Scientist

Eikon Therapeutics Appoints Ching-Pin Chang, M.D., Ph.D. as Executive Vice President and Chief Scientific Officer TMCnet News [September 03, 2026] | / | Eikon Therapeutics Appoints Ching-Pin Chang, M.D., Ph.D. as Executive Vice President and Chief Scientific Officer MILLBRAE, Calif., Sept. 03, 2026 (GLOBE NEWSWIRE) - Eikon Therapeutics, Inc. (Nasdaq: EIKN) ("Eikon"), a late-stage clinical biopharmaceutical company dedicated to developing innovative medicines to address serious unmet medical needs, today announced the appointment of Ching-Pin ("CP") Chang, M.D., Ph.D. as Executive Vice President and Chief Scientific Officer. Dr. Chang is a physician-scientist and accomplished research leader with more than two decades of experience spanning academic medicine, foundational research, and drug discovery. He joins Eikon from Bristol Myers Squibb, where he most recently served as Vice President, Head of Cardiovascular Discovery Biology and Translational Pharmacology. "CP is an exceptional physician-scientist whose pioneering basic research in developmental genetics and cardiomyopathies while a student, post-doctoral fellow, and faculty member at Stanford University led to leadership roles in the biopharmaceutical industry, where he demonstrated an ability to translate deep insights about human disease biology into transformative therapies," said Roger M. Perlmutter, M.D., Ph.D., Chairman and Chief Executive Officer of Eikon Therapeutics. "His scientific judgment, translational expertise, and experience building high-performing research organizations will be invaluable as we apply our differentiated discovery capabilities to create important new medicines." Prior to joining Bristol Myers Squibb, Dr. Chang served as Head of Cardiovascular Research at Gilead Sciences and then as Vice President of Disease Biology at MyoKardia, where he built a disease biology program focused on understanding and targeting the genetic causes of cardiomyopathies and the characterization of mavacamten, which was later approved for the treatment of hypertrophic cardiomyopathy. "It's an honor to join Eikon and work alongside leaders who have helped develop some of the most important medicines of our time," said Dr. Chang. "This is an exciting moment for the company as its late-stage portfolio advances and technology and AI opens new possibilities across drug discovery and development. With its ability to generate novel biological data at exceptional scale, Eikon is well positioned to capitalize on these advances and bring breakthrough therapeutics to patients with serious illnesses." In addition to his industry experience, Dr. Chang built an accomplished academic career centered on developmental genetics, especially as related to cardiomyopathies. He established his own laboratory at Stanford to study genetic, epigenetic, and RNA-based mechanisms underlying abnormal cardiovascular development and heart failure. He later moved his laboratory to Indana University School of Medicine where he held the Charles Fisch Endowed Chair of Cardiology and also directed Molecular and Translational Medicine at the Krannert Institute of Cardiology. Dr. Chang completed his medical degree at National Taiwan University before moving to the United States, where he earned his Ph.D. in cancer biology at Stanford University, focusing on molecular interactions between protooncogenes and oncogenic mechanisms. He went on to complete medical residency training at Massachusetts General Hospital, a cardiology fellowship at Stanford University, and a physician-scientist research fellowship at the Howard Hughes Medical Institute, a training arc that grounded him both in clinical practice and in fundamental research. About Eikon Therapeutics Eikon is a late-stage clinical biopharmaceutical company dedicated to building a global, fully-integrated organization developing innovative medicines to address serious unmet medical needs. Eikon's initial focus is oncology, where it is advancing a pipeline of drug candidates targeting areas of high unmet need that could eventually become critical medicines for the treatment of various cancers. Eikon deploys its technology platform, including its proprietary single molecule tracking system, to develop internally-derived novel therapies, while also leveraging the deep expertise of its management team to in-license promising assets. Eikon's vision is to become a generational leader, by purposefully integrating traditional biology research with advanced engineering to develop better medicines faster. For more information, visit www.eikontx.com. Forward-Looking/Safe Harbor Statements This press release contains forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. All statements in this press release that are not historical facts are hereby identified as forward-looking