1556 CSL324, a G-CSF receptor antagonist, blocks neutrophil migration markers that are upregulated in hidradenitis suppurativa

Neutrophils contribute to the pathophysiology of hidradenitis suppurativa (HS), a chronic debilitating inflammatory skin disease, yet their exact role remains be fully defined. Granulocyte colony-stimulating factor (G-CSF), major regulator neutrophil development and survival, can blocked by novel, human anti-G-CSF receptor (G-CSFR) monoclonal antibody CSL324. We investigated activation migration neutrophils in HS impact blocking G-CSFR with Neutrophil numbers were significantly higher lesions compared biopsies from healthy donors (HD)(p<0.0001). In peripheral blood samples, mean counts patients than HD. pathways increased demonstrated an phenotype, CXCR1 on surface HS. G-CSF was key driver transcriptomic changes elevated serum HD (p=0.013). Administration CSL324 randomized, double-blind, placebo-controlled study CSL324_1001 inhibited G-CSF-induced similar transcriptional those observed cohort, as highlighted expression genes related migratory capacity. Our data suggests that are due increase G-CSF-driven migration. counteracted reducing cell levels chemokine receptors.