Other Resources
Publications
2020
Thrombo-Inflammation in Cardiovascular Disease: An Expert Consensus Document from the Third Maastricht Consensus Conference on Thrombosis
Publication Source | Thromb. Haemost. 020 Apr;120(4):538-564 |
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Link | https://pubmed.ncbi.nlm.nih.gov/32289858/ |
Abstract | Thrombo-inflammation describes the complex interplay between blood coagulation and inflammation that plays a critical role in cardiovascular diseases. The third Maastricht Consensus Conference on Thrombosis assembled basic, translational, and clinical scientists to discuss the origin and potential consequences of thrombo-inflammation in the etiology, diagnostics, and management of patients with cardiovascular disease, including myocardial infarction, stroke, and peripheral artery disease. This article presents a state-of-the-art reflection of expert opinions and consensus recommendations regarding the following topics: (1) challenges of the endothelial cell barrier; (2) circulating cells and thrombo-inflammation, focused on platelets, neutrophils, and neutrophil extracellular traps; (3) procoagulant mechanisms; (4) arterial vascular changes in atherogenesis; attenuating atherosclerosis and ischemia/reperfusion injury; (5) management of patients with arterial vascular disease; and (6) pathogenesis of venous thrombosis and late consequences of venous thromboembolism |
Document Type | Expert Consensus Document |
Pharmacodynamic Effects of Vorapaxar in Prior Myocardial Infarction Patients Treated With Potent Oral P2Y12 Receptor Inhibitors With and Without Aspirin: Results of the VORA‐PRATIC Study
Publication Source | Journal of American Heart Association, Vol. 9, No.8 |
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Background | Vorapaxar as an adjunct to dual antiplatelet therapy (DAPT) reduces thrombotic events in patients with prior myocardial infarction at the expense of increased bleeding. Withdrawal of aspirin has emerged as a bleeding reduction strategy. The pharmacodynamic effects of vorapaxar with potent P2Y12 inhibitors as well as the impact of dropping aspirin is unexplored and represented the aim of the VORA‐PRATIC (Vorapaxar Therapy in Patients With Prior Myocardial Infarction Treated With Newer Generation P2Y12 Receptor Inhibitors Prasugrel and Ticagrelor) study. |
Link | https://www.ahajournals.org |
Document Type | Publication |
Tetraspanin CD9 Regulates GPIIb-IIIa-Mediated Platelet Function: Identification of Unique Protein Interactomes
Publication Source | ISTH Academy. Kotha J. 07/11/20; 296839; PB1734 |
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Background | Tetraspanins are transmembrane proteins involved in cellular events such as adhesion, motility, and proliferation. CD9 (Tspan-29) is highly expressed on the platelet surface. Previously, it was determined that CD9 and the platelet integrin, GPIIb-IIIa form noncovalent complexes that are dependent upon the GPIIb-IIIa conformation state. |
Link | https://academy.isth.org |
Document Type | Poster / Current Abstract |
2019
We need predictive safety biomarkers
Publication Source | European Biotechnology, Summer Edition 2019, Volume 18 - https://european-biotechnology.com/ |
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Background | Every year, drug developers lose billions of euros because of late-stage clinical or postmarking safety problems with drugs. A recently kicked-off IMI consortium now wants to qualify a set of safety biomarkers that allow for the prediction of drug-induced injury of kidney, liver, vasculature, CNS, and pancreas. EUROPEAN BIOTECHNOLOGY spoke with Dr Michael Merz, the coordinator of the TransBioLine Project, and consortium member Prof Dr Stefan Wnendt about the plans and impact of the Project. |
Link | "We need predictive biomarkes" |
Document Type | Interview |
Pharmacodynamic Effects of Vorapaxar in Patients With and Without Diabetes Mellitus: Results of the OPTIMUS-5 Study
Publication Source | JACC: Basic to Translational Science 2019-11-01 4(7): 763-775 |
