Gilead Sciences Presents Groundbreaking Data on Primary Biliary Cholangitis and Viral Hepatitis at EASL 2026
At the European Association for the Study of the Liver (EASL) Congress 2026, Gilead Sciences, Inc. (Nasdaq: GILD) unveiled new clinical insights aimed at advancing treatment options for primary biliary cholangitis (PBC) and viral hepatitis. The presentations, delivered during the May 27-30 event in Barcelona, highlight the company’s commitment to addressing critical gaps in liver disease management.
Advancing PBC Treatment with Livdelzi
Gilead’s focus on PBC centered around Livdelzi® (seladelpar), a first-in-class delpar (selective PPAR-delta agonist) approved for treating PBC in combination with ursodeoxycholic acid (UDCA) for patients with inadequate responses or as monotherapy for those unable to tolerate UDCA. The company presented findings from 29 abstracts, including late-breaking data from the Phase 3 RESPONSE trial (NCT04620733) and interim results from the ASSURE study (NCT03301506).
The RESPONSE trial data evaluated Livdelzi’s efficacy and safety in PBC patients with risk factors for disease progression, such as elevated liver stiffness and metabolic syndrome. Meanwhile, the ASSURE study explored the relationship between biochemical response and liver stiffness trends over 36 months, particularly in individuals with alkaline phosphatase (ALP) levels between 1 to 1.67x the upper limit of normal (ULN). These findings, according to Dr. Swati Tole, Senior Vice President of Clinical Development at Gilead, provide a “multidimensional view of Livdelzi’s potential” to address both disease activity and patient-reported symptoms like pruritus.
Expanding Viral Hepatitis Research
In addition to PBC, Gilead shared updates on its viral hepatitis initiatives, emphasizing the need for innovative therapies to combat persistent challenges in the field. While specific details about new compounds were not disclosed, the company reiterated its dedication to “advancing understanding and care” through ongoing research and collaboration with the global medical community.
Implications for Patient Care
The
Worth a look
- Unions Slam Ineffectiveness of French Education Ministry’s Heatwave Plan
- Florida Amendment 3: Property Tax Cuts vs. Public Services Impact
- Breakthrough Salk Study Uncovers Mechanism Behind Immunotherapy Resistance: Interferons, Mitochondrial Dysfunction, and PGE2″ Interferons, mitochondrial dysfunction and PGE2: Salk study reveals mechanism behind immunotherapy resistance. Boost its search engine visibility with relevant keywords for maximum impact. Immunotherapy resistance remains one of the biggest hurdles in cancer treatment. According to a recent study published in the journal Nature Communications, scientists at the Salk Institute have made a groundbreaking discovery that sheds light on the underlying mechanisms behind this resistance. The study reveals that interferons, a type of protein that plays a crucial role in the immune system, can contribute to mitochondrial dysfunction in cancer cells. This dysfunction can lead to the production of prostaglandin E2 (PGE2), a molecule that promotes tumor growth and resistance to immunotherapy. In their study, the researchers found that PGE2 production was a key factor in the development of immunotherapy resistance in cancer cells. The team used a combination of experimental and computational models to investigate the relationship between interferons, mitochondrial dysfunction, and PGE2 production. The findings of the study suggest that targeting PGE2 production could be a potential strategy for overcoming immunotherapy resistance. The researchers propose that blocking PGE2 receptors or inhibiting its production could help restore the function of mitochondria in cancer cells, making them more susceptible to immunotherapy. The study’s authors hope that their findings will pave the way for the development of new therapies that can overcome immunotherapy resistance and improve treatment outcomes for cancer patients. Key Takeaways: – Interferons contribute to mitochondrial dysfunction in cancer cells – Mitochondrial dysfunction leads to PGE2 production, promoting tumor growth and resistance to immunotherapy – Targeting PGE2 production could be a potential strategy for overcoming immunotherapy resistance – Restoring mitochondrial function in cancer cells could make them more susceptible to immunotherapy Keywords: immunotherapy resistance, interferons, mitochondrial dysfunction, PGE2, Salk Institute, cancer treatment, breakthrough study, Nature Communications. (archyworldys.com)