statements for this purpose. These statements may be identified by words such as "aims," "anticipates," "believes," "could," "estimates," "expects," "forecasts," "goal," "intends," "may," "plans," "possible," "potential," "seeks," "will" and variations of these words or similar expressions that are intended to identify forward-looking statements, although not all forward-looking statements contain these words. Forward-looking statements in this press release include, but are not limited to, statements regarding: the therapeutic potential, safety, and efficacy of Eikon's product candidates; the timing for anticipated data readouts; expected milestones and business objectives for 2026 and beyond; and other statements regarding Eikon's future operations, financial performance, financial position, prospects, objectives, strategies and other future events. These forward-looking statements are based upon management's current expectations and assumptions, and are subject to a number of risks, uncertainties and other factors that could cause actual results and events to differ materially and adversely from those indicated by such forward-looking statements including, among others: its limited operating history; its significant net losses incurred since inception and the likelihood of incurring additional losses for the foreseeable future; its need for substantial additional funding; the early stage of development of many of its product candidates and the possibility that its product candidates may fail in development; its dependence on the success of its current product candidates; its ability to leverage its technology platform to enable more informed drug research and development; legal and regulatory risks; intellectual property-related risks; and those risks, uncertainties and other factors discussed under the caption "Risk Factors" and elsewhere in Eikon's Quarterly Report on Form 10-Q for the quarter ended June 30, 2026, filed with the Securities and Exchange Commission ("SEC") on August 13, 2026, and in other public filings with the SEC in the future. As a result, you should not place undue reliance on any forward-looking statements. The forward-looking statements made in this press release speak only as of the date of this press release, and Eikon undertakes no obligation to update such forward-looking statements, whether as a result of new information, future developments or otherwise, except as required by law. Contacts: Investors Alfred "Freddie" Bowie, Ph.D., CFO [email protected] Media Colin Sanford [email protected] [ Back To TMCnet.com's Homepage] |

J&J-Bristol Myers milvexian misses Phase 3 LIBREXIA ACS endpoint in full ESC readout. The 14,194-patient study found no reduction in cardiovascular death, heart attack or ischemic stroke with milvexian, confirming the trial's earlier futility stop. Published August 29, 2026 · 1:53 PM ET Johnson & Johnson and Bristol Myers Squibb's milvexian failed to reduce major cardiovascular events in the Phase 3 LIBREXIA ACS trial, according to the full results presented Saturday at ESC Congress 2026. The readout puts numbers around an efficacy failure that the companies had already signaled when they stopped the study for futility in November 2025. After a median follow-up of 10 months, cardiovascular death, myocardial infarction or ischemic stroke occurred in 5.4% of patients assigned to milvexian and 5.1% of those receiving placebo. The hazard ratio was 1.05, with a 95% confidence interval of 0.91 to 1.21 and a p-value of 0.50, leaving no evidence that the 25 mg twice-daily regimen improved the trial's primary efficacy endpoint. The European Society of Cardiology's full LIBREXIA ACS readout also showed no difference in the principal safety endpoint of intracranial or fatal bleeding. That endpoint occurred in 0.3% of patients in each group, with a hazard ratio of 1.04 and a 95% confidence interval of 0.58 to 1.87. Full results confirm the efficacy miss. LIBREXIA ACS randomized 14,194 patients at 893 sites in 44 countries to oral milvexian 25 mg twice daily or matched placebo. Participants had experienced an acute coronary syndrome within seven days and had either undergone cardiac catheterization with percutaneous coronary intervention or were being managed conservatively. They also had to carry at least two factors associated with a higher risk of recurrent ischemic events, and all received antiplatelet therapy selected by the investigator. The neutral result was not limited to the primary composite. ESC reported no difference between milvexian and placebo in the individual components of cardiovascular death, myocardial infarction and ischemic stroke, and no improvement in major secondary efficacy endpoints including all-cause mortality. In other words, the trial did not reveal an efficacy signal elsewhere