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Pharmacologic Targeting of the ATX/LPA Axis Attenuates Bleomycin-Induced Pulmonary Fibrosis

Pharmacologic Targeting of the ATX/LPA Axis Attenuates Bleomycin-Induced Pulmonary Fibrosis

Ioanna Ninou, Eleanna Kaffe, Stefan Müller, David C Budd, Christopher S Stevenson, Christoph Ullmer, Vassilis Aidinis

Pulm Pharmacol Ther. 2018 Oct;52:32-40.

PMID: 30201409

Abstract:

Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease with a dismal prognosis and a largely unknown etiology. Autotaxin (ATX) is a secreted lysophospholipase D, largely responsible for extracellular production of lysophosphatidic acid (LPA), a bioactive phospholipid. LPA has numerous effects in most cell types, signaling through at least 6 receptors (LPAR) exhibiting wide spread distribution and overlapping specificities. The ATX/LPA axis has been suggested as a therapeutic target in different chronic inflammatory and fibroproliferative disorders, including pulmonary fibrosis. In this report, we examined head-to-head the efficacy of a potent inhibitor of ATX (PF-8380), that has not been tested in pulmonary fibrosis models, and an antagonist of LPAR1 (AM095) in bleomycin (BLM)-induced pulmonary fibrosis. Both compounds abrogated the development of pulmonary fibrosis and prevented the distortion of lung architecture, exhibiting qualitative and quantitative differences in different manifestations of the modeled disease.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP1144035539	PF-8380		1144035-53-9	Price
AP1345614596	AM095		1345614-59-6	Price

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