Kinnate Biopharma Inc. Selected to Deliver Oral Presentation on its RAF Inhibitor Candidate Program at the Virtual IASLC 2022 Targeted Therapies of Lung Cancer Meeting

On February 14, 2022 Kinnate Biopharma Inc. (Nasdaq: KNTE) ("Kinnate"), a biopharmaceutical company focused on the discovery and development of small molecule kinase inhibitors for difficult-to-treat, genomically defined cancers, reported that it has been selected to deliver an oral presentation of preclinical data from its KIN-2787 program at the upcoming virtual IASLC 2022 Targeted Therapies of Lung Cancer meeting taking place February 22-26, 2022 (Press release, Kinnate Biopharma, FEB 14, 2022, View Source [SID1234608057]). The presentation will be delivered by study collaborator and presenting author Tadashi Manabe, M.D., Ph.D., Postdoctoral Scholar-Fellow, Department of Medicine, Division of Hematology and Oncology at the University of California, San Francisco (UCSF).

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"We continue to make progress in our clinical trial of KIN-2787 and expect initial data in the third quarter of 2022," said Richard Williams, MBBS, Ph.D., Chief Medical Officer at Kinnate. "Among other indications, KIN-2787 is being developed for the treatment of patients with non-small cell lung cancer driven by BRAF Class II or Class III alterations and we are looking forward to sharing preclinical data on its antitumor activity at this upcoming IASLC meeting."

In this study, KIN-2787 activity was assessed by suppression of downstream MAPK pathway signaling and subsequent cell growth inhibition across BRAF-altered and/or RAS-altered versus wild type panels of human non-small cell lung cancer (NSCLC) cell lines. In contrast to approved therapies, targeting Class I BRAF alterations, KIN-2787 was most active in Class II and Class III BRAF-altered NSCLC cells. KIN-2787 also inhibited cellular proliferation in BRAF alteration-positive human NSCLC cell lines. Additionally, KIN-2787 was active in in vitro cell growth inhibition assays against a parental BRAF Class I-driven NSCLC cell line and retained activity in an experimentally acquired vemurafenib-resistant BRAF p61 splice variant-expressing derived cell line. In vivo, KIN-2787 efficacy was evaluated using a BRAF-alteration driven human NSCLC cell line and patient-derived xenograft models. The ongoing KN-8701 trial (NCT# 04913285) of KIN-2787 is actively enrolling patients across multiple centers in the United States.

"Together, Class II and III alterations represent as many as 65% of all oncogenic BRAF alterations in NSCLC. While there are approved RAF inhibitors being used in combination treatment of BRAF Class I-altered NSCLC, there are currently no RAF-targeted therapies for the treatment of NSCLC patients with tumors driven by BRAF Class II or III alterations, which is likely a contributing factor in the inferior clinical outcomes often seen with these patients," said Dr. Manabe. "I am pleased to share findings from this study which show that KIN-2787 is a potent and selective pan-RAF inhibitor with demonstrated capabilities in overcoming well-characterized resistance mechanisms."

"KIN-2787 is a promising next-generation RAF inhibitor with unique properties that has shown potent activity against a variety of oncogenic BRAF-driven lung cancers in preclinical studies. The preclinical data are exciting, and I have great enthusiasm for its continued clinical development as a potential new targeted therapy that could help address the current unmet needs for oncogene-driven lung cancer patients," added Trever Bivona, M.D., Ph.D., study collaborator and Professor, Hematology and Oncology, at UCSF.

Details of the meeting presentation are as follows:

Abstract title: Antitumor Activity of KIN-2787, a Next-Generation Pan-RAF Inhibitor, in Preclinical Models of Human BRAF-Alteration Driven Non-Small Cell Lung Cancer (NSCLC)
Session: Best Fellows Oral Abstract Session
Session date and time: Wednesday, February 23, 2022 at 4:15pm ET
Additional information on the virtual IASLC 2022 Targeted Therapies of Lung Cancer meeting is available at: View Source