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Last update 08 May 2025

LPAR3

Last update 08 May 2025

Basic Info

Synonyms

Edg-7, EDG7, endothelial differentiation, lysophosphatidic acid G-protein-coupled receptor, 7

+ [9]

Introduction

Receptor for lysophosphatidic acid (LPA), a mediator of diverse cellular activities. May play a role in the development of ovarian cancer. Seems to be coupled to the G(i)/G(o) and G(q) families of heteromeric G proteins.

Drugs associated with LPAR3

ART24

Target

LPAR3

Mechanism

LPAR3 agonists [+2]

Active Org.

Adiso Therapeutics Ltd. [+1]

Originator Org.

APC Microbiome Institute [+1]

Active Indication

Neuroinflammatory Diseases [+1]

Inactive Indication

Clostridium difficile infection [+2]

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Ki-16198

Target

LPAR1 x LPAR3

Mechanism

LPAR1 antagonists [+1]

Active Org.-

Originator Org.

Kirin Brewery Co. Ltd.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BMS-002

Target

LPAR1 x LPAR3

Mechanism

LPAR1 antagonists [+1]

Active Org.-

Originator Org.

Bristol Myers Squibb Co.

Active Indication-

Inactive Indication

Diabetic Nephropathies

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with LPAR3

NCT04891965

/ CompletedPhase 1

A Randomized, Placebo-Controlled, Double-Blind, Phase 1 Study of ART24 in Subjects Recently Cured of a Clostridioides Difficile Infection (CDI)

This is a randomized, placebo-controlled, double-blind, multi-site study in which up to approximately 36 subjects with a recent C. difficile infection (CDI) who have completed a standard of care course of CDI antibiotics and have achieved clinical cure based on signs and symptoms, will be randomized to 7 or 28 daily doses of ART24 or placebo. Subjects will be followed for 6 months after the last dose of study drug.

Start Date27 Feb 2020

Sponsor / Collaborator

Adiso Therapeutics, Inc.

100 Clinical Results associated with LPAR3

100 Translational Medicine associated with LPAR3

0 Patents (Medical) associated with LPAR3

521

Literatures (Medical) associated with LPAR3

01 Dec 2025·Neural Regeneration Research

LPAR3: a shared target for neurodegenerative diseases?

Article

Author: Acton, Susan ; Chesnel, Laurent

01 Jul 2025·Cellular Signalling

LPAR3 and COL8A1, as matrix stiffness-related biomarkers, promote nasopharyngeal carcinoma metastasis by triggering EMT and angiogenesis

Article

Author: Zhang, Kaiwen ; Wu, Rui ; You, Bo ; Gu, Miao ; Yi, Lu ; Zhang, Xin ; Xie, Haijing ; Xia, Tian ; You, Yiwen ; Yin, Haimeng ; Pan, Si

Matrix stiffness affects the progression of nasopharyngeal carcinoma, but the underlying mechanism is still unknown. Here, we demonstrated that nasopharyngeal carcinoma tissues with distant metastasis contain large collagen deposits and strong matrix stiffness. First, we performed RNA-seq analysis of nasopharyngeal carcinoma cells cultured on polyacrylamide hydrogel systems and found that LPAR3 and COL8A1 are potential matrix stiffness markers. Based on in vivo and in vitro experiments, matrix stiffness mainly affected tumor metastasis rather than proliferation. Subsequently, we found that matrix stiffness triggers the formation of epithelial-mesenchymal transition by increasing the expression of LPAR3 in nasopharyngeal carcinoma, which is related to metastasis. In addition, matrix stiffness promotes the expression of COL8A1 secreted by nasopharyngeal carcinoma and is related to tumor angiogenesis. Simultaneous inhibition of LPAR3 and COL8A1 genes significantly reduced nasopharyngeal carcinoma invasion and metastasis. Based on the investigation, we confirmed that matrix stiffness governs the progression of nasopharyngeal carcinoma and that LPAR3 and COL8A1, as matrix stiffness related biomarkers, promote nasopharyngeal carcinoma metastasis by inducing epithelial-mesenchymal transition and angiogenesis. Overall, the in-depth exploration of matrix stiffness may provide a strategy for clinical treatment intervention and provide promising targets for clinical nasopharyngeal carcinoma treatment.

01 Jun 2025·Experimental Eye Research

Lysophosphatidic acid receptor 3 (LPAR3) regulates ocular surface chloride transport via calcium signaling

Article

Author: Kuo, Yien-Ming ; Pasricha, Neel D ; Gao, Qi ; Cil, Onur ; Chen, Feeling Y ; de Souza Goncalves, Livia ; Verkman, Alan S ; Lindgren, Ethan S ; Yan, Rongshan ; Chan, Matilda F

Dry eye is a multifactorial disease associated with impaired tear film homeostasis, damaging the ocular surface epithelium. Lysophosphatidic acid receptors (LPARs) are G-protein coupled receptors involved in Ca²⁺ and cAMP signaling via PLC and adenylyl cyclase activation. LPAR activation is involved in cell proliferation and wound healing in human corneal epithelial cells (HCECs) and in neuropathic pain. This study investigates the expression and functions of LPARs in ocular surface epithelial cells. Functional measurements of ocular surface potential difference (OSPD) were done in mice with topically applied, selective LPAR modulators. LPAR3 immunostaining was performed in mouse and human cornea and conjunctiva, and mouse lacrimal gland. LPAR-induced Ca²⁺ signaling was studied in primary and immortalized HCECs. The general LPAR agonist, linoleoyl LPA, and the LPAR3 selective agonist, 2S-OMPT, stimulated ocular surface Cl^- secretion via Ca²⁺-activated Cl^- channels (CaCCs). LPAR3 was expressed in the corneal and conjunctival epithelia of mice and humans, as well as in mouse lacrimal gland. Activation of LPAR and LPAR3 in HCECs transiently elevated intracellular Ca²⁺ through the Gq/PLC signaling pathway. LPAR3 agonists may potentially have therapeutic efficacy in ocular surface diseases, including dry eye disease.

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LPAR3

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