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Summary | Vorapaxar reduces thrombotic cardiovascular events at the expense of increased bleeding. However, the differential pharmacodynamic (PD) effects of vorapaxar according to diabetes mellitus (DM) status are unknown. Moreover, although withdrawal of aspirin has emerged as a bleeding reduction strategy, the PD effects of stopping aspirin in patients treated with vorapaxar also are unknown. In this prospective PD investigation, vorapaxar was associated with reduced platelet-mediated thrombogenicity without affecting clot kinetics irrespective of DM status. However, platelet-mediated thrombogenicity increased after aspirin withdrawal, particularly among patients with DM. (Optimizing anti-Platelet Therapy In diabetes MellitUS-5 Study [OPTIMUS-5]; NCT02548650) |
Link | https://jacc.org |
Document Type | Publication |
Receptor Occupancy Assay for Assessment of Therapeutic Agents
Summary | Receptor occupancy (RO), the measurement of the binding of a therapeutic to its cellular target, is increasingly important in the development of biologically based therapeutic agents. RO assay measurements can be used to determine minimal drug thresholds and guide dosing decisions during the clinical development of a drug. RO assays using flow cytometry describe the qualitative or quantitative measurement of the binding of a therapeutic agent to its cell surface target. Therefore, RO assays can measure the number of cell surface receptors bound by a therapeutic agent or can be designed to address more complicated scenarios such as receptor signaling, internalization or shedding events once a receptor engages a therapeutic agent. |
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Link | Receptor Occupancy Assay for Assessment of Therapeutic Agents |
Document Type | White Paper |
Evaluation of the pharmacodynamics of a ticagrelor reversal agent PB2452
Publication Source | ESC Congress 2019 |
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Background | Ticagrelor is a P2Y12 antagonist used in combination with aspirin to reduce the risk of recurrent thrombotic cardiovascular events in patients with acute coronary syndrome. Ticagrelor is associated with a risk for spontaneous major bleeding or bleeding associated with invasive procedures, particularly cardiac surgery. A rapid-acting reversal agent for ticagrelor would be advantageous. The pharmacodynamic effects of ticagrelor and a ticagrelor reversal agent are best evaluated using a panel of platelet function tests that have different sensitivities and methodologies and using a variety of agonists at different concentrations. |
Link | https://esc365.escardio.org |
Document Type | Video Presentation |
Antibody-Based Ticagrelor Reversal Agent in Healthy Volunteers
Publication Source | N Engl J Med 2019; 380:1825-1833 |
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Background | Ticagrelor is an oral P2Y12 inhibitor that is used with aspirin to reduce the risk of ischemic events among patients with acute coronary syndromes or previous myocardial infarction. Spontaneous major bleeding and bleeding associated with urgent invasive procedures are concerns with ticagrelor, as with other antiplatelet drugs. The antiplatelet effects of ticagrelor cannot be reversed with platelet transfusion. A rapid-acting reversal agent would be useful. |
Link | https://nejm.org |
Document Type | Publication |
Nickel reduces calcium dependent dimerization in neural cadherin
Publication Source | Metallomics, 2019,11, 475-482 |
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Abstract | Cadherins are the transmembrane component in adherens junctions, structures that link the actin cytoskeletons in adjacent cells within solid tissues including neurological synapses, epithelium and endothelium. Cell–cell adhesion by cadherins requires the binding of calcium ions to specific sites in the extracellular region. Given the complexity of the cell adhesion microenvironment, we are investigating whether other divalent cations might affect calcium-dependent dimerization of neural (N) cadherin. The studies reported herein characterize the impact of binding physiological magnesium(II) or neurotoxic nickel(II) on calcium-dependent N-cadherin function. Physiological levels of magnesium have only a small effect on the calcium-binding affinity and calcium-induced dimerization of N-cadherin. However, a tenfold lower concentration of nickel decreases the apparent calcium-binding affinity and calcium-induced dimerization of N-cadherin. Competitive binding studies indicate that the apparent dissociation constants for nickel and magnesium are 0.2 mM and 2.5 mM, respectively. These Kd values are consistent with concentrations observed for a range of divalent cations in the extracellular space. Results from these studies indicate that calcium-induced dimerization by N-cadherin is attenuated by natural and non-physiological divalent cations in the extracellular microenvironment |
