CIGB-552 is a cell-penetrating peptide with antitumor properties, exhibiting an IC50 of 23 μM in H460 cells. It increases the level of COMMD1 protein and significantly inhibits the NF-κB signaling pathway. Furthermore, CIGB-552 promotes apoptosis (apoptosis) of tumor cells and induces accumulation of reactive oxygen species (ROS) within them. Additionally, it possesses anti-inflammatory and anti-angiogenic effects. CIGB-552 is applicable in research related to lung and colon cancer.

CIGB-552, when applied at concentrations of 20-60 μM for 5 hours, increases the protein levels of the tumor suppressor COMMD1. At 25 μM for 0-12 hours, it facilitates the ubiquitin-mediated degradation of RelA and suppresses NF-κB signaling in H460 cells. With 25 μM exposure over 0-24 hours, CIGB-552 elevates pro-apoptotic proteins and reduces anti-apoptotic proteins in H460 cells. Administering CIGB-552 at 25 μM for 24-48 hours induces apoptosis in lung cancer cells. Additionally, at 25 μM for 8 hours, it decreases the antioxidant capacity of H460 cells, leading to oxidative damage of proteins and lipids. In a 37.5 μM dose for 1 hour, it induces the accumulation of reactive oxygen species (ROS) by inhibiting SOD1 activity, selectively killing tumor cells. At 75-150 μM for 24 hours, CIGB-552 significantly inhibits TNF-α-induced NF-κB activation. Furthermore, using 2.5-25 μM for 24 hours, it exerts anti-angiogenic effects by inhibiting hypoxia-induced HIF-1 activation through COMMD1.

CIGB-552, administered at 1 mg/kg through subcutaneous injection three times a week for three weeks, significantly impedes tumor growth in mice with lung cancer and extends survival time without notable toxicity. Additionally, CIGB-552, delivered at doses of 0.2-1.4 mg/kg via subcutaneous injection twice weekly for two weeks, effectively suppresses tumor growth in mice with colon cancer and exhibits anti-angiogenic properties.