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First-In-Class Thiosemicarbazone Metal Complexes Targeting the Sigma-2 Receptor (S2R) as an Innovative Strategy

Alessandra Barbanente1, Joanna Kopecka2, Daniele Vitone1

  • 1Department of Chemistry, University of Bari Aldo Moro, Via E. Orabona, 4, 70125 Bari, Italy.

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Summary

FA4-copper complexes show potent activity against pancreatic cancer by inducing cell death. This novel therapy warrants further investigation for pancreatic cancer treatment.

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Area of Science:

  • Oncology
  • Medicinal Chemistry
  • Molecular Biology

Background:

  • Pancreatic cancer has a high incidence and low survival rate, necessitating novel therapeutic strategies.
  • The sigma-2 receptor (S2R) is implicated in tumor progression and represents a therapeutic target.
  • Thiosemicarbazones (TSCs) are a class of compounds investigated for their anti-cancer properties.

Purpose of the Study:

  • To synthesize and evaluate copper(II) and platinum(II) complexes of FA4, a sigma-2 receptor-targeting thiosemicarbazone.
  • To compare the efficacy of these novel complexes against pancreatic cancer models.
  • To investigate the mechanism of action of the most potent compound.

Main Methods:

  • Synthesis of FA4-metal complexes (Cu(II) and Pt(II)) and control TSC 1-metal complexes.
  • In vitro cytotoxicity assays to determine efficacy.
  • Apoptosis assays and analysis of endoplasmic reticulum (ER) and mitochondrial stress.
  • In vivo studies using a preclinical PANC-1 pancreatic cancer model.

Main Results:

  • FA4-copper complexes demonstrated significantly higher in vitro cytotoxicity compared to FA4-platinum complexes and control TSCs.
  • FA4-copper induced apoptotic cell death through ER and mitochondrial stress, exhibiting greater potency than FA4 alone.
  • In vivo studies confirmed that FA4-copper was more effective than FA4, TSC 1, and TSC 1-copper in a preclinical pancreatic cancer model.

Conclusions:

  • FA4-copper complexes represent a promising therapeutic strategy for pancreatic cancer.
  • Targeting the sigma-2 receptor with FA4-copper warrants further clinical investigation.
  • The induction of ER and mitochondrial stress is a key mechanism for FA4-copper's anti-cancer activity.