Lucicebtide acetate is a CCAAT/enhancer-binding protein β (CEBPB) inhibitor. It can be used in research on glioblastoma multiforme and recurrent melanoma.

KCL008 (Her2+/ER-/PR-):18.56 μM, C/EBPβ (ATF5):24.6 nM, KCL012 (Her2-/ER-/PR-):15.32 μM

Lucicebtide acetate (compound ST101 acetate) is a cell-penetrating specific peptide antagonist that binds C/EBPβ with nanomolar affinity and interferes with its heterodimer formation by targeting the leucine zipper structural domain of CCAAT/enhancer binding protein β (C/EBPβ). In contrast, Lucicebtide acetate binds weakly to C/EBPγ, with a strength difference of over 3000-fold. [1]
In a competitive ELISA, Lucicebtide acetate effectively inhibited the interaction of C/EBPβ with ATF5 with an IC50 of 24.6 nM, and induced the targeted degradation of C/EBPβ. In U251-LS and HCT116 cell lines, Lucicebtide acetate (20 μM for 24 h) reduced C/EBPβ protein expression by approximately 44% and 40%, respectively, while it did not have a significant effect on C/EBPγ protein levels. [1]
Lucicebtide acetate was also able to induce cell cycle arrest in cancer cells, with IC50s of 18.56 μM and 15.32 μM for KCL008 (Her2+/ER-/PR-) and KCL012 (Her2-/ER-/PR-) breast cancer cells, respectively, and did not show significant toxicity in normal human mammary epithelial cells (HMECs). toxicity to normal human mammary epithelial cells (HMECs). [1]

In animal studies, Lucicebtide acetate (injected subcutaneously at a dose of 50 mg/kg three times a week for three weeks) successfully induced significant tumor regression in mice bearing a subcutaneous xenograft model of U251 glioblastoma, and demonstrated a long-lasting antitumor effect. [1]