Corvus Presents New Data on its Investigational ITK Inhibitor CPI-818 at the American Society of Hematology (ASH) Annual Meeting & Exposition - Seite 2

The poster highlighting updated data from the Phase 1/1b study was presented on Sunday, Dec. 6 by Michael S. Khodadoust, MD, PhD, Division of Medical Oncology, Stanford University School of Medicine. Key highlights from the presentation include:

• Of the seven evaluable patients with PTCL, there have been two objective tumor responses as of the cut-off date of October 5, 2020 (the “Cut-Off Date”):
  • One patient, who previously failed chemotherapy and high dose chemotherapy with autologous bone marrow transplantation, achieved a complete response (CR) with CPI-818 at month 8 that remained ongoing after 12 months on study. The patient received CPI-818 for 12 months and the CR persisted beyond discontinuation of therapy (per the study protocol, the patient stopped receiving therapy after 12 months on study). As of December 1, 2020, this patient was off all therapy for lymphoma and remains disease free at 14+ months.
  • One patient who failed multiple prior therapies achieved a partial response at four months on therapy and remained on study as of the Cut-Off Date.
    
    
• Of the 11 evaluable patients with CTCL:
  
  • One patient achieved a complete response in lymph node disease and continued to have stable cutaneous disease at more than 12 months on therapy as of November 2, 2020.
  • Three patients achieved stable disease on therapy for between 3 and 5 months..
    
    
• There was a dose dependent increase in receptor occupancy, with trough occupancy >75% observed at the 200, 400 and 600 mg doses.
  
  
• No dose limiting toxicities and no grade 3 or 4 treatment related adverse events were observed as of the Cut-Off Date.
  

The ITK Inhibitor CPI-818 Blocks Activation of T Cells from Autoimmune Lymphoproliferative Syndrome (ALPS) Patients and Is Active in a Murine Model of ALPS (Abstract #95)

ALPS is a rare genetic disease affecting children that manifests with lymphadenopathy, splenomegaly, cytopenias (low blood counts) and autoimmunity. The disease is caused by a mutation in the Fas gene, which provides instructions for making a signaling protein involved in the induction of apoptosis. The mutation results in immune dysregulation due to abnormally high levels of “double negative” T cells (CD4 and CD8 double negative), which infiltrate the blood, spleen and lymphoid tissues. A similar mutation occurs in Fas-deficient MRL/lpr mice, which are used as a model for this disease. These mice are frequently also used as a model for autoimmune disease.