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Last update 08 May 2025

PTGDS

Last update 08 May 2025

Basic Info

Synonyms

Beta-trace protein, Cerebrin-28, Glutathione-independent PGD synthase

+ [13]

Introduction

Catalyzes the conversion of PGH2 to PGD2, a prostaglandin involved in smooth muscle contraction/relaxation and a potent inhibitor of platelet aggregation (PubMed:20667974). Involved in a variety of CNS functions, such as sedation, NREM sleep and PGE2-induced allodynia, and may have an anti-apoptotic role in oligodendrocytes. Binds small non-substrate lipophilic molecules, including biliverdin, bilirubin, retinal, retinoic acid and thyroid hormone, and may act as a scavenger for harmful hydrophobic molecules and as a secretory retinoid and thyroid hormone transporter. Possibly involved in development and maintenance of the blood-brain, blood-retina, blood-aqueous humor and blood-testis barrier. It is likely to play important roles in both maturation and maintenance of the central nervous system and male reproductive system (PubMed:20667974, PubMed:9475419). Involved in PLA2G3-dependent maturation of mast cells. PLA2G3 is secreted by immature mast cells and acts on nearby fibroblasts upstream to PTDGS to synthesize PGD2, which in turn promotes mast cell maturation and degranulation via PTGDR (By similarity).

Drugs associated with PTGDS

Pizuglanstat

Target

PTGDS

Mechanism

PTGDS inhibitors

Active Org.

Taiho Pharmaceutical Co., Ltd.

Originator Org.

Taiho Pharmaceutical Co., Ltd.

Active Indication

Muscular Dystrophy, Duchenne

Inactive Indication-

Drug Highest PhasePhase 3

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AT-56

Target

PTGDS

Mechanism

PTGDS inhibitors

Active Org.

Shandong University

Originator Org.

Shandong University

Active Indication

Peripheral T-Cell Lymphoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

KMN-010034

Target

PTGDS

Mechanism

PTGDS inhibitors

Active Org.-

Originator Org.

Cayman Chemical Co., Inc.

Active Indication-

Inactive Indication-

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with PTGDS

JPRN-jRCT2071230028

/ CompletedPhase 1IIT

A phase 1 open-label study evaluating the effects of food on TAS-205 in healthy volunteers

Start Date20 Jul 2023

Sponsor / Collaborator-

NCT04825431

/ CompletedPhase 1

A Phase 1 Open-label Study Evaluating the Pharmacokinetics and Mass Balance of [14C] TAS-205 in Healthy Volunteers

To evaluate the pharmacokinetics, mass balance recovery, metabolite profile and metabolite identification of [14C]TAS-205 following oral single doses.

Start Date22 Mar 2021

Sponsor / Collaborator

Taiho Pharmaceutical Co., Ltd.

JPRN-jRCT2041200055

/ RecruitingPhase 3IIT

A phase 3, randomized, placebo-controlled, double-blind and open-label, extension study of TAS-205 in patients with Duchenne muscular dystrophy - REACH-DMD

Start Date22 Dec 2020

Sponsor / Collaborator-

100 Clinical Results associated with PTGDS

100 Translational Medicine associated with PTGDS

0 Patents (Medical) associated with PTGDS

790

Literatures (Medical) associated with PTGDS

01 May 2025·Journal of the Neurological Sciences

Beta-trace protein in chronic inflammatory demyelinating polyradiculoneuropathy and Guillain-Barré syndrome – clinical utilization and a new insight into pathophysiological mechanisms

Article

Author: Hansson, Magnus ; Gustafsson, Rasmus ; Kmezic, Ivan ; Press, Rayomand

INTRODUCTIONBeta-trace protein (BTP) is primarily used as a marker for traumatic CSF leakage. Spinal leptomeningeal cells adjacent to the spinal nerve roots are a major producer of this protein, which has prompted interest in its relevance to inflammatory polyradiculoneuropathies. BTP has not previously been investigated in patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculopathy (CIDP).MATERIAL AND METHODSBTP was measured in the cerebrospinal fluid (CSF) and plasma in patients with GBS, CIDP, disease-free controls, non-inflammatory polyneuropathies, and multiple sclerosis.RESULTSPre-treatment levels of BTP in plasma were increased in patients with CIDP, but not GBS compared to all controls. Pre-treatment levels of BTP in CSF were increased in patients with CIDP compared to all controls but in patients with GBS compared only to disease-free controls. In patients with GBS and CIDP, levels of BTP in CSF were increased compared to disease-free controls irrespective of Q.alb, and the levels correlated with axonal damage markers in CSF and plasma. Elevated pre-treatment levels of BTP in CSF predicted therapy failure 3 months after initiation of immunotherapy in CIDP.CONCLUSIONSBTP in CSF and plasma may be a potential biomarker to aid in the diagnosis of CIDP. BTP in CSF could be a potentially more informative biomarker than albumin in a subgroup of patients with GBS and CIDP who have a normal or mildly elevated Q.alb. BTP in CSF may be predictive for therapy response in patient with CIDP, but needs to be validated in larger studies.

