Antitumor efficacy, pharmacokinetic and biodistribution studies of the anticancer peptide CIGB-552 in mouse models
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Maribel G Vallespí1, Gilmara Pimentel, Ania Cabrales-Rico
1Pharmaceutical Department, Center for Genetic Engineering and Biotechnology, P.O. Box 6162, Havana, 10600, Cuba.
Abstract:
Accumulation of the COMMD1 protein as a druggable pharmacology event to target cancer cells has not been evaluated so far in cancer animal models. We have previously demonstrated that a second-generation peptide, with cell-penetrating capacity, termed CIGB-552, was able to induce apoptosis mediated by stabilization of COMMD1. Here, we explore the antitumor effect by subcutaneous administration of CIGB-552 in a therapeutic schedule. Outstandingly, a significant delay of tumor growth was observed at 0.2 and 0.7 mg/kg (p < 0.01) or 1.4 mg/kg (p < 0.001) after CIGB-552 administration in both syngeneic murine tumors and patient-derived xenograft models. Furthermore, we evidenced that (131)I-CIGB-552 peptide was actually accumulated in the tumors after administration by subcutaneous route. A typical serine-proteases degradation pattern for CIGB-552 in BALB/c mice serum was identified. Further, biological characterization of the main metabolites of the peptide CIGB-552 suggests that the cell-penetrating capacity plays an important role in the cytotoxic activity. This report is the first in describing the antitumor effect induced by systemic administration of a peptide that targets COMMD1 for stabilization. Moreover, our data reinforce the perspectives of CIGB-552 for cancer targeted therapy.
Insights
The peptide CIGB-552 effectively delays tumor growth in cancer models by stabilizing the COMMD1 protein. This cell-penetrating peptide shows promise for targeted cancer therapy, with accumulation observed in tumor tissues.
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- The COMMD1 protein's role in cancer therapy is underexplored.
- Previous research identified CIGB-552, a cell-penetrating peptide, that induces apoptosis via COMMD1 stabilization.
Purpose of the Study:
- To evaluate the antitumor effect of systemically administered CIGB-552 in cancer models.
- To investigate the biodistribution and metabolic profile of CIGB-552.
Main Methods:
- Subcutaneous administration of CIGB-552 in syngeneic murine and patient-derived xenograft tumor models.
- Radioiodination of CIGB-552 with (131)I to track tumor accumulation.
- Analysis of CIGB-552 degradation in mouse serum and characterization of its metabolites.
Main Results:
- Significant delay in tumor growth was observed across multiple cancer models at various CIGB-552 doses (p < 0.01 and p < 0.001).
- (131)I-CIGB-552 demonstrated accumulation within tumor tissues following subcutaneous administration.
- A typical serine-protease degradation pattern was identified in mouse serum, and metabolites retained cell-penetrating capacity.
Conclusions:
- Systemic administration of CIGB-552 exhibits significant antitumor activity in preclinical cancer models.
- CIGB-552 demonstrates tumor accumulation and a defined metabolic profile, supporting its therapeutic potential.
- The findings highlight CIGB-552 as a promising candidate for targeted cancer therapy by stabilizing COMMD1.
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