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Last update 08 May 2025

PTGES2

Last update 08 May 2025

Basic Info

Synonyms

C9orf15, chromosome 9 open reading frame 15, FLJ14038

+ [9]

Introduction

Isomerase that catalyzes the conversion of PGH2 into the more stable prostaglandin E2 (PGE2) (in vitro) (PubMed:12804604, PubMed:17585783, PubMed:18198127). The biological function and the GSH-dependent property of PTGES2 is still under debate (PubMed:17585783, PubMed:18198127). In vivo, PTGES2 could form a complex with GSH and heme and would not participate in PGE2 synthesis but would catalyze the degradation of prostaglandin E2 H2 (PGH2) to 12(S)-hydroxy-5(Z),8(E),10(E)-heptadecatrienoic acid (HHT) and malondialdehyde (MDA) (By similarity) (PubMed:17585783).

Drugs associated with PTGES2

Compound 3(University of Salerno)

Target

PTGES2

Mechanism

PTGES2 modulators

Active Org.

Sun Pharma Advanced Research Company Ltd. [+1]

Originator Org.

University of Salerno

Active Indication

Pancreatic Ductal Adenocarcinoma [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PTGES2

100 Translational Medicine associated with PTGES2

0 Patents (Medical) associated with PTGES2

471

Literatures (Medical) associated with PTGES2

01 Apr 2025·Pest Management Science

Arachidonic acid metabolism is involved in the detoxification and recognition of Phytophthora sojae to benzoxazinones

Article

Author: Zhang, Zhuoqun ; Wen, Jingzhi ; Du, Xiuming ; Zhao, Yifan ; Liu, Haixu ; An, Tai ; Xu, Ying

AbstractBACKGROUNDPhytophthora sojae (Kaufmann and Gerdemann), a pathogenic oomycete, causes one of the most destructive soybean diseases, Phytophthora root and stem rot (PRR). Previous studies have shown that benzoxazines (BXs) such as 6‐methoxy‐benzoxazolin‐2‐one (MBOA) and benzoxazoline‐2‐one (BOA) in maize root exudates inhibit the chemotaxis of zoospores, as well as the mycelial growth and pathogenicity of P. sojae. However, the molecular mechanism by which BXs regulate the growth, development and pathogenicity of P. sojae is still not well understood at present.RESULTSBy analyzing the transcriptome data, it was determined that PsPTGES2 (encoding prostaglandin E synthase 2), PsGST1 (encoding glutathione S transferase), and PsEPHX2 (encoding soluble epoxide hydrolase) in the arachidonic acid (AA) pathway were involved in the response of P. sojae to MBOA and BOA. Polyethylene glycol (PEG)‐mediated protoplast transformation was performed to construct silenced transformants of PsPTGES2, PsGST1, and PsEPHX2. Our data demonstrated that PsPTGES2, PsGST1, and PsEPHX2 were involved in mycelial growth, oospore formation, zoospore encystment, cyst germination in P. sojae. PsPTGES2 and PsGST1 were involved in the pathogenicity. The silencing transformants PsPTGES2 and PsGST1 reduced the metabolic ability to AA and the resistance to BOA. Moreover, the zoospores of the silencing transformants PsPTGES2, PsGST1, and PsEPHX2 decreased the chemotaxis to genistein and repellency to BOA.CONCLUSIONAA metabolism is involved in the growth, development and pathogenicity of P. sojae and the detoxification and recognition of P. sojae to BXs. The study results provide a solid theoretical basis for developing effective strategies to control the infection and pathogenicity of P. sojae. © 2024 Society of Chemical Industry.

