
Sun Pharma announces top-line results of tildrakizumab 100 mg Phase 3 studies
Sun Pharmaceutical Industries announced top-line results from two Phase 3 clinical studies evaluating the efficacy and safety of tildrakizumab 100 mg (ILUMYA) administered over 24 weeks for treatment of active psoriatic arthritis.
Treatment with tildrakizumab 100 mg (ILUMYA) resulted in greater improvements in PsA signs and symptoms at Week 24 compared to treatment with placebo. Both the INSPIRE-1 and INSPIRE-2 studies achieved the primary endpoint, with a higher proportion of patients in the INSPIRE-1 and INSPIRE-2 studies treated with tildrakizumab achieving ACR20 responses at week 24, compared to those receiving placebo (p < 0.05).
"We are excited to share that both the INSPIRE-1 and INSPIRE-2 clinical trials have successfully met their primary endpoints. These top-line results reinforce the therapeutic potential of ILUMYA as a treatment option for patients with active psoriatic arthritis. We extend our sincere gratitude to the patients, healthcare professionals and administrators whose contributions made the studies possible. We look forward to sharing the complete clinical data in the near future, said Marek Honczarenko, MD, PhD, Senior Vice President and Head of Global Specialty Development at Sun Pharma.
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What we think is happening We propose that when blood-vessel cells turn into "zombies", they pump out substances that make blood thicker and prone to forming tiny clots. These clots slow down circulation, so less oxygen reaches muscles and organs. This is one reason people feel drained. During exercise, the problem worsens. Instead of the vessels relaxing to allow adequate bloodflow, they tighten further. This means that muscles are starved of oxygen and patients experience a crash the day after exercise. In the brain, the same faulty cells let blood flow drop and leak, bringing on brain fog and dizziness. In the gut, they weaken the lining, allowing bits of bacteria to slip into the bloodstream and trigger more inflammation. Because blood vessels reach every corner of the body, even scattered patches of these "zombie" cells found in the blood vessels can create the mix of symptoms seen in long-COVID and ME/CFS. Immune exhaustion locks in the damage Some parts of the immune system kill senescent cells. They are natural-killer cells, macrophages and complement proteins, which are immune molecules capable of tagging and killing pathogens. But long-COVID and ME/CFS frequently have impaired natural-killer cell function, sluggish macrophages and complement dysfunction. Senescent endothelial cells may also send out a chemical signal to repel immune attack. So the "zombie cells" actively evade the immune system. This creates a self-sustaining loop of vascular and immune dysfunction, where senescent endothelial cells persist. In a healthy person with an optimally functioning immune system, these senescent endothelial cells will normally be cleared. But there is significant immune dysfunction in ME/CFS and long-COVID, and this may enable the "zombie cells" to survive and the disease to progress. Where the research goes next There is a registered clinical trial in the US that is investigating senescence in long-COVID. Our consortium is testing new ways to spot signs of ageing in the cells that line our blood vessels. First, we expose healthy endothelial cells in the lab to blood from patients to see whether it pushes the cells into a senescent, or "zombie," state. At the same time, we are trialling non-invasive imaging and fluorescent probes that could one day reveal these ageing cells inside the body. In selected cases, tissue biopsies may later confirm what the scans show. Together, these approaches aim to pinpoint how substances circulating in the blood drive cellular ageing and how that, in turn, fuels disease. Our aim is simple: find these ageing endothelial cells in real patients. Pinpointing them will inform the next round of clinical trials and open the door to therapies that target senescent cells directly, offering a route to healthier blood vessels and, ultimately, lighter disease loads. (The Conversation) NSA NSA