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Updated: May 25, 2026

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
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Mitigating Excessive Mitochondrial Fission Through the Development of a Selective Macrocyclic Inhibitor Targeting

Mulate Zerihun1, Sayan Chakraborty1, Ayetenew Abita1

  • 1The Azrieli Faculty of Medicine in the Galilee, Bar-Ilan University, Safed 1311502, Israel.

Journal of Medicinal Chemistry
|May 23, 2026
PubMed
Summary

Researchers developed CVP-764, a macrocyclic peptide, to inhibit mitochondrial fission proteins Fis1 and Mid51. This compound protects heart cells from stress by maintaining mitochondrial integrity and improving viability, showing promise for cardiovascular disease treatment.

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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Dynamics
  • Drug Discovery

Background:

  • Mitochondrial fragmentation, regulated by Fis1 and Mid51, is linked to cardiovascular disease.
  • Targeting protein-protein interactions (PPIs) in mitochondrial dynamics offers therapeutic potential.

Purpose of the Study:

  • To identify and optimize inhibitors of the Fis1/Mid51 PPI.
  • To evaluate the therapeutic efficacy and safety of these inhibitors in a cellular model of cardiovascular stress.

Main Methods:

  • Homologous sequence analysis and structure-guided design were used to identify peptide inhibitors.
  • Fluorescence polarization assays assessed binding affinity.
  • H9c2 cardiomyocytes were used to evaluate cellular effects under stress.
  • In silico ADMET profiling and preliminary in vivo toxicity studies were performed.

Main Results:

  • A linear peptide inhibitor (CVP-240) and its macrocyclic derivative (CVP-764) were developed, targeting the Fis1/Mid51 PPI.
  • CVP-764 demonstrated high affinity binding to Mid51, selectively disrupted Fis1/Mid51 signaling, and showed nanomolar binding.
  • In cardiomyocytes, CVP-764 preserved mitochondrial function, reduced oxidative stress, and enhanced cell viability.
  • Macrocyclization improved stability and cell permeability; in silico and in vivo studies suggested a favorable safety profile.

Conclusions:

  • CVP-764 is a potent and selective inhibitor of the Fis1/Mid51 interaction.
  • The macrocyclic derivative exhibits enhanced stability, cell permeability, and a promising safety profile.
  • CVP-764 represents a promising lead compound for therapeutic intervention in pathological mitochondrial fission associated with cardiovascular disease.