Researchers Test New Therapuetic Target Against Boehringer Ingelheim’s IPF Candidate

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by Maureen Newman |

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Dr. Claudia A. Staab-Weijnitz and Dr. Oliver Eickelberg at the Comprehensive Pneumology Center in the University of Munich are studying a new drug target for idiopathic pulmonary fibrosis (IPF) that addresses a protein potentially involved in the pathway of IPF pathogenesis. By attenuating the protein in a model of IPF, the researchers were able to decrease signs of excessive fibrosis.

The protein of interest is FK506-binding protein 10 (FKBP10), a protein that influences collagen stiffness and abundance. Since mutations in FKBP10 lead to stiffer collagen, the researchers were interested if increased collagen production and stiffness in IPF could correlate to changes in FKBP10 in IPF patients. They reported their findings in the article, “FK506-binding Protein 10 is a Potential Novel Drug Target for Idiopathic Pulmonary Fibrosis,” which was published in the American Journal of Respiratory and Critical Care Medicine.

To determine a possible correlation, the researchers measured how much FKBP10 is expressed in the lungs of IPF patients. Looking at 99 patients and 43 controls, the researchers determined that FKBP10 is higher in IPF patients than in healthy individuals. The results were significant and may apply to a broader population, as the researchers tested both American German patients with IPF.

Taking cells from the lungs of IPF patients, the researchers wanted to know if they could reduce the amount of collagen produced by IPF cells when given a treatment that suppresses FKBP10. The researchers used siRNA molecules to prevent protein production of FKBP10 and successfully knocked down FKBP10 production. As a result, the IPF cells secreted less collagen and produced fewer mediators of fibrosis.

To compare, the researchers also treated IPF cells with nintedanib, a drug in clinical trials by Boehringer Ingelheim designed to treat IPF. “Importantly, FKBP10 knockdown significantly decreased total collagen secretion by about 20%, in an amount similar to the effects observed with nintedanib,” stated the researchers.

This study was important to indicate that FKBP10 is an interesting target for IPF treatments. Although the researchers chose to knock down FKBP10 in an in vitro model using a gene-based approach, drug targets may be designed to inhibit FKBP10. The field of IPF may look forward to developing treatments that focus on FKBP10 to reduce fibrosis.

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