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Nuvectis Announces Positive Data for NXP900 in Triple Negative Breast Cancer Preclinical Models with an Integrin-Linked Kinase (ILK) Loss
Data Published in Cancer Research, a journal of the American Association for Cancer Research Publication highlights potent activity of NXP900, a
About this update from Nuvectis Pharma, Inc.
[{"type":"text","content":"Data Published in Cancer Research, a journal of the American Association for Cancer Research Publication highlights potent activity of NXP900, a differentiated inhibitor of the SRC/YES1 Kinases Fort Lee, NJ, Feb. 22, 2022 (GLOBE NEWSWIRE) -- Nuvectis Pharma, Inc. (NASDAQ: NVCT) (“Nuvectis” or the “Company”), a biopharmaceutical company focused on the development of precision medicines for serious conditions of unmet medical need in oncology, today announced a publication in Cancer Research by scientists from the University of Edinburgh titled Loss of Integrin-Linked Kinase Sensitizes Breast Cancer to SRC Inhibitors, highlighting NXP900's robust activity in preclinical models of Triple Negative Breast Cancer (“TNBC”) with Integrin-Linked Kinase (“ILK”) loss. NXP900 is Nuvectis’ novel and highly-selective SRC/YES1 inhibitor that effectively shuts down SRC-mediated signaling by inhibiting both the catalytic and scaffolding functions of SRC/YES1 kinases, without triggering immunosuppressive effects. A copy of the publication is available on Nuvectis' website at www.nuvectis.com/NXP900. The study was led by Dr. Valerie G. Brunton, Ph.D., Professor and Chair of Cancer Therapeutics at the Institute of Genetics and Cancer at the Cancer Research UK Edinburgh Centre in Edinburgh, Scotland. Dr. Brunton and the team at the University of Edinburgh demonstrated that loss of ILK sensitizes TNBC to treatment with SRC inhibitors, and that treatment with NXP900 (referred to as “eCF506” in the publication) was superior to treatment with bosutinib, an approved multi-kinase inhibitor that is known to inhibit the catalytic function of SRC kinase. Importantly, it was shown that NXP900 completely blocked the growth of ILK-knock-out tumors (subcutaneously injected in an immunodeficient mouse model) demonstrating superiority vs bosutinib. The studies also showed that NXP900 was significantly more potent in the same TNBC model (without ILK knock-out) versus bosutinib. This further supports the notion that complete shutdown of SRC-mediated signaling is key to unlocking the full potential of SRC inhibition as an anti-cancer treatment strategy “Our findings are that loss of ILK sensitizes breast cancer to SRC/YES1 inhibitors and that this exposes a therapeutic vulnerability in breast cancer, representing a potential avenue for clinical development.\" said Dr...