01 Apr 2025·Current Medicinal Chemistry

Nepetin Attenuates Atopic Dermatitis in HaCaT Cells and BALB/c Mice through MyD88-MKK3/6-Akt Signaling

Article

Author: Gong, Guowei ; Zheng, Yuzhong ; Ganesan, Kumar ; Tsim, Karl Wah Keung ; Xiao, Jian ; Dong, Tina Tingxia

Introduction::Nepetin is a type of O-methylated flavone (6-hydroxy luteolin) and has been found in many herbal medicines that exhibit various pharmacological properties, including anti-inflammatory responses. Here, we aimed to investigate the efficacy of nepetin in attenuating inflammatory responses in cultured keratinocytes and 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD) in BALB/c mice.Methods::Various assay methods including cell viability, flow cytometry, fluorometry, confocal microscopy, western blot, ELISA techniques, staining methods, score and scratch frequency assessment, etc. were employed to explore the mechanisms.Results::LPS-treated keratinocytes showed a significant increase in inflammatory mediators (i- NOS, COX-2, PGES2, and NO) and cytokines (IL-1β, IL-6, and TNF-α) in a dose-dependent manner. Treatment with nepetin prevented LPS-induced cell death and inhibited inflammatory mediators and the production of cytokines in cultured keratinocytes. This inhibition was achieved by nepetin, which inhibited LPS-induced ROS production and the translocation of NF-κB in the cultures, thereby inhibiting the generation of inflammatory mediators and/or cytokines. In a mouse model of AD, treatment with nepetin reduced skin inflammation symptoms in a dose-dependent manner, as evidenced by the significant reduction of inflammation-related cytokines, skin lesions, and behavior scores.Conclusion::Based on the present in vitro and in vivo study, nepetin is the safest bioactive compound with potential therapeutic applications for AD-related skin lesions and adverse skin reactions.

01 Apr 2025·Bioorganic & Medicinal Chemistry Letters

Development of novel GI-centric prostaglandin E2 receptor type 4 (EP4) agonist prodrugs as treatment for ulcerative colitis and other intestinal inflammatory diseases

Article

Author: Tsai, Kevin ; Yu, Hongbing ; Yang, Hyungjun ; Lassueur, Kristiana ; Chen, Gang ; Cantelli, Christophe R ; Ma, Caixia ; Jacobson, Kevan ; Chan, Jocelyn J ; Young, Robert N ; Kantham, Srinivas ; Vallance, Bruce A

Prostaglandin E₂ receptor type 4 (EP4) agonists have been shown to be effective in treating experimental ulcerative colitis (UC) in animals and in human clinical trials, but their development has been impeded by unacceptable systemic side effects. In this study, a series of methylene phosphate prodrugs of a highly potent and selective prostaglandin EP4 receptor agonist were designed to target and remain localized in the gastrointestinal (GI) tract after either oral or rectal instillation. The prodrugs were designed to be converted to liberate active EP4 agonist by intestinal alkaline phosphate (IAP), a ubiquitous enzyme found at the luminal of the intestinal wall thus exposing the colon epithelial barrier while reducing systemic exposure to the active agonist. The prodrugs were shown to hydrolyze in plasma and after contact with GI tissue slices from ileum and colon. When optimized prodrugs were dosed orally, systemic peak exposure to the active agonist was not reduced, presumably due to IAP activity in the duodenum and small intestine. However, when dosed rectally, the prodrugs gave much reduced levels of EP4 agonist in the blood. An optimized prodrug was shown to be retained in the colon, when compared with free agonist after rectal administration in healthy mice and to be efficacious in a model of UC (the DSS mouse model). Plasma exposure to the active agonist was also much reduced in the mouse model of UC after 4 days of rectal dosing but after 7 days, one DSS mouse showed elevated systemic levels of the free agonist in the blood. The concept of efficacy and intestinal retention of an EP4 agonist-methylene phosphate prodrug was proven for rectal instillation but in DSS treated mice, severe disease appears to compromise the epithelia barrier sufficiently to allow some absorption of the prodrug to occur. Thus, further optimization of these prodrugs is required before a candidate can be selected for development for treating severe ulcerative colitis.

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PTGES2

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