Link | https://pubs.rsc.org |
Document Type | Publication |
Oxidative Burst Analysis by Flow Cytometry
Summary | The growing number of monoclonal antibody therapies have provided better, more targeted treatment for the different types of cancers. With these exciting new therapies, the side effects of immune suppression have been declining over the years. However, even these new therapies can be associated with increased opportunistic infections [1-3]. The complex network of pathways and cells that encompass immune response regulation make the assessments of immune suppression one of the most challenging aspects to monitor in recovering patients. Understanding the mechanisms by which new therapies contribute to immune suppression and increase the incidence of opportunistic infections is a key aspect for immune-oncology. |
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Link | Oxidative Burst Analysis by Flow Cytometry |
Document Type | White Paper |
2018
Effects of genetic variation in protease activated receptor 4 after an acute coronary syndrome: Analysis from the TRACER trial
Publication Source | Blood cells, molecules & diseases vol. 72 (2018): 37-43 |
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Abstract | Variation in platelet response to thrombin may affect the safety and efficacy of PAR antagonism. The Thr120 variant of the common single nucleotide polymorphism (SNP) rs773902 in the protease-activated receptor (PAR) 4 gene is associated with higher platelet aggregation compared to the Ala120 variant. We investigated the relationship between the rs773902 SNP with major bleeding and ischemic events, safety, and efficacy of PAR1 inhibition in 6177 NSTE ACS patients in the TRACER trial. There was a lower rate of GUSTO moderate/severe bleeding in patients with the Thr120 variant. The difference was driven by a lower rate in the smaller homozygous group (recessive model, HR 0.13 [0.02–0.92] P = 0.042). No significant differences were observed in the ischemic outcomes. The excess in bleeding observed with PAR1 inhibition was attenuated in patients with the Thr120 variant, but the interactions were not statistically significant. In summary, lower major bleeding rates were observed in the overall TRACER cohort with the hyperreactive PAR4 Thr120 variant. The increase in bleeding with vorapaxar was attenuated with the Thr120 variant, but we could not demonstrate an interaction with PAR1 inhibition. These findings warrant further exploration, including those of African ancestry where the A allele (Thr120) frequency is ~65%. |
Link | https://www.sciencedirect.com/ |
Document Type | Publication |
Inhibitory Mechanisms of Very Low-dose Rivaroxaban in Non-ST-elevation Myocardial Infarction
Publication Source | Blood Adv. 2018 Mar 27;2(6):715-730 |
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Abstract | Very low–dose (VLD) factor Xa (FXa) inhibition, in combination with acetylsalicylic acid (ASA) and clopidogrel, is associated with improved outcomes in patients with acute coronary syndrome (ACS) with a tolerable bleeding risk profile. To date, there are no data documenting platelet inhibition and the anticoagulatory effects of VLD FXa inhibition on top of guidelineadherent dual-antiplatelet therapy (DAPT) in patients with ACS. Patients with non–ST-elevation myocardial infarction (NSTEMI) receiving oral DAPT (ASA 1 clopidogrel, n 5 20; or ASA 1 ticagrelor, n 5 20) were prospectively enrolled in a nonrandomized study. Coagulation- and platelet-dependent thrombin generation (TG), measured by means of the calibrated automated thrombogram, were significantly decreased after in vitro and in vivo addition of rivaroxaban. As shown by a total thrombus-formation analysis approach, rivaroxaban treatment led to a significantly decreased coagulation-dependent (AR-chip) thrombus formation in patients treated with ASA plus P2Y12 inhibitor (clopidogrel/ticagrelor), whereas the pure platelet-dependent (PL-chip) thrombus formation was not affected at all. Adjunctive rivaroxaban therapy was not associated with significant differences in platelet aggregation assessed by light-transmission aggregometry (LTA). Nevertheless, according to fluorescence-activated cell sorter analysis, VLD rivaroxaban treatment resulted in a significantly reduced expression of platelet HMGB-1, whereas P-selectin exposure was not affected. Furthermore, an enhanced effect of rivaroxaban on total thrombus formation and TG was observed in particular in clopidogrel nonresponder patients defined as adenosine 59-diphosphate-induced LTA $40%. VLD rivaroxaban reduces thrombus formation and platelet-dependent TG in patients with ACS receiving DAPT, which can be of potential ischemic benefit. This trial was registered at www.clinicaltrials.gov as #NCT01417884. |
