Equillium Presents Clinical Data from EQUALISE Phase 1b Study in Lupus Patients at the American Society of Nephrology Annual Meeting
Sustained decrease in proteinuria observed in subgroup of patients with systemic lupus erythematosus, without lupus nephritis, following two doses of itolizumab
Dose dependent decreases in inflammatory marker CD6 following itolizumab administration
Excerpt from the Press Release:
LA JOLLA, Calif.–(BUSINESS WIRE)–Equillium, Inc. (Nasdaq: EQ), a clinical-stage biotechnology company developing itolizumab to treat severe autoimmune and inflammatory disorders with high unmet medical need, today announced interim data from the Type A portion of the Phase 1b EQUALISE study that showed promising clinical activity in patients with systemic lupus erythematosus (SLE), and pharmacokinetic and pharmacodynamic data supporting the anti-CD6 mechanism of itolizumab. The data were presented in two separate posters, both by Chaim Putterman, M.D., Professor of Medicine, Albert Einstein College of Medicine, at the American Society of Nephrology annual meeting.
“These data provide additional insights into the promise of itolizumab as a potential therapy for patients with lupus,” said Dr. Putterman. “I am especially intrigued by the decreases in proteinuria of up to 53 percent in patients with elevated baseline levels of proteinuria or albuminuria. I look forward to additional data generated in the ongoing EQUALISE study of itolizumab in the TYPE B cohort of patients with lupus nephritis.”
In poster #1624, highlighting the exploratory subgroup analysis of SLE patients with elevated baseline levels of proteinuria or albuminuria, the data showed a decline in proteinuria of up to 53% following two doses of itolizumab. Proteinuria is used as a biomarker for potential kidney damage. Subcutaneous dosing of itolizumab was well tolerated with most adverse events being mild to moderate injection site reactions.
In a separate pharmacokinetic and pharmacodynamic poster (#1623), the data demonstrated dose-proportional increases in drug exposure and rapid and dose-dependent decreases of CD6 cell surface expression on CD4 cells in patients SLE.
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