Phase 2 trial of GLPG3667 for SLE now recruiting patients in US

Novel oral therapy from Galapagos aims to ease lupus severity

Marisa Wexler, MS avatar

by Marisa Wexler, MS |

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Galapagos officially has launched a Phase 2 clinical trial that will test its oral therapy GLPG3667 — designed to ease disease severity in people with systemic lupus erythematosus (SLE) — at a half dozen sites in the U.S.

The first participant has been randomized, or assigned to a treatment group, in the placebo-based study, the company announced in a press release. The trial is double-blind, meaning neither participants nor researchers will know which patients are receiving GLPG3667 and which are given the placebo.

Called GALACELA (NCT05856448), the trial is expected to enroll 140 adults with SLE, ages 18 to 75, who are experiencing notable disease activity despite treatment with at least one standard therapy, such as an antimalarial or immunosuppressant. It’s enrolling patients at study centers in California, Florida, North Carolina, and Texas.

“We are proud to have reached this important milestone in our journey to improve the lives of patients living with autoimmune diseases,” said Daniele D’Ambrosio, MD, PhD, therapeutic area head immunology at Galapagos.

“We are excited about GLPG3667’s potential to make a meaningful difference for people living with SLE,” D’Ambrosio added.

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Phase 2 trial of GLPG3667 expected to enroll 140 SLE patients

In the trial, participants will be given GLPG3667 or the placebo once daily for 32 weeks, or nearly eight months.

Its main goal is to compare the proportion of patients who achieve a response in the SLE responder index (SRI)-4 by the study’s end. The SRI-4 is a composite assessment of lupus severity; a response on SRI-4 basically means that some measures of disease activity have gotten less severe, while others have remained stable.

Several other standardized measures of lupus severity and activity also will be evaluated in the trial, along with assessments of the safety and pharmacological profile of GLPG3667 in people with SLE.

Lupus is caused by the immune system launching an attack that erroneously targets the body’s own healthy tissues. This autoimmune attack is coordinated by signaling molecules called cytokines, which bind to receptors on immune cells, activating a chain of events that ultimately spur them to go on the offensive.

GLPG3667 is designed to block the activity of a protein known as tyrosine kinase 2, or TYK2, which plays a key role in the molecular processes underlying immune cells’ response to cytokines. By blocking TYK2, the experimental therapy is expected to diminish immune cells’ reactions to these inflammatory signaling molecules, ultimately reducing the autoimmune attack that drives SLE.

Previous experiments done in healthy human volunteers have indicated that immune cells in people treated with GLPG3667 are less responsive to certain cytokines known to play a central role in SLE, implying that the therapy works as intended.

“Although significant progress has been made in the management of SLE over the past decade, flares … and mortality continue to remain a significant concern,” D’Ambrosio said, adding that researchers “look forward to advancing this candidate medicine in clinical development.”