Last update 19 Sep 2024

TAFI

Last update 19 Sep 2024

Basic Info

Synonyms

羧肽酶B2, Carboxypeptidase B2, carboxypeptidase B2 (plasma, carboxypeptidase U)

+ [10]

Introduction

Cleaves C-terminal arginine or lysine residues from biologically active peptides such as kinins or anaphylatoxins in the circulation thereby regulating their activities. Down-regulates fibrinolysis by removing C-terminal lysine residues from fibrin that has already been partially degraded by plasmin.

Drugs associated with TAFI

S-62798

Target

TAFI

Mechanism

TAFI inhibitors

Active Org.

Les Laboratoires Servier SAS

Originator Org.

Les Laboratoires Servier SAS

Active Indication

Pulmonary Embolism

Inactive Indication-

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

DS-1040

Target

TAFI

Mechanism

TAFI inhibitors

Active Org.

Daiichi Sankyo Co., Ltd.

Originator Org.

Daiichi Sankyo Co., Ltd.

Active Indication

Pulmonary Embolism

Inactive Indication

Acute Ischemic Stroke [+2]

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AZD-9684

Target

TAFI

Mechanism

TAFI inhibitors

Active Org.-

Originator Org.

AstraZeneca Pharmaceuticals Co., Ltd.

Active Indication-

Inactive Indication

Thrombosis

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with TAFI

EUCTR2019-003514-14-AT / Not yet recruitingPhase 2

A Multicentre, Randomized, Double-blind, Placebo-controlled Dose-finding Study of S62798 in Patients with Intermediate-High Risk Acute Pulmonary Embolism on heparin

Start Date06 Jul 2020

Sponsor / Collaborator

Institut de Recherches Intern Servier

EUCTR2019-003514-14-GR / Not yet recruitingPhase 2

A Multicentre, Randomized, Double-blind, Placebo-controlled Dose-finding Study of S62798 in Patients with Intermediate-High Risk Acute Pulmonary Embolism on heparin

Start Date20 May 2020

Sponsor / Collaborator

Institut de Recherches Intern Servier

EUCTR2019-003514-14-IT / Not yet recruitingPhase 2

A Multicentre, Randomized, Double-blind, Placebo-controlled Dose-finding Study of S62798 in Patients with Intermediate-High Risk Acute Pulmonary Embolism on heparin - NA

Start Date05 May 2020

Sponsor / Collaborator

Institut de Recherches Intern Servier

100 Clinical Results associated with TAFI

100 Translational Medicine associated with TAFI

0 Patents (Medical) associated with TAFI

1,264

Literatures (Medical) associated with TAFI

01 Dec 2024·Molecular Biology Reports

ATR1 A1166C (rs5186), FII G20210A (rs1799963), FV G1691A (rs6025), FXIII 97G > T (rs11466016) and MTHFR A1298C (rs1801131) polymorphisms and the risk of ST-elevation myocardial infarction in young Mexican individuals

Article

Author: Jiménez-Alvarado, Rosa María ; Isordia-Salas, Irma ; Leaños-Miranda, Alfredo ; Santiago-Germán, David ; Carrillo-Juárez, Reyes Ismael

BACKGROUNDPrevious studies had identified genetic variants associated with Myocardial Infarction, but results are inconclusive. We examined the association between FII G20210A (rs1799963), FV G1691A (rs6025), FXIII 97G > T (rs11466016), ATR1 A1166C (rs5186) and MTHFR A1298C (rs1801131) polymorphisms and ST elevation Myocardial Infarction in young Mexican individuals.METHODSWe included a total of 350 patients with Myocardial Infarction <45 years old and 350 controls matched by age and gender. The polymorphisms were analyzed by PCR-RFLP using specific restriction enzymes. DNA fragments were separated by electrophoresis in 2% gel of agarose and visualized using SYBR green.RESULTSThe A1166C (p = 0.004) but not FXIII 97G > T (p = 0.19), G20210A (p = 0.32), G1691A (p = No significant) and A1298C (p = 0.21) polymorphisms were associated with increased risk for ST elevation Myocardial Infarction. Moreover, dyslipidemia, hypertension, smoking and family history of atherothrombotic disease were associated.CONCLUSIONSWe found that A1166C represented increased risk for ST elevation Myocardial Infarction. However, G20210A, G1691A, 97G > T, and A1298C were not associated. In addition, we had determined that Glu298Asp, PLA1/A2, TAFI Thr325Ile, ACE I/D, AGT M235T and PAI-1 4G/5G polymorphisms represented increased risk in the same group of patients. However, MTHFR C677T, AGT T174M, FV G1691A, TSP-1 N700S, MTHFR C677T and TAFI 174 M polymorphisms were no associated. Our results suggest that in young patients with ST Myocardial Infarction, those polymorphisms could contribute to premature endothelial dysfunction, atherothrombosis, vasoconstriction, increased platelet aggregation, muscle cell migration and proliferation. Further studies are required to try to better assess gene-gene and gene-modifiable factors interaction.

