YAP1

STOCKHOLM, Sept. 26, 2023 /PRNewswire/ -- Beactica Therapeutics AB, the Swedish precision oncology company, today announced that it has entered into a research collaboration agreement with the National Center for Advancing Translational Sciences (NCATS), one of 27 institutes and centers at the U.S. National Institutes of Health (NIH). The collaboration will focus on the translation of novel proteolysis-targeting degraders of TEAD under development by Beactica for treatment of cancer. Under the agreement, NCATS will gain access to proprietary targeted degraders of TEAD from Beactica to evaluate their efficacy in disease-relevant preclinical models. NCATS will also map systematically the drug-combination landscape for selected preclinical candidates by performing a high-throughput drug-combination screen using a collection of about 3,000 oncology-focused, mechanistically annotated drugs. Pharmacological modulation of the Hippo signalling pathway has translational potential in both regenerative and oncology indications. Small-molecule modulators of the TEAD transcription factors have recently emerged as a novel anti-cancer drug-class, to specifically target Hippo-pathway-deficient cancers. "We are very pleased to be selected by NCATS and look forward to collaborating with them to maximize the therapeutic potential of our targeted degraders of TEAD." said Dr Per Källblad, CEO of Beactica Therapeutics. "Their extensive expertise and capabilities will accelerate our project's progress, enhancing its potential to positively impact patients". About YAP–TEAD YAP1 (Yes-associated protein 1) is a coactivator that together with TEAD 1–4 (TEA Domain) transcription factors play key roles in the Hippo signalling pathway that regulate cell proliferation, apoptosis, and stemness. Dysregulation of the Hippo pathway and subsequent activation of TEAD has been reported in a wide range of cancers such as squamous cell carcinoma, head and neck, gynaecological, and gastrointestinal cancers. The first clinical proof-of-concept for drugging the Hippo–YAP–TEAD pathway was recently achieved with the TEAD inhibitor VT3989, which was presented at the American Association for Cancer Research (AACR) Annual Meeting in April 2023. About Beactica Therapeutics Beactica Therapeutics AB is a privately held precision oncology company committed to the fight against cancer. The company is advancing a pipeline of novel small molecule therapeutics with a focus to treat genetically defined cancers with significant unmet medical need. Beactica's approach is centered around targeting synthetically lethal disease proteins with allosteric modulators and targeted protein degraders. Beactica deliver value to patients and shareholders by advancing its programmes to clinical proof of concept. For more information, please visit . Beactica Therapeutics Contact Per Källblad M.Sc. Ph.D. CEO [email protected] Tel: +46 18 56 08 80 The following files are available for download: SOURCE Beactica Therapeutics AB

Fort Lee, NJ, Sept. 21, 2023 (GLOBE NEWSWIRE) -- Nuvectis Pharma, Inc. (NASDAQ: NVCT) ("Nuvectis" or the "Company"), a clinical-stage biopharmaceutical company focused on the development of innovative precision medicines for the treatment of serious conditions of unmet medical need in oncology, today announced upcoming scientific presentations for NXP800 at the 2023 AACR Special Conference In Cancer Research: Ovarian Cancer (October 5-7, 2023, Boston, MA) and for NXP800 and NXP900 at the 2023 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics (October 11-15, 2023 Boston, MA). Abstract Titles and Presenters Presentation Details 2023 AACR Special Conference in Cancer Research: Ovarian Cancer NXP800 Activation of the integrated stress response by NXP800, an orally available, clinical-stage, investigational agent in ARID1A-mutated, platinum resistant ovarian cancer Presenter: Paul Workman The Institute of Cancer Research London, United Kingdom Session Title Proffered Talks I Session Type Oral Session Date / Time October 6th, 9:50-10:50 AM 2023 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics NXP800 From targeted phenotypic screen to NXP800: A clinical stage activator of the integrated stress response for the treatment of ARID1A-mutated ovarian carcinoma Presenter: Paul Workman The Institute of Cancer Research London, United Kingdom Session Title Drug Screening Session Type Oral Session Date / Time October 14th, 4:00-5:40 PM NXP800 Results of a phase 1 dose escalation clinical trial of NXP800, a novel GCN2 activator, in patients with advanced or metastatic solid tumors (B044) Presenter: Simon Rodney The Institute of Cancer Research and The Royal Marsden Hospital NHS Foundation Trust London, United Kingdom Session Title Poster Session B Session Type Poster Session Date / Time October 13th, 12:30-4:00 PM NXP900 NXP900, a novel YES1/SRC kinase inhibitor demonstrates inhibition of YAP1 nuclear localization and potent single agent anti-tumor activity in esophageal squamous cancer models (B162) Presenter: Neil O. Carragher University of Edinburgh, Edinburgh, United Kingdom Session Title Poster Session B Session Type Poster Session Date / Time October 13th, 12:30-4:00 PM About Nuvectis Pharma, Inc. Nuvectis Pharma, Inc. is a clinical-stage biopharmaceutical company focused on the development of innovative precision medicines for the treatment of serious conditions of unmet medical need in oncology. The Company is currently developing two drug candidates, NXP800 and NXP900. NXP800 is an oral small molecule currently in a Phase 1b clinical trial investigating its potential to treat platinum resistant, ARID1a-mutated ovarian carcinoma. The FDA granted Fast Track Designation to the NXP800 development program in platinum resistant, ARID1a-mutated ovarian carcinoma, and Orphan Drug Designation for the treatment of cholangiocarcinoma. NXP900 is an oral small molecule SRC/YES1 kinase family (SFK) inhibitor currently in a Phase 1a dose escalation clinical trial. 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An international team of researchers has demonstrated that a combination of inhibitors may suppress tumor growth and prevent relapse in patients with certain cancers, including head and neck squamous cell carcinoma and lung adenocarcinoma. Their findings support the future development of innovative therapeutic approaches targeting these cancers. An international team of researchers has demonstrated that a combination of inhibitors may suppress tumor growth and prevent relapse in patients with certain cancers, including head and neck squamous cell carcinoma and lung adenocarcinoma. Their findings support the future development of innovative therapeutic approaches targeting these cancers. The team's work is published in the journal Oncogene on August 17, 2023. Scientists know that in humans and other mammals, the Hippo signaling pathway plays a key role in the rapid increase of cells that occurs with cancers in the body. Yes-associated protein 1, or YAP, is a protein that is critical in regulating the progression of tumor growth, and it plays an important role in the beginning and spread of a variety of cancers. When the Hippo pathway is dysregulated, it triggers the activation of YAP and this contributes to head and neck squamous cell carcinoma. Both the Hippo pathway and YAP have attracted attention as signaling pathways that regulate cancer cell characteristics. Epidermal growth factor receptor, or EGFR, is a protein on cells that contributes to their growth. When a mutation occurs in the gene for EGFR, it can grow too much, leading to cancer. EGFR is frequently amplified and highly overexpressed in head and neck squamous cell carcinoma, and mutated and activated in lung adenocarcinoma. So the EGFR inhibitor, a drug that blocks the cancer's growth, is used as a targeted therapy in fighting these cancers. In earlier work, the research team clarified the mechanism by which EGFR activates YAP through the Hippo pathway. However, EGFR-targeted monotherapy has shown a low response rate. Based on this evidence, researchers believe that EGFR inhibitors may temporarily inactivate YAP, but when YAP is re-activated, it increases resistance to the EGFR inhibitors used to fight the cancer. Scientists do not yet fully understand how the YAP is re-activated. The team focused their current study on AXL, a receptor-type tyrosine kinase. They set out to clarify the mechanism that causes the cancer cells' resistance to EGFR inhibitors, specifically focusing on the novel regulatory mechanism of YAP by AXL. Receptor-type tyrosine kinases like AXL play an important role in cell processes. When it is working properly, AXL is mainly expressed in immune cells, and does the work of removing dead cells and controlling the duration of immune responses. But when AXL becomes dysregulated, they can contribute to cancers, including lung adenocarcinoma, acute leukemia, and head and neck squamous cell carcinoma. The team used comprehensive transcriptional analysis and in vitro experiments in their study. With this research, the team clarified that AXL stimulates YAP through a novel mechanism when AXL combines with EGFR. This combination activates YAP via the EGFR-LATS1/2 axis. LATS1/2, or large tumor suppressor kinases, are important members of the Hippo pathway. The team determined that the combination of AXL and EGFR inhibitors working together inactivates YAP and suppresses the viability of head and neck squamous cell carcinoma and lung adenocarcinoma cells. "The combination therapy targeting both EGFR and AXL or YAP simultaneously may effectively suppress tumor growth and prevent resistance and relapse in patients with EGFR-altered cancers, including head and neck squamous cell carcinoma and lung adenocarcinoma," said Toshinori Ando, assistant professor at the Center of Clinical Oral Examination, Hiroshima University Hospital. Looking ahead, the team plans to try to generate effective drugs that can target EGFR, AXL, and YAP. "We think that intrinsic YAP activation or acquired re-activation after EGFR-targeted therapy in head and neck squamous cell carcinoma and lung adenocarcinoma has not been clarified yet. We will continue the research," said J. Silvio Gutkind, distinguished professor, Department of Pharmacology, University of California, San Diego.