that could offset the missed primary endpoint. Milvexian did have the expected pharmacodynamic effect. Patients taking the drug showed prolonged activated partial thromboplastin time, which the investigators said indicated anticoagulant activity at the tested dose. That finding makes the result more informative than a simple failure to demonstrate drug exposure, but it does not establish why inhibiting factor XIa failed to reduce events in this post-ACS setting. The safety data are more nuanced than the efficacy result. Intracranial or fatal bleeding was not increased, which is relevant because the development thesis for factor XIa inhibitors has centered on reducing thrombosis while avoiding some of the bleeding burden associated with conventional anticoagulation. LIBREXIA ACS did not demonstrate the hoped-for reduction in ischemic events, however, so the favorable comparison on that narrow safety endpoint could not rescue the study's benefit-risk proposition for this indication. The trial had already been stopped for futility. The endpoint miss itself was not a surprise by the time the ESC numbers arrived. On November 14, 2025, Bristol Myers Squibb and Johnson & Johnson announced that they would stop LIBREXIA ACS after a preplanned interim review by the independent data monitoring committee concluded that the trial was unlikely to meet its primary efficacy endpoint. At that time, the companies said no new safety concerns had been identified and that the other two Phase 3 LIBREXIA studies would continue. ClinicalTrials.gov now lists the ACS study as completed, with an actual primary completion and study completion date of February 6, 2026 and actual enrollment of 14,194 patients. The August 29 ESC presentation is therefore important because it provides the full numerical outcome rather than simply repeating the earlier futility decision. Investors already knew the ACS program had failed to clear its planned efficacy bar; the new information shows the size and direction of the difference between milvexian and placebo and confirms that the formal analysis did not overturn the interim conclusion. The setting was always a demanding test for an additional antithrombotic drug. Patients after an acute coronary syndrome remain at risk of recurrent ischemic events even after modern interventions and antiplatelet therapy, but adding anticoagulation can raise bleeding risk. Factor XIa inhibition has attracted attention because factor XI participates in thrombus formation while appearing less central to normal hemostasis than some established anticoagulation targets. LIBREXIA ACS tested whether that mechanism could add protection on top of standard post-ACS therapy without creating an unacceptable bleeding penalty. Milvexian's broader Phase 3 program continues. Johnson & Johnson and Bristol Myers Squibb are developing milvexian across three major thrombotic indications. In 2023, Johnson & Johnson said the FDA had granted Fast Track designation for the acute coronary syndrome, atrial fibrillation and secondary stroke-prevention programs. The companies described the combined LIBREXIA program as involving nearly 50,000 patients, although milvexian remains investigational and is not approved for any indication. The two remaining Phase 3 studies address different clinical questions from ACS. LIBREXIA AF compares milvexian with apixaban in patients with atrial fibrillation and was listed by ClinicalTrials.gov in July as active but not recruiting, with 20,284 participants and an estimated primary completion date of October 31, 2026. LIBREXIA STROKE is evaluating milvexian against placebo on top of antiplatelet therapy after acute ischemic stroke or high-risk transient ischemic attack; Johnson & Johnson's trial registry shows enrollment complete and a study end date in December 2026. Those distinctions matter because the ACS failure does not automatically determine the outcome of the atrial-fibrillation or stroke studies. The patient populations, background therapies, comparators and efficacy endpoints differ, and the ESC investigators specifically cautioned that the remaining trials test milvexian in clinically distinct settings. The ACS result nevertheless removes one large potential indication from the development case unless future analysis produces a materially different regulatory path. Bristol Myers Squibb had described milvexian as a potential multi-billion-dollar asset when the ACS study was halted in 2025. With the full ACS data now confirming no efficacy benefit, the commercial breadth of that thesis depends more heavily on the two remaining Phase 3 programs. The next concrete milestones are the planned completion of LIBREXIA AF later in 2026 and LIBREXIA STROKE afterward, though completion dates do not necessarily indicate when topline results will be released.

