Neuro-protectant Peptides for Ischemic Stroke

Fragmentation of RANKL Eliminates Side-effect while Boosting Effect.

Core Benefit

  • First-in-class drug with new mechanism of action.
  • Potentially also effective for sepsis by controlling excessive inflammatory response, and osteoporosis by blocking osteoclast differentiation.

Background and Technology

Recent studies have shown that administration of recombinant receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) reduces infarct volume and brain edema in ischemic stroke with reduced expression in inflammatory cytokines through a Toll-like receptor 2/4 (TLR2/4) signaling pathway in microglia [1]. However, RANKL also activated osteoclast which causes osteoporosis.

To overcome the problem, the researchers have developed RANKL fragment peptides which block the activation of microglia, macrophage, and osteoclast [2]. Since the peptides can attenuate inflammatory immune response, and competitively inhibits RANKL/RANK pathway of osteoclast, they can be an alternative of TLR2/4 antagonists or RANKL antagonists, and possibly applicable for sepsis and osteoporosis.

[1] Proc Natl Acad Sci U S A. 2014 Jun 3; 111(22): 8191-6. doi: 10.1073/pnas.1400544111.
[2] Scientific Reports 6, Article number: 38062 (2016) doi:10.1038/srep38062

Facts and Data

  1. The invented 30-amino acid peptide significantly reduced secretion of IL-6, TNF-alpha from LPS stimulated mouse/human macrophage, mouse microglia cell lines, and prevented neuronal death of LPS stimulated neuron/glia mixed primary culture.
  2. The peptide inhibited RNANK/RANKL dependent M1 macrophage differentiation and osteoclast progenitor cell maturation.
  3. In mouse ischemic stroke/reperfusion model, i administration after 6 hours of onset of stroke successfully delivered the peptide through the blood brain barrier, reduced infarct volume to less than a half(n=7) and NSS(neurological severity score) from around 2 to 1.

NOTE: The peptide used was not protected or modified for protease degradation avoidance.




Associate Prof.  Munehisa Shimamura, Graduate School of Medicine, Osaka University, Japan


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Product No: TP0521

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