01 Sep 2024·STAR Protocols

Protocol for the simultaneous quantification of oxidative purine lesions in DNA using LC-MS/MS analysis

Article

Author: Chatgilialoglu, Chryssostomos ; Terzidis, Michael A ; Krokidis, Marios G

Most DNA damages induced through oxidative metabolism are single lesions which can accumulate in tissues. Here, we present a protocol for the simultaneous quantification of oxidative purine lesions (cPu and 8-oxo-Pu) in DNA. We describe steps for enzymatic digestion of DNA and sample pre-purification, followed by quantification through liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. We optimized this protocol in commercially available calf thymus DNA and used genomic and mitochondrial DNA extracted from cell cultures and animal and human tissues.

01 Aug 2024·Journal of Thrombosis and Haemostasis

Fibrinolysis is impaired in patients with primary immune thrombocytopenia

Article

Author: Wolberg, Alisa S ; Rast, Jasmin ; Fillitz, Michael ; de Moreuil, Claire ; Reitsma, Stéphanie E ; Pabinger, Ingrid ; Wolberg, Alisa S. ; Reitsma, Stéphanie E. ; Gebhart, Johanna ; de Laat, Bas ; Schramm, Theresa ; Ay, Cihan ; Quehenberger, Peter ; Mehic, Dino

BACKGROUNDPatients with primary immune thrombocytopenia (ITP) have an increased risk of thrombosis, which may be due to altered fibrinolysis.OBJECTIVESTo elucidate the clinical impact of delayed fibrinolysis in ITP patients.METHODSA turbidimetric clot formation and lysis assay and a fluorometric plasmin generation (PG) assay were performed and levels of plasminogen-activator-inhibitor-1 (PAI-1), tissue-plasminogen-activator (tPA), tPA-PAI-1 complexes, α2-antiplasmin, TAFI and D-Dimer were assessed in 86 adult primary ITP patients and 78 healthy controls (HC).RESULTSITP patients showed significantly delayed clot formation, increased clot density, and prolonged clot lysis time (CLT) compared to HC with a median (IQR) CLT of 28.0 (13.7-34.7) minutes in patients and 17.3 (12.0-28.0) minutes in HC, while in PG only the lag time was prolonged. In ITP patients compared to controls, PAI-1 was higher (1.2 (0.8-2.6) vs 1.1 (0.6-2.1) U/mL), and tPA antigen and activity were lower (tPA antigen: 2.6 (1.1-4.4) vs 3.7 (3.2-4.7) ng/mL; tPA activity ≤0 U/mL: 26% vs 7%). TPA-PAI-1 complex levels were positively associated with CLT in multiple linear regression analysis (β=0.241, p=0.019), whereas PG parameters were not associated with CLT. Six patients, who developed thrombosis during follow-up, had higher levels of tPA-PAI-1 complexes.CONCLUSIONProlonged CLT and delayed onset of PG may indicate a hypofibrinolytic tendency in ITP patients, as also indicated by high PAI-1 and low tPA levels. No association was found between fibrinolytic potential and the bleeding phenotype, whereas higher tPA-PAI-1 complex levels were associated with prolonged CLT and increased in patients with future thrombosis.

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