Link | Inhibitory mechanisms of very low-dose rivaroxaban |
Type | Publication |
Sequential Treatment Escalation with Dapagliflozin and Saxagliptin Improves Beta Cell Function in Type 2 Diabetic Patients on Previous Metformin Treatment: An Exploratory Mechanistic Study
Publication Source | Journal of American Heart Association, Vol. 9, No.8 |
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Background | Vorapaxar as an adjunct to dual antiplatelet therapy (DAPT) reduces thrombotic events in patients with prior myocardial infarction at the expense of increased bleeding. Withdrawal of aspirin has emerged as a bleeding reduction strategy. The pharmacodynamic effects of vorapaxar with potent P2Y12 inhibitors as well as the impact of dropping aspirin is unexplored and represented the aim of the VORA‐PRATIC (Vorapaxar Therapy in Patients With Prior Myocardial Infarction Treated With Newer Generation P2Y12 Receptor Inhibitors Prasugrel and Ticagrelor) study. |
Link | https://www.ahajournals.org |
Document Type | Publication |
Experimental study on the hemostatic effect of cyanoacrylate intended for catheter securement
Publication Source | Hormone and Metabolic Research 2018; 50(05): 403 - 407 |
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Purpose | We investigated the effect of sequential treatment escalation with dapagliflozin and saxagliptin on beta cell function in patients with T2DM insufficiently controlled on metformin monotherapy during a hyperglycaemic clamp investigation. Twenty-six patients (19 males, age 63.5±7.0 years; duration of diabetes 8.8±4.7 years; HbA1c 63.9±15.8 mmol/mol; mean±SD) were enrolled in the study. During a first treatment period (TP1) all patients received 10 mg dapagliflozin for one month, followed by the addition of 5 mg saxagliptin or placebo for another month (TP2). At baseline and at the end of each treatment period, fasting glucose and insulin levels were analysed, and a hyperglycaemic clamp with the measurement of plasma C-peptide, insulin, proinsulin, and glucagon was performed. |
Link | https://eref.thieme.de/ |
Type | Publication |
Evaluation of the Cy-Quant VASP/P2Y12 ELISA Kit for Sample Stability and Batch Processing
Summary | The platelet P2Y12 receptor is involved in ADP mediated platelet activation. A variety of methods and assays are available to measure P2Y12 function, such as the VerifyNow® (Instrumentation Laboratory), light transmission aggregometry (LTA), and the Cy-Quant VASP/P2Y12 ELISA (Stago). The purpose of this study was to evaluate suitability of batch processing of samples and to determine effects of sample stability for the Cy-Quant VASP/P2Y12 ELISA method. |
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Link | Evaluation of the Cy-Quant VASP/P2Y12 ELISA kit |
Document Type | Current Abstract |
2017
The Role of Platelet Function Testing in Improving Clinical Outcomes
Publication Source | The Medical Roundtable, November 1, 2017; CV43571 |
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Discussion Topics |
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Link | https://themedicalroundtable.com/ |
Document Type | Expert Round Table |
Effects on α‐ and β‐cell function of sequentially adding empagliflozin and linagliptin to therapy in people with type 2 diabetes previously receiving metformin: An exploratory mechanistic study
Publication Source | Diabetes, obesity & metabolism vol. 19,4 (2017): 489-495. |
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Abstract | Aims: To investigate the effect of sequential treatment escalation with empagliflozin and linagliptin on laboratory markers of α- and β-cell function in people with type 2 diabetes mellitus (T2DM) insufficiently controlled on metformin monotherapy. |
Link | https://dom-pubs.onlinelibrary.wiley.com/ |
