Anti-Fibrotic Peptide


Researchers at MUSC have identified a specific fragment of the mesenchymal-epithelial transition factor (MET) receptor as a peptide with robust antifibrotic properties. Preliminary studies show that the purified peptide markedly reduces collagen and other extracellular matrix proteins in scleroderma lung fibroblasts and in TGF-β-stimulated normal lung fibroblasts.

Overview: In terms of kidney fibrosis, there are approximately 26 million adults with chronic kidney diseases (CKD), and the number of these patients is expected to double by 2020. The current CKD market is estimated to be just under $15 billion, growing at a 6% annual growth rate and potentially reaching $20 billion by 2016. Currently, there are no available therapies capable of increasing kidney function by repairing or reversing kidney damage. The liver fibrosis therapeutics market was valued at $264M in 2010, and is expected to grow to $445M with a CAGR of 7.8% by 2017. The pulmonary fibrosis therapy market in the US and EU is projected to be worth more than $1.1B by 2017. The mechanism for fibrosis is similar across all disease states so we see applications to expand this technology.

Pulmonary fibrosis represents the terminal stage of a diverse group of lung diseases including scleroderma associated interstitial lung disease (SSc-ILD). The molecular mechanisms underlying the pathogenesis of SSc-ILD are not well understood, and treatment is often toxic and inefficacious. Earlier studies have identified hepatocyte growth factor (HGF) as an antifibrotic agent that protects against tissue fibrosis in several animal models. It has been previously demonstrated that antifibrotic effects mediated by the HGF receptor, also known as cellular mesenchymal-epithelial transition factor (c-MET, MET), are impaired in lung fibroblasts isolated from subset of patients with severe SSc-ILD. Lung fibroblasts from SSc-ILD patients with poor pulmonary outcomes express the D1398G variant of the HGF receptor, and that D1398G MET receptor mutant generated in vitro does not exert any of MET’s antifibrotic effects in lung fibroblasts.

Applications: Pulmonary fibrosis
Advantages: Collagen reduction, extracellular matrix protein reduction
Key Words: Pulmonary fibrosis, antifibrotic, fibroblasts, interstitial lung disease

Publication: Atanelishvili, Ilia, et al. "M10, a caspase cleavage product of the hepatocyte growth factor receptor, interacts with Smad2 and demonstrates antifibrotic properties in vitro and in vivo." Translational Research (2015).

Inventors: Galina Bogatkevich, Yuichiro Shirai, & Richard Silver
Patent Status: PCT Application Filed 7/21/2016

MUSC-FRD Technology ID: P1454

Patent Information:
For Information, Contact:
Scott Davis
Sr Licensing Manager
MUSC Foundation for Research Development
Galina Bogatkevich
Yuichiro Shirai
Richard Silver
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