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LPA Antagonists for the Treatment of IPF

LPA 拮抗剂用于治疗 IPF

基本信息

批准号：
8393147
负责人：
WEIZHONG CAI
金额：
$ 35.41万
依托单位：
ANGION BIOMEDICA CORPORATION
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-08-01 至 2013-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8393147
关键词：
Animal Model Area Biological Biological Assay Biology Bleomycin Body Weight Chemicals Chemistry Cicatrix Clinical Trials Collagen Coupled Coupling Disease Edg4 Protein Etiology Evaluation Fibroblasts Fibrosis GTP-Binding Proteins Gene Expression Goals Grant Hamman-Rich syndrome Hepatic Histology In Vitro Individual Inflammation Injury Intellectual Property Investigational Drugs Kidney Laboratories Lead Liver Lung Lysophospholipids Measures Mediating Modeling Molecular Models Mus Organ Patients Pharmaceutical Chemistry Phase Positioning Attribute Preparation Process Production Program Development Property Property Rights Pulmonary Fibrosis Regulation Research Research Personnel Role Series Signal Transduction Small Business Innovation Research Grant Solubility Structure Structure of parenchyma of lung Systemic Scleroderma Testing Therapeutic Tissues Toxicology Transgenes Transgenic Mice United States Universities Weight analog clinically relevant drug development drug discovery effective therapy efficacy evaluation experience in vitro Assay in vivo in vivo Model indium-bleomycin lysophosphatidic acid molecular modeling overexpression prevent repaired small molecule vzg-1 Receptor

项目摘要

DESCRIPTION (provided by applicant): Idiopathic pulmonary fibrosis (IPF) is a progressive, agonizing, debilitating and routinely fatal disease that afflicts 200,000 individuals in the United States and five million patients worldwide. There are currently no effective treatments available for this devastating illness. Although the etiology of IPF is currently unknown, various insults ar thought to disrupt the tight regulation between inflammation and repair of lung tissue leading to excess production of collagen by fibroblasts and the formation of excessive scar tissue, irreversibly destroying lung structure and function. The role of lysophosphatidic acid (LPA) signaling in IPF has been firmly established; through a G protein-coupled LPA1 receptor, LPA mediates recruitment of fibroblasts into the pulmonary interstitium which hyper-accelerates normal repair processes, resulting in fibrosis. A selective LPA1 receptor antagonist may intervene in the dysregulated inflammation/repair cycle, prevent fibrosis, and benefit afflicted individuals. Our long-term goal is to develop small molecule antagonists of the LPA1 receptor as potential therapeutics for IPF. The objective of this application is to identify such antagonists and evaluate them in two clinically relevant animal models of IPF. PUBLIC HEALTH RELEVANCE: Small molecule LPA1 antagonists are potential therapeutics for idiopathic pulmonary fibrosis (IPF).

描述（由申请人提供）：特发性肺纤维化（IPF）是一种进行性、痛苦、衰弱和常规致命的疾病，在美国折磨着20万人