Effect of Intravenous FX06 as an Adjunct to Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction

Atar, Dan; Petzelbauer, Peter; Schwitter, Jiirg; Huber, Kurt; Rensing, Benno J.; Kasprzak, Jarosław D.; Butter, Christian; Grip, Lars; Hansen, Peter Riis; Süselbeck, Tim; Clemmensen, Peter; Marin-Galiano, Marcos; Geudelin, Bernard; Buser, Peter

doi:10.1016/j.jacc.2008.12.017

Cited by 137 publications

(71 citation statements)

References 50 publications

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“…In renal allotransplantation, the tissue-protective effect was associated with a reduced alloimmune response and prolonged graft survival. In conjunction with recent clinical trials showing an excellent tolerability and safety of B␤ in patients, 17,18 our data suggest that intrasurgical administration of this peptide could be used to prevent IR-triggered alloimmune processes and reduce the risk of rejection in renal transplantation. Compared with other experimental strategies that try to prevent IR injury and rejection by blocking individual adhesion molecules or chemokines, the use of B␤ 15-42 might be more promising because of its broader mechanism of action.…”

Section: Discussionsupporting

confidence: 79%

Bβ15–42 Attenuates the Effect of Ischemia-Reperfusion Injury in Renal Transplantation

Sörensen

Rong

Susnik

et al. 2011

Journal of the American Society of Nephrology

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Renal ischemia-reperfusion contributes to reduced renal allograft survival. The peptide B␤ 15-42 , a breakdown product of fibrin, attenuates inflammation induced by ischemia-reperfusion in the heart by competitively blocking the binding of leukocytes to endothelial VE-cadherin, but whether it could improve outcomes in renal transplantation is unknown. Here, we tested the ability of B␤ to ameliorate the effects of renal ischemic injury during allogenic kidney transplantation in mice. In our renal transplantation model (C57BL/6 into BALB/c mice), treatment with B␤ 15-42 at the time of allograft reperfusion resulted in significantly improved survival of recipients during the 28-day follow-up (60% versus 10%). B␤ 15-42 treatment decreased leukocyte infiltration, expression of endothelial adhesion molecules, and proinflammatory cytokines. Treatment significantly attenuated allogenic T cell activation and reduced cellular rejection. Moreover, B␤ 15-42 significantly reduced tubular epithelial damage and apoptosis, which we reproduced in vitro. These data suggest that B␤ 15-42 may have therapeutic potential in transplant surgery by protecting grafts from ischemia-reperfusion injury.

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Section: Discussionsupporting

confidence: 79%

Bβ15–42 Attenuates the Effect of Ischemia-Reperfusion Injury in Renal Transplantation

Sörensen

Rong

Susnik

et al. 2011

Journal of the American Society of Nephrology

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“…17 The substance was well tolerated in a phase 2 clinical trial in patients with ST-elevation myocardial infarction. 18 In our patient, we noted no signs of tolerability problems or compromised safety. The improvement of the vascular leak syndrome, however, also coincided with a decrease in the plasma viral load.…”

Section: Discussionmentioning

confidence: 44%

Severe Ebola virus disease with vascular leakage and multiorgan failure: treatment of a patient in intensive care

Wolf

Kann

Becker³

et al. 2015

The Lancet

205

192

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“…This work has been translated into a multicenter phase IIa clinical trial investigating the effects of Bβ15-42 (FX06) on myocardial infarct size. In summary, Bβ15-42 significantly reduced the size of the necrotic core zone of infarcts while total late enhancement was not significantly different between control and Bβ15-42-treated groups (68).…”

Section: Fibrin Fragmentsmentioning

confidence: 72%

Novel Aspects of Fibrin(ogen) Fragments during Inflammation

Jennewein

Tran

Paulus

et al. 2011

Mol Med

208

139

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Coagulation is fundamental for the confinement of infection and/or the inflammatory response to a limited area. Under pathological inflammatory conditions such as arthritis, multiple sclerosis or sepsis, an uncontrolled activation of the coagulation system contributes to inflammation, microvascular failure and organ dysfunction. Coagulation is initiated by the activation of thrombin, which, in turn, triggers fibrin formation by the release of fibrinopeptides. Fibrin is cleaved by plasmin, resulting in clot lysis and an accompanied generation of fibrin fragments such as D and E fragments. Various coagulation factors, including fibrinogen and/or fibrin [fibrin(ogen)] and also fibrin degradation products, modulate the inflammatory response by affecting leukocyte migration and cytokine production. Fibrin fragments are mostly proinflammatory, however, Bβ15-42 in particular possesses potential antiinflammatory effects. Bβ15-42 inhibits Rho-kinase activation by dissociating Fyn from Rho and, hence prevents stress-induced loss of endothelial barrier function and also leukocyte migration. This article summarizes the state-of-the-art in inflammatory modulation by fibrin(ogen) and fibrin fragments. However, further research is required to gain better understanding of the entire role fibrin fragments play during inflammation and, possibly, disease development.

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Effect of Intravenous FX06 as an Adjunct to Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction

Cited by 137 publications

References 50 publications

Bβ15–42 Attenuates the Effect of Ischemia-Reperfusion Injury in Renal Transplantation

Bβ15–42 Attenuates the Effect of Ischemia-Reperfusion Injury in Renal Transplantation

Severe Ebola virus disease with vascular leakage and multiorgan failure: treatment of a patient in intensive care

Novel Aspects of Fibrin(ogen) Fragments during Inflammation

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