Selective Reprogramming of Pulmonary Macrophages for Treatment of Idiopathic Pulmonary Fibrosis

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2019-LOW-68624
Researchers at Purdue University have developed molecular agonists to reverse idiopathic pulmonary fibrosis (IPF) by reprograming fibrotic macrophages to the non-fibrotic state. IPF is a lung disease that is characterized by rigidification of the lung resulting and a gradual loss in ability to mediate gas exchange leaving patients in a hypoxic state that increases gradually over the course of the disease. Current treatment options for IPF are only able to slow the rate of disease progression and none are able to reverse the existing fibrosis. With around 40,000 new cases of IPF diagnosed each year, a curative treatment option would be beneficial in treating IPF. Activated macrophages and activated fibroblasts are two cell types play a prominent from in IPF. Activated macrophages secrete signals that activate lung fibroblasts, the cells responsible for fibrotic tissue generation. Therefore, shutting down the activated macrophage secretion signals would provide a potential curative treatment option for IPF. Researchers at Purdue University have identified molecules that target Toll-like receptor 7 selectively on the macrophage surface to shut down signals secreted that activate fibroblasts. These molecules have been tested in histological and mouse models.

Advantages:
-Selective targeting of fibrotic macrophages

Potential Applications:
-Reverse idiopathic pulmonary fibrosis
-Possible combination therapy with existing therapeutics
Jul 8, 2020
PCT-Patent
WO
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Jul 9, 2019
Provisional-Patent
United States
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Jul 8, 2019
Provisional-Patent
United States
(None)
(None)
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