Two companies to treat KRAS positive solid tumors
Release date: 2020-01-09 Views: 0
Today, Verastem Oncology announced that it has reached an exclusive global license agreement with Chugai Pharmaceutical of Japan, and Verastem has obtained global development and promotion rights for RAF / MEK inhibitor CH5126766 (CKI27) developed by Chugai. Currently, CH5126766 is being developed to treat patients with solid tumors carrying KRAS mutations.
Previous preclinical studies have shown that FAK inhibitors can enhance the immune response by reducing immunosuppressive cells, increasing cytotoxic T cells, and reducing matrix density, thereby allowing tumor-killing immune cells to enter the tumor. The defactinib developed by Verastem is an oral small molecule inhibitor of FAK and PYK2. At present, the two partners have carried out a treatment based on defactinib and CH5126766 in phase 2 trials of single-agent treatment of patients with low-grade serous ovarian cancer (LGSOC) and non-small cell lung cancer (NSCLC) with KRAS mutations. Mutated LGSOC, NSCLC, and Phase 1/2 clinical trials in patients with colorectal cancer (CRC) have verified the efficacy of the combined therapy of CH5126766 and defactinib. Detailed data for the trial will be released in the first half of this year.
According to the terms of the agreement, Verastem will be responsible for the development and global promotion of CH5126766, and will pay Chugai Company a $ 3 million prepayment and CH5126766's future sales share.
"Based on the results of clinical trials of defactinib monotherapy in patients with KRAS mutations in NSCLC, we conducted a series of preclinical studies to identify drug classes that have synergies with defactinib. We found that the combination of defactinib with the MEK inhibitor CH5126766 has the highest Level of synergy, "said Mr. Dan Paterson, President and Chief Operating Officer of Verastem Oncology," These early clinical results drive our partnership with Chugai to accelerate the treatment of patients with highly aggressive and recurrent KRAS mutation cancer Joint development plan. "
"CH5126766 is a unique inhibitor of the RAS / RAF / MEK signaling pathway," said Neal Rosen, MD, Memorial Sloan-Kettering Cancer Center. "CH5126766 can block MEK compared to other MEK inhibitors being developed. Kinase activity and RAF's ability to phosphorylate MEK. This unique mechanism allows CH5126766 to block MEK signaling but does not cause compensatory activation that limits the efficacy of other inhibitors. The clinical data of the combination therapy of Defactinib and CH5126766 is for KRAS mutant solid tumors Patients bring hope. "
 Verastem Oncology Announces Global Licensing Agreement with Chugai Pharmaceutical Co., Ltd. to Develop and Commercialize RAF / MEK Inhibitor CH5126766, Retrieved January 08, 2020, from http://www.businesswire.com/news/home/20200108005086/ en
 Verastem pens KRAS-focused drug licensing deal with Chugai, Retrieved January 08, 2020, from http://www.fiercebiotech.com/biotech/verastem-pens-kras-focused-drug-licence-deal-chugai-pharmaceutical
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