Alzprotect, a French biopharmaceutical company, has successfully completed the open-label extension (OLE) phase following its Phase 2a clinical trial of AZP2006 (ezeprogind®), a treatment for Progressive Supranuclear Palsy (PSP). The results of this 6-month extension highlight the potential of AZP2006 to slow or stabilize disease progression, particularly when administered early.
Key Findings:
- Delay in Disease Progression: During the initial Phase 2a trial, patients treated with AZP2006 for 3 months showed early signs of delayed disease progression compared to those receiving a placebo.
- Stabilization in Early Disease: In the OLE phase, patients who began AZP2006 treatment early in their disease course showed significant stabilization of PSP symptoms, outperforming those who initially received a placebo during Phase 2a.
- Benefits for Late-Stage PSP: Patients who switched from placebo to AZP2006 during the OLE phase also experienced stabilization, suggesting AZP2006 could benefit patients in more advanced stages of the disease.
- Overall Progression: From baseline to the end of the OLE, the progression of PSP was significantly less in patients who had been receiving AZP2006 from the start, compared to those initially on placebo.
- Safety Profile: No notable safety concerns arose during the OLE phase, confirming the safety of long-term AZP2006 treatment.
- Precision in Symptom Tracking: The use of both the PSPRS-28 and the more precise PSPRS-10 scales reinforced the finding that patients who began active treatment early showed consistent stabilization of their PSP symptoms.
These results emphasize the importance of early intervention with AZP2006 in PSP treatment, with potential long-term benefits. Even late-stage patients showed improvement, highlighting AZP2006’s promise as a viable therapeutic option.
Alzprotect remains committed to further developing AZP2006 to provide a new treatment for PSP patients.
Dr. Artin Karapet, Chief Medical Officer, remarked, “The positive outcomes from the OLE phase mark a significant milestone for PSP patients. These findings demonstrate that AZP2006 can stabilize disease progression, even in advanced stages. Early and continuous treatment may be key to slowing the progression of PSP, offering renewed hope to the PSP community.”
Phil Verwaerde, Chief Executive Officer, added, “The results strongly support AZP2006’s potential to stabilize PSP, especially with early intervention. The stabilization in late-stage patients underscores the promise of this therapy in improving patient outcomes.”
AZP2006 works through a unique mechanism of action, distinct from existing treatments. It stimulates lysosome homeostasis—essential for maintaining brain function—by facilitating the entry of the Prosaposin-Progranulin complex into neurons, directly targeting the root causes of neurodegeneration.
