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Preventive Use of MPL-C Immunomodulator Reduces Cardiac Infarct Size

Strategic Insights

— 1 min read

Researchers from the Medical College of Wisconsin, the Good Samaritan Hospital Heart Institute, the University of Southern California, and the Hatter Institute have found that the preventive use of MPL-C immunomodulator significantly reduces cardiac infarct size by more than 50% compared to controls. This discovery was made through preclinical data presented at the American Heart Association 68th Scientific Sessions. According to the data, MPL-C may act through a cellular electrophysiologic system, believed to play an important role in cardioprotection against ischemia and reperfusion injury.

Key Takeaways:

  • The preventive use of MPL-C immunomodulator reduced cardiac infarct size by more than 50% in three animal models compared to controls.
  • MPL-C may influence a cellular electrophysiologic system known as the adenosine triphosphate-sensitive potassium (KATP) channel, which is associated with eflux of potassium from the cell, preservation of cellular energy (ATP), and prevention of intracellular calcium overload.
  • The activation of the KATP channel is believed to be important in preconditioning myocardial tissue against ischemia.
  • The use of MLP-C mimicked the effect on 5'-nucleotidase produced by ischemic preconditioning, where the heart is transiently rendered ischemic prior to induction of prolonged ischemia.
  • MPL-C cardioprotective effect was eliminated when a KATP blocker was administered in one of the studies.
  • The data suggest that MPL-C could be a useful chemical mimetic of ischemic preconditioning, which could be beneficial in protecting cardiac tissue against prolonged ischemia.

Statistics:

  • The preventive use of MPL-C reduced cardiac infarct size by 50% or more in three animal models.
  • The administration of a KATP blocker eliminated the MPL-C cardioprotective effect.
  • The data demonstrated that MPL-C may significantly influence the activity of 5'-nucleotidase, an enzyme that helps to regulate adenosine metabolism.
  • The animal study showed that the use of MPL-C mimicked the effect on 5'-nucleotidase produced by ischemic preconditioning.

Sources:

  • Ribi ImmunoChem Research, Inc.
  • American Heart Association 68th Scientific Sessions
  • Medical College of Wisconsin
  • Good Samaritan Hospital Heart Institute
  • University of Southern California
  • Hatter Institute, University College Hospital, London
  • PR Newswire

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