GLMD News & Events

Galmed announces that following a restructuring of the acquisition terms, it consummated the acquisition of Colospan a commercial-stage medical device company that has developed a clinically differentiated solution to one of colorectal surgery's most pressing problems: anastomotic leak complications and the diverting stomas used to manage them. Restructured Anti-Dilutive Financial Terms: To diminish the dilutive event on GLMD's existing shareholders, Galmed and Colospan agreed that in lieu of issuing $2.0 million in Galmed ordinary shares at closing, the cash payment shall be increased by $800K. The remaining balance has been structured as a transparent, risk-mitigated earnout capped at $2.0 million, commencing in Q3 2027. This single-digit percentage earnout on net sales revenues is tied to clear performance tiers: a 7% payout on net sales revenue over $5.0 million, escalating to 9% for net sales revenue over $12.0 million. In addition, the parties agreed to an acceleration of the earnout upon the earlier of a strategic transaction involving substantially all of the acquired business or related intellectual property of Colospan, or Galmed raising at least $17.5 million in aggregate gross proceeds through equity financings. Galmed is laying the groundwork for a pan-European launch of CG-100, a less invasive intraluminal bypass device designed to protect colorectal anastomoses and reduce the need for diverting stomas. CG-100 benefits from strong safety and efficacy clinical data based on 4 clinical trials conducted in Europe between 2014 and 2024. In addition to generating top-line revenue already in 2026, "real-life" data from patients using CG-100 is planned to be submitted to the FDA to support Colospan' s Pivotal study. Strategic Synergy: Establishing a unified GI platform by leveraging drug development expertise with medical device commercialization.

Galmed and Tissue Dynamics announced results from a preclinical study evaluating a combination of Aramchol Meglumine, an SCD1 inhibitor, and a selective PPARalpha agonist. The study identified a previously unrecognized metabolic pathway involved in the progression of cardiac fibrosis and heart failure and demonstrated that the two-drug combination effectively targets this mechanism. Progressive cardiac fibrosis, driven by ischemic injury or age-related metabolic dysfunction, results in pathological scarring of the heart muscle, leading to tissue stiffening and impaired systolic and diastolic function. Cardiac fibrosis is a major contributor to heart failure progression and remains an area of significant unmet medical need. The study demonstrated that a combination of Aramchol Meglumine and a selective PPARalpha agonist modulates two key pathological processes-mitochondrial stress and associated lipogenesis-that contribute to the development and progression of cardiac fibrosis and heart failure. In inflammatory human cardiac organoids, the treatment reduced fibrotic burden by approximately fourfold while preserving cardiac muscle density and maintaining metabolic function. Based on these findings, a new patent application has been filed, and preparations are underway to support future IND-enabling activities.

Galmed and Tissue Dynamics announced results from a preclinical study evaluating a combination of Aramchol Meglumine, an SCD1 inhibitor, and a selective PPARalpha agonist. The study identified a previously unrecognized metabolic pathway involved in the progression of cardiac fibrosis and heart failure and demonstrated that the two-drug combination effectively targets this mechanism. Progressive cardiac fibrosis, driven by ischemic injury or age-related metabolic dysfunction, results in pathological scarring of the heart muscle, leading to tissue stiffening and impaired systolic and diastolic function. Cardiac fibrosis is a major contributor to heart failure progression and remains an area of significant unmet medical need. The study demonstrated that a combination of Aramchol Meglumine and a selective PPARalpha agonist modulates two key pathological processes-mitochondrial stress and associated lipogenesis-that contribute to the development and progression of cardiac fibrosis and heart failure. In inflammatory human cardiac organoids, the treatment reduced fibrotic burden by approximately fourfold while preserving cardiac muscle density and maintaining metabolic function. Based on these findings, a new patent application has been filed, and preparations are underway to support future IND-enabling activities.