMAKRAS for the treatment of adult patients with KRAS Locally advanced or metastatic non-small cell lung cancer (NSCLC) with a G12C mutation, as determined by an FDA-approved test, having received at least one prior systemic treatment. LUMAKRAS has received accelerated approval based on overall response rate (ORR) and duration of response (DoR). Continued approval for this indication may depend on verification and description of clinical benefit in one or more confirmatory trials.
Amgen and Carmot Therapeutics entered into a collaborative research and licensing agreement announced in 2014 with goals that included identifying KRASG12C targeted therapies. As part of this collaboration, Carmot and Amgen successfully applied Chemotype Evolution to identify novel binding sites and covalent inhibitors of KRASG12C. Amgen then used these findings to develop LUMAKRAS. Under the terms of the agreement, Carmot is entitled to research funding, milestone payments and a royalty on commercial sales of the products resulting from the collaboration.
“The rapid development of LUMAKRAS illustrates the value of Chemotype Evolution and its ability to complement the design of drugs based on structure and medicinal chemistry,” commented Stig K. Hansen, PhD, co-founder and CEO of Carmot. “Chemotype Evolution is a transformative technology that can accelerate drug discovery for difficult targets. KRAS has been considered a go-to target for decades, but the evolution of the chemotype, combined with published findings, allowed Carmot and Amgen to quickly acquire new knowledge that helped Amgen discover the AMG 510, now. LUMAKRAS.
More generally, we have significantly extended the capabilities of Chemotype Evolution and used it to develop a portfolio of programs in metabolic diseases and cancer. Just as Chemotype Evolution has provided essential new information on KRAS function, Carmot has used the technology to generate in-depth information in other areas of the disease ”.
About Carmot Therapeutics, Inc. Carmot Therapeutics (“Carmot”) is focused on the discovery and development of disease-modifying therapies for patients with metabolic diseases and cancer. Carmot applies Chemotype Evolution (CE), pioneering drug discovery technology, in combination with unique biological expertise to identify innovative and superior therapies. In metabolic diseases, Carmot combines CE with new knowledge of incretin receptor signaling to develop a large and valuable pipeline of peptide and small molecule therapies. Carmot’s GLP-1 / GIP Dual Receptor Modulator has entered phase 2 of development and has the potential to be the best in a new class of treatments for type 2 diabetes and associated indications. Additionally, Carmot is using CE to identify novel covalent inhibitors and develop novel therapies targeting major oncogenic pathways, internally and with partners. Carmot has successfully applied CE with strategic partners, including collaboration with Amgen who supported Amgen’s development of LUMAKRAS (sotorasib), the first KRAS inhibitor to be approved.
About Non-Small Cell Lung Cancer and the KRAS G12C Mutation Lung cancer is the leading cause of cancer-related deaths worldwide, and it is responsible for more deaths worldwide than colon cancer, breast cancer and prostate cancer combined. Overall survival rates for NSCLC are improving, but remain low for patients with advanced disease, and 5-year survival is only 7% for those with metastatic disease.
KRAS The G12C is the most common KRAS mutation in NSCLC. In the United States, approximately 13% of patients with non-squamous NSCLC have the KRAS G12C mutation. Unmet medical needs remain high and treatment options are limited for patients with NSCLC KRAS G12C mutation whose first-line treatment did not work or has stopped working. Results with current therapies are suboptimal with median progression-free survival of approximately 4 months after second-line treatment of KRAS G12C mutated NSCLC.
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