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HOUSTON--(BUSINESS WIRE)-- Sporos BioDiscovery, Inc. (a portfolio company of Sporos Bioventures, LLC.), a precision oncology company developing a diversified pipeline of small molecule therapeutic programs targeting cancer vulnerabilities in the tumor and tumor microenvironment, today announced that it will present two posters highlighting preclinical data from the company’s novel TEAD1 / TEAD4 isoform selective inhibitor, SPR1, at the American Association for Cancer Research (AACR) Annual Meeting 2024, taking place April 5-10, 2024, in San Diego, CA. “We look forward to presenting two posters at this year’s AACR meeting that highlight the significant preclinical work we have done to characterize SPR1 as a potential best-in-class TEAD inhibitor. In addition, our team’s expert biological analysis has uncovered a new therapeutic vulnerability that could broaden the potential use of SPR1, a TEAD1/4 inhibitor, to a new subset of cancers with certain homozygous deletions,” said Stephen Rubino, Ph.D., President of Sporos BioDiscovery. Presentation Details: Title: TEAD1/4 inhibitors exhibit deeper biological impact and broader activity compared to TEAD1-only inhibitors in both monotherapy and combination without additional kidney toxicity Session Category: Experimental and Molecular Therapeutics Session Title: New Targets Session Date and Time: Tuesday Apr 9, 2024, 1:30 p.m. - 5:00 p.m. PT Abstract Number: 5913 Poster Number: 27 Title: VGLL4 is the target of the 3p25 homozygous deletion and presents a novel therapeutic vulnerability for TEAD1/4 but not TEAD1 inhibitors Session Category: Experimental and Molecular Therapeutics Session Title: YAP/TAZ/TEAD Modulators Session Date and Time: Wednesday Apr 10, 2024, 9:00 a.m. - 12:30 p.m. PT Abstract Number: 7266 Poster Number: 3 About Sporos BioDiscovery Sporos BioDiscovery, Inc. is a biotechnology research & development company with a diversified pipeline of several small molecule precision oncology therapeutic programs in development, including its lead candidate SPR1, a novel TEAD inhibitor program. Sporos BioDiscovery, Inc. is a portfolio company of Sporos Bioventures, LLC, a private biotechnology company focused on transforming the drug development process across oncology.

STOCKHOLM, Feb. 14, 2024 /PRNewswire/ -- Beactica Therapeutics AB, the Swedish precision oncology company, today announced that its TEAD programme has been selected for a late-breaking presentation at the American Association for Cancer Research's Annual Meeting 2024. The conference will take place on April 5-10, 2024 in San Diego, California. Dr Peter Brandt, Head of Chemistry, will present a poster entitled Degraders of TEAD transcription factors based on interface 3 binders on Sunday April 7, 2024, at 1:30 PM – 5:00 PM. The location is at the San Diego Convention Center, Section 52, abstract presentation number: LB029. The session title is Late-Breaking Research: Chemistry. The presentation will include new positive results from studies with novel proteolysis-targeting degraders of TEAD based on interface 3-binding ligands under development by Beactica. This will include head-to-head in vitro comparisons with other classes of TEAD modulators in clinical development such as palmitoylation inhibitors and direct YAP–TEAD protein–protein interaction inhibitors. The work to be presented contains contributions by Beactica's collaborators at the National Center for Advancing Translational Sciences (NCATS), one of 27 institutes and centers at the U.S. National Institutes of Health (NIH). Organised by the American Association for Cancer Research, the AACR Annual Meeting is the largest and most important cancer drug discovery event in the world. It has an anticipated attendance of more than 20 000 scientists, clinicians, advocates, and other attendees. The event spans integrative cancer science, global impact, individualised patient care and showcases the best and most up-to-date cancer science available. About TEAD TEAD 1–4 (Transcriptional Enhanced Associate Domain) are transcription factors that together with its coactivators YAP (Yes-associated protein) and TAZ (transcriptional coactivator with PDZ-binding motif) play key roles in the Hippo signalling pathway that regulates 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 achieved with the TEAD inhibitor VT3989 and 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

A groundbreaking scientific study has unveiled a remarkable discovery that may have far-reaching implications for the treatment of heart disease. The implications are immense offering glimpses of a future where heart disease may no longer be an irreversible condition but a challenge that can be overcome through medical intervention. The potential for developing novel therapies that leverage the body's innate regenerative capacity holds great promise for millions of individuals affected by heart disease worldwide. A groundbreaking scientific study published in Nature Cardiovascular Research has unveiled a remarkable discovery that may have far-reaching implications for the treatment of heart disease. The intensive investigations utilizing single-cell genomics and genetic experiments were conducted by a team of scientists in theCardiomyocyte Renewal Laboratory and McGill Gene Editing Laboratory at The Texas Heart Institute, including James F. Martin Vivian L. Smith Chair in Regenerative Medicine and Vice Chairman and Professor of Molecular Physiology and Biophysics at Baylor College of Medicine, and co-first authors Xiao Li, PhD, and Rich Gang Li, PhD. Titled "YAP Induces a Neonatal Like Pro-Renewal Niche in the Adult Heart," this research sheds light on the potential of the human heart to achieve self-repair and regeneration. Heart disease remains a leading cause of death worldwide, with myocardial infarction, also known as a heart attack, causing irreparable damage to cardiac muscle cells. While current treatments focus on alleviating symptoms and improving blood flow, they fall short in addressing the crucial issue of lost cardiomyocytes (CMs), leading to further complications such as heart failure. However, this groundbreaking study offers hope for a paradigm shift in regenerative medicine. Heart disease remains a leading cause of death worldwide, with myocardial infarction, also known as a heart attack, causing irreparable damage to cardiac muscle cells. While current treatments focus on alleviating symptoms and improving blood flow, they fall short of addressing the crucial issue of lost cardiomyocytes (CMs), leading to further complications such as heart failure. However, this groundbreaking study offers hope for a paradigm shift in regenerative medicine. Contrary to longstanding beliefs, the study reveals that regeneration of CMs requires a complex microenvironment, where a dynamic synergy between CMs, resident immune cells, and cardiac fibroblasts is the driving force behind cardiac renewal. Through intricate signaling mechanisms, these cell types coordinately instruct and support each other, facilitating CM proliferation and effectively repairing damaged heart tissue. "Understanding heart regeneration on a molecular level is an important step towards developing innovative therapeutics that can facilitate CM regeneration," said the team in their lay summary. "Our study challenges the existing paradigm, suggesting that targeting the microenvironment rather than a specific cell type is instrumental in healing the injured heart." The implications of this groundbreaking discovery are immense, offering glimpses of a future where heart disease may no longer be an irreversible condition but a challenge that can be overcome through medical intervention. The potential for developing novel therapies that leverage the body's innate regenerative capacity holds great promise for millions of individuals affected by heart disease worldwide. The work is supported by the National Heart, Lung, and Blood Institute (HL127717, HL130804, and HL118761 to JFM), the American Heart Association (AHA) (849706 to SL, 903651 to RGL, and 903411 to FM), the Don McGill Gene Editing Laboratory of The Texas Heart Institute (XL), and the Vivian L. Smith Foundation (JFM)