Recombinant Nematode Anticoagulant Protein c2 in non-ST Segment Elevation Acute Coronary Syndrome and Beyond

Fluture, Adrian; Giugliano, Gregory R.; Giugliano, Robert P.

doi:10.2217/14796678.3.4.365

Cited by 2 publications

(1 citation statement)

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“…In a double blind placebo-controlled trial, rNAPc2 was found to be safe and well-tolerated at doses ranging from 0.3 to 5 μg/kg body weight in preventing thrombin generation during coronary angioplasty in combination with aspirin, clopidogrel, and heparin (Moons et al, 2003). A more recent phase II clinical study demonstrated that in patients with non ST-elevation acute coronary syndrome managed with standard antithrombotics and an early invasive approach, additional proximal inhibition of the coagulation cascade with rNAPc2 was well tolerated and not associated with an increase in major or minor bleedings as compared with a placebo treatment (Fluture et al, 2007;Giugliano et al, 2007). A novel finding in the ANTHEM-TIMI-32 trial was that the doses of rNAPc2 suppressing thrombin generation through 48 h were associated with a ≥50% reduction in ischemia on continuous ECG.…”

Section: Nematode Anticoagulant Protein (Napc2)mentioning

confidence: 99%

Tissue Factor in Cardiovascular Disease

Holy¹,

Tanner²

2010

Cardiovascular Pharmacology - Heart and Circulation

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Tissue factor (TF) is the major trigger of the coagulation cascade and thereby crucially involved in the maintenance of vascular hemostasis. By binding factor VIIa, the resulting TF:VIIa complex activates the coagulation factors IX and X ultimately leading to fibrin and clot formation. In the vessel wall, TF expression and activity is detectable in vascular smooth muscle cells and fibroblasts and, at a much lower level, in endothelial cells and can be induced by various stimuli including cytokines. In addition, TF is found in the bloodstream in circulating cells such as monocytes, in TF containing microparticles, and as a soluble splicing isoform. Besides its well-known extracellular role as a trigger of coagulation, TF also functions as a transmembrane receptor, and TF-dependent intracellular signaling events regulate the expression of genes involved in cellular responses such as proliferation and migration. TF indeed appears to be involved in the pathogenesis of neointima formation and tumor growth, and increased levels of TF have been detected in patients with cardiovascular risk factors or coronary artery disease as well as in those with cancer. Therefore, pharmacological or genetic inhibition of TF may be an attractive target for the treatment of cardiovascular disease and cancer. Different strategies for inhibition of TF have been developed such as inhibition of TF synthesis and blockade of TF action. Clinical applications of such strategies need to be tested in appropriate trials, in particular for evaluating the advantages of targeted versus systemic delivery of the inhibitors.

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Section: Nematode Anticoagulant Protein (Napc2)mentioning

confidence: 99%