AstronauTx turns sleep into new dementia target. AstronauTx has exercised its Saniona option, advancing a sleep-focused neurodegeneration candidate toward IND-enabling studies. Sleep has become one of the most talked-about levers in longevity science, credited with everything from metabolic health to cognitive resilience. AstronauTx, a UK biotech founded by SV Health's Dementia Discovery Fund, is now translating that interest into a drug pipeline. The company has exercised its option under a 2023 research collaboration with Danish biopharma Saniona, securing exclusive worldwide rights to develop, manufacture and commercialise a development candidate, ATX0926, that emerged from the partnership [1]. The molecule targets a novel, still-undisclosed ion channel, discovered using Saniona's IonBase platform, that AstronauTx believes influences glymphatic flow, the process by which the brain clears metabolic waste, largely during sleep. ATX0926 is now expected to enter IND-enabling studies, the battery of safety and manufacturing work required before a drug can be tested in humans. Sleep architecture as a disease driver, not just a symptom. AstronauTx's underlying thesis, unusual enough to be worth spelling out, is that changes in sleep architecture do not simply accompany neurodegenerative disease; they may help cause it. The company is working on the premise that slow-wave sleep, the deep sleep stage most associated with memory consolidation and brain clearance, is a modifiable risk factor for conditions including dementia. Improving it, rather than simply monitoring it, is the stated goal. "Exercising this option reflects the strength of the science that has come out of our collaboration with Saniona and our conviction in this target and its mechanism of promoting glymphatic flow as a potential new approach to treating neurological disease," said Jane Rhodes, CEO of AstronauTx. The company says its approach leans on quantifiable endpoints, including EEG-based sleep architecture metrics and measures of cognitive function and glymphatic flow, rather than symptom-based scales alone, an attempt to bring more objective biomarkers to a field that has historically struggled with them. What Saniona gets out of the deal. For Saniona, the option exercise converts years of discovery work into near-term value and a longer-term royalty stream. The company will receive AstronauTx Series A shares worth US$5 million, priced on the same terms as AstronauTx's October 2023 Series A round, and will book that amount as income. Beyond the equity, Saniona is eligible for up to US$172 million in development, regulatory and commercial milestones, split roughly $97 million for the earlier stages and $75 million for commercial success, plus tiered royalties on any eventual product sales. "AstronauTx's decision to exercise its option is a strong endorsement of both the scientific progress achieved through our collaboration and Saniona's ion channel discovery platform," said Thomas Feldthus, CEO of Saniona. "It demonstrates our ability to generate and advance high-quality development candidates together with world-class partners while enabling us to retain meaningful long-term value through equity ownership, milestones and royalties." The deal adds to a growing list of external validations for Saniona's ion channel platform, which also underpins research collaborations with Boehringer Ingelheim and Cephagenix, alongside licensing arrangements with Jazz Pharmaceuticals, Acadia Pharmaceuticals and Medix. For AstronauTx, backed by a $61 million Series A that included the Novartis Venture Fund and Bristol Myers Squibb, ATX0926 becomes the clearest test yet of whether sleep biology can be turned into a clinical-stage neurology pipeline. LTUI: 2700 AstronauTx. Powered by: Longevity level(s): * Level 6: Aging disease prevention therapeutics Overview. AstronauTx is a biotechnology company headquartered in London, United Kingdom, focused on developing small-molecule therapeutics targeting neurodegenerative diseases, particularly Alzheimer's disease. The company employs a novel approach centered on enhancing slow-wave sleep architecture and restoring glymphatic function to reduce pathological protein accumulation in the brain. By modulating astrocyte biology and correcting disrupted brain physiology, AstronauTx aims to deliver both symptomatic relief and disease-modifying benefits. The company's platform represents a distinctive strategy to address neurodegeneration through physiological restoration rather than conventional symptomatic management. Access all data points on DLT: * Financial Data * Patents * Technology * Management * Advisory Board * News * Classifications * Similar Companies