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Neutralizing RGMa with Elezanumab Promotes Cerebroprotection and Recovery in Rabbit Middle Cerebral Artery Occlusion.

Peer B Jacobson1, Andrea Mothe2, Aharon Levy3

  • 1Department of Translational Sciences, Imaging Research, AbbVie Inc., 1 North Waukegan Rd, North Chicago, IL, 60064, USA. peerbjacobson@gmail.com.

Translational Stroke Research
|June 16, 2023
PubMed
Summary
This summary is machine-generated.

Elezanumab, an antibody targeting repulsive guidance molecule A (RGMa), improved motor function and reduced neuroinflammation in a rabbit stroke model. This therapy shows potential for treating acute ischemic stroke (AIS) even with delayed intervention.

Keywords:
Acute ischemic strokeCerebroprotectionElezanumabMCAORGMaRabbit

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Area of Science:

  • Neuroscience
  • Immunology
  • Regenerative Medicine

Background:

  • Repulsive guidance molecule A (RGMa) inhibits neuronal growth and survival, and is elevated after central nervous system injury.
  • RGMa neutralization offers neuroprotection and promotes neuroplasticity in preclinical models.
  • Current acute ischemic stroke (AIS) treatments have limited time windows and strict patient criteria, highlighting a need for new therapies.

Purpose of the Study:

  • To evaluate elezanumab, a human anti-RGMa monoclonal antibody, for its efficacy in improving neuromotor function and reducing neuroinflammation in a rabbit model of AIS.
  • To assess the therapeutic potential of elezanumab with delayed intervention times up to 24 hours post-stroke.

Main Methods:

  • A rabbit embolic permanent middle cerebral artery occlusion (pMCAO) model was used to simulate AIS.
  • Rabbits received weekly intravenous infusions of elezanumab at various doses and time windows (6 and 24 hours post-stroke).
  • Neuromotor function was assessed, and neuroinflammation was evaluated by measuring microglial and astrocyte activation.

Main Results:

  • Elezanumab significantly improved neuromotor function when administered 6 hours after stroke in two replicate studies.
  • All elezanumab treatment groups, including the 24-hour delayed intervention group, showed significantly reduced neuroinflammation.
  • Microglial and astrocyte activation were significantly modulated by elezanumab treatment.

Conclusions:

  • Elezanumab demonstrates neuroprotective effects and improves functional recovery in a preclinical AIS model.
  • The antibody's ability to expand the time window for intervention distinguishes it from current AIS therapies.
  • Further clinical trials are warranted to determine the optimal dose and time window for elezanumab in human AIS patients.