01 Apr 2025·Liver International

Spatial and Single‐Cell Transcriptomics Reveals the Regional Division of the Spatial Structure of MASH Fibrosis

Article

Author: Lin, Xun‐ge ; Li, Tao‐yuan ; Li, Ni ; Liang, Xu‐jing ; Liu, Yun‐yan ; Pan, Yun ; Ye, Li‐hong ; Dai, Er‐hei ; Xiao, Min‐xi ; Zhang, Hai‐cong ; Li, Min‐ran ; Li, Jin‐zhong ; Li, Jun‐qing ; Liu, Zhi‐quan ; Huang, Xin ; Li, Jie‐ying ; Yang, Liu ; Dai, Hai‐mei ; Cao, Yang

ABSTRACTObjectiveTo elucidate the regional distribution of metabolic dysfunction‐associated steatohepatitis (MASH) fibrosis within the liver and to identify potential therapeutic targets for MASH fibrosis.MethodsLiver sections from healthy controls, patients with simple steatosis and MASH patients were analysed using spatial transcriptomics integrated with single‐cell RNA‐seq.ResultsSpatial transcriptomics analysis of liver tissues revealed that the fibrotic region (Cluster 9) was primarily distributed in lobules, with some fibrosis also found in the surrounding area. Integration of the single‐cell‐sequencing data set (GSE189175) showed a greater proportion of inflammatory cells (Kupffer cells and T cells) and myofibroblasts in MASH. Six genes, showing high‐ or low‐specific expression in Cluster 9, namely, ADAMTSL2, PTGDS, S100A6, PPP1R1A, ASS1 and G6PC, were identified in combination with pathology. The average expression levels of ADAMTSL2, PTGDS and S100A6 on the pathological HE staining map were positively correlated with the increase in the degree of fibrosis and aligned strongly with the distribution of fibrosis. ADAMTSL2+ myofibroblasts play a role in TNF signalling pathways and in the production of ECM structural components. Pseudotime analysis indicated that in the early stages of MASH, infiltration by T cells and Kupffer cells triggers a significant inflammatory response. Subsequently, this inflammation leads to the activation of hepatic stellate cells (HSCs), transforming them into myofibroblasts and promoting the development of liver fibrosis.ConclusionThis study is the first to characterise lineage‐specific changes in gene expression, subpopulation composition, and pseudotime analysis in MASH fibrosis and reveals potential therapeutic targets for this condition.

09 Mar 2025·British Journal of Cancer

Targeting PTGDS Promotes ferroptosis in peripheral T cell lymphoma through regulating HMOX1-mediated iron metabolism

Article

Author: Liu, Bingyu ; Shang, Juanjuan ; Zhou, Xiangxiang ; Zhou, Xiaoli ; Wang, Xin ; Guo, Qianqian ; Hu, Shunfeng ; Lu, Tiange

AbstractBackgroundPeripheral T cell lymphoma (PTCL) is characterized by high heterogeneity, strong aggressiveness, and extremely poor prognosis. Ferroptosis, a novel form of programmed cell death, has been involved in tumor development and targeting ferroptosis holds great potential for tumor therapy.MethodsLentiviral transfection was performed to regulate gene expression, followed by Tandem mass tag (TMT)-mass spectrometry and RNA-sequencing. Tumor xenograft models were established for in vivo experiments.ResultsHigh expression of prostaglandin D2 synthase (PTGDS) was closely associated with poor prognosis of PTCL patients. PTGDS knockdown and AT56 treatment significantly inhibited the progression of PTCL through regulating cell viability, proliferation, apoptosis, cell cycle and invasion in vitro and in vivo. We further revealed that targeting PTGDS promoted ferroptosis process and enhanced the sensitivity of PTCL cells to ferroptosis inducers Sorafenib in vitro and in vivo. Mechanically, PTGDS interacted with heme-degrading enzymes HMOX1, and targeting PTGDS increased the level of iron and induced ferroptosis in PTCL through promoting HMOX1-mediated heme catabolism and ferritin autophagy process. Through the construction of H25A mutation, the specific gene site of HMOX1 corresponding to its role was identified.ConclusionsTaken together, our findings firstly identified that targeting PTGDS promotes the ferroptosis in PTCL through regulating HMOX1-mediated iron metabolism, and highlighted novel therapeutic strategies to improve the efficacy of ferroptosis-targeted therapy in PTCL patients.

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