Lucicebtide (ST101) effect on hPBMCs-derived M2-type macrophages.

Reprogramming immunosuppressive M2-like macrophage to immune-active M1-like macrophage represents a promising strategy to improve responses to immunotherapy. Lucicebtide (previously referred to as ST101) is a peptide antagonist of the transcription factor C/EBPβ, a key activator of the transcriptional program in immunosuppressive macrophages. We show that Lucicebtide exposure reprograms human Perypheral Blood Mononuclear cells (hPBMSc)-derived M2-like macrophage to the pro-inflammatory M1-like phenotype. RNAseq tracriptional profiling of M2-like macrophages untreated or treated with Lucicebtide induces a substantial dowregulation of the M2-program and a subset of known C/EBPβ targets. Taken togheter, these data highlight the ability of Lucicebtide to rewire the M2-like immunosuppressive program and support combinatorial stategies to potentiate immunotherapy approaches. RNA-seq profiling of hPMBCs-derived M2-like cultures untreated or treated with 10 μM Lucicebtide.