Last update 01 Nov 2024

TXA2 synthase x LTRs

Last update 01 Nov 2024

Basic Info

Related Targets

TXA2 synthaseLTRs

Drugs associated with TXA2 synthase x LTRs

LASSBio-341

Target

CysLT x TXA2 synthase

Mechanism

CysLT antagonists [+1]

Active Org.

Federal University of Rio de Janeiro

Originator Org.

Federal University of Rio de Janeiro

Active Indication

Inflammation

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

SC-106

Target

LTRs x TXA2 synthase

Mechanism

LTRs antagonists [+1]

Active Org.-

Originator Org.

Scotia

Active Indication-

Inactive Indication

Rheumatoid Arthritis

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TXA2 synthase x LTRs

100 Translational Medicine associated with TXA2 synthase x LTRs

0 Patents (Medical) associated with TXA2 synthase x LTRs

Literatures (Medical) associated with TXA2 synthase x LTRs

01 Oct 2023·Prostaglandins & Other Lipid Mediators

Defining the contractile prostanoid component in hyperosmolar-induced bronchoconstriction in human small airways

Review

Author: Al-Ameri, Mamdoh ; Belikova, Maria ; Säfholm, Jesper ; Orre, Ann-Charlotte

Exercise-induced bronchoconstriction (EIB) is thought to be triggered by increased osmolarity at the airway epithelium. The aim of this study was to define the contractile prostanoid component of EIB, using an ex vivo model where intact segments of bronchi (inner diameter 0.5-2 mm) isolated from human lung tissue and subjected to mannitol. Exposure of bronchial segments to hyperosmolar mannitol evoked a contraction (64.3 ± 3.5 %) which could be prevented either by elimination of mast cells (15.8 ± 4.3 %) or a combination of cysteinyl leukotriene (cysLT₁), histamine (H₁) and thromboxane (TP) receptor antagonists (11.2 ± 2.3 %). Likewise, when antagonism of TP receptor was exchanged for inhibition of either cyclooxygenase-1 (8 ± 2.5 %), hematopoietic prostaglandin (PG)D synthase (20.7 ± 5.6 %), TXA synthase (14.8 ± 4.9 %), or the combination of the latter two (12.2 ± 4.6 %), the mannitol-induced contraction was prevented, suggesting that the TP-mediated component is induced by PGD₂ and TXA₂ generated by COX-1 and their respective synthases.

01 Feb 2021·Prostaglandins & Other Lipid MediatorsQ3 · BIOLOGY

Metabolism and biological functions of 12(S)-hydroxyheptadeca-5Z,8E,10E-trienoic acid

Q3 · BIOLOGY

Review

Author: Okuno, Toshiaki ; Yokomizo, Takehiko

12(S)-hydroxyheptadeca-5Z,8E,10E-trienoic acid (12-HHT) is a 17-carbon hydroxy fatty acid that is biosynthesized either by enzymatic pathways, like thromboxane synthase (TXAS) and cytochrome P450 or a non-enzymatic pathway. TXAS catalyzes the isomerization reaction from PGH₂ to 12-HHT, malondialdehyde, and TXA₂ at a ratio of 1:1:1. Furthermore, 12-HHT has been considered as a mere byproduct of TXA₂ biosynthesis, and its biological function has long been uncertain. BLT2 was initially identified as a low-affinity leukotriene B₄ (LTB₄) receptor, which is also activated by various hydroxy-eicosatetraenoic acids (HETEs), suggesting that BLT2 may be activated by other endogenous ligands apart from LTB₄ and HETEs. By unbiased ligand screening using crude lipids from rat organs, 12-HHT has been identified as an endogenous agonist for BLT2. The 12-HHT-BLT2 axis induces mast cell migration and contributes to allergic inflammation. BLT2 is also expressed in epithelial cells of the small intestine and skin in mice and contributes to in vivo epithelial barrier functions.

02 Apr 2019·Journal of Investigational Allergology and Clinical ImmunologyQ3 · MEDICINE

Angioedema-Induced by Nonsteroidal Anti-inflammatory Drugs: A Genotype-Phenotype Correlation in A Brazilian Population

Q3 · MEDICINE

Article

Author: Sole, D ; Filippelli-Silva, R ; Veronez, C L ; Pesquero, J B ; Martin, R P ; Ensina, L F

This paper discusses about the angioedema-induced by nonsteroidal anti-inflammatory drugs, genotype-phenotype correlation in Brazilian population.Nonsteroidal anti-infammatory drugs (NSAIDs) are the leading cause of hypersensitivity reactions in Latin America, both in adults and children.Therefore, in this study, we used whole-exome sequencing (WES) to detect genetic markers.That determine a hypersensitivity response in patients with NSAID-induced isolated angioedema (NIA).Four unrelated patients with NIA and their parents were selected and agreed to participate in the study.Nine genes related to the COX and 5-LO signaling pathways (ALOX5, PTGS2, CYSLTR1, CYSLTR2, LTC4S, PTGER1, PTGER2, TBXA2R, TBXAS1) were filtered in the VCF file according to variant segregation anal. in order to propose the genotype-phenotype associationTaken together, our data enable us to conclude that there is probably no single genetic marker of NIA in our cohort of patients.NIA is most likely determined by a combination of genetic alterations.

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