Systemic Lupus Erythematosus (SLE)
B cells, a type of immune cell, are over-activated in SLE and produce antibodies that recognize the body’s own cellular components (autoantibodies) leading to abnormal immune response damaging healthy tissue and organs. These processes may be present years before a patient experiences the symptoms. Blocking B cell activation may be the key to treating SLE. While Bruton’s tyrosine kinase (BTK) inhibitors have been shown to inhibit B cell activation in laboratory settings, none are currently available to treat SLE.
Blocking B cell activation may be the key to treating SLE.
In the last 60 years, only one new medicine, belimumab (Benlysta) has been approved to treat lupus. However, currently available treatments fail to provide a long-lasting benefit to many patients. Consequently, SLE remains a significant, medically underserved disease.
AC0058 is a BTK inhibitor that blocks B cell activation, which may be the key to treating SLE.
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For detailed information about completed and ongoing clinical studies for AC0058, ACEA’s BTK inhibitor, please visit www.clinicaltrials.gov.
For detailed information about completed and ongoing clinical studies for Abivertinib (AC0010), ACEA’s dual EGFR/BTK inhibitor, please visit www.clinicaltrials.gov.