Document Type | Publication |
The Impact of the Packaging System on the Stability of Blood Samples Used for Safety Assessments in Clinical Trials
Publication Source | Pharm.Ind. 70, Nr. 2, 284-289(2017) |
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Background | Reliable shipment of clinical blood, serum and plasma samples from remote sites to central labs for standardized analyses is increasingly important in medicnal product trials. This study investigates the benefits of dedicated packaging for protecting such samples from extreme seasonal temperature fluctuations during shipment. In this paper we describe the thermal properties of MLM's Safeguard Box which was tested with respect to the stability of real samples under stress conditions. |
Link | The Impact of the Packaging System in Clinical Trials |
Document Type | Publication |
Thrombin Generation Assay
Summary | Thrombin is the final product of the intrinsic and extrinsic pathways, converting soluble fibrinogen into fibrin. It also serves as a potent activator of platelet function. As a key enzyme in hemostasis and thrombosis, it is imperative that reliable monitoring of thrombin be performed in study subjects during pharmacologic safety trials, and in patients dosed with hemostasis-modulating medication. |
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Link | Thrombin Generation Assay |
Document Type | White Paper |
Functional and Phenotypic Microparticle Analysis
Summary | Circulating stimuli, including inflammatory cytokines and some therapeutics, activate platelets and endothelial cells. Measurement of circulating mciroparticles serves as an indicator of in vivo vascular function, and in clinical studies is used to identify risk of thrombosis and bleeding. |
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Link | Functional and Phenotypic Microparticle Analysis |
Document Type | White Paper |
2016
Light Transmission Aggregometry
Summary | Aggregometry remains the gold standard for evaluating platelet function due to the capability to tailor testing and to adequately assess drug dose response. It is the reference method used clinically to test for platelet disorders. |
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Link | Light Transmission and Luminescence Aggregometry |
Document Type | White Paper |
Platelet Function Analyzed by Flow Cytometry
Summary | Flow cytometry is a sensitive technique for assessing specific components of platelet function, including degranulation, receptor signaling and surface protein activation. |
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Link | Platelet Function Analyzed by Flow Cytometry |
Document Type | White Paper |
Platelet-Leukocyte Aggregate
Summary | Increasing evidence implicates platelets as key cellular mediators of inflammation and vascular disease. Platelets express and secrete a variety of molecules and inflammatory mediators, such as platelet factor 4, P-selectin, CD40L, vWF, CD63, thrombospondins, MMPs, polyphosphates, ADP, thromboxane, nitric oxide, IL-1β and GPIb. Many of these mediators promote recruitment of leukocytes to sites of endothelial damage or tissue inflammation and this pathway likely contributes to pathogenesis of inflammatory and cardiovascular diseases, such as atherosclerosis, diabetes, and rheumatoid arthritis. |
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Link | Platelet-Leukocyte Aggregate |
Document Type | White Paper |
Specialty Platelet Testing
Summary | Platelets are the intended, and sometimes unintended, targets of countless therapeutics. There is also an increasing appreciation that pathologies such as coronary artery disease, diabetes, and cancer alter platelet function. |
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Link | Specialty Platelet Testing |
Document Type | White Paper |
Coagulation Testing
Summary | Inflammation, endothelial damage, and platelet activation trigger secondary hemostasis, comprising initiation and propagation of the coagulation cascade and the formation of insoluble fibrin to consolidate and stabilize the thrombus. |
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Link | Coagulation Testing |
Document Type | White Paper |
2015
Characterization of pancreatic NMDA receptors as possible drug targets for diabetes treatment
Publication Source | Nature medicine vol. 21,4 (2015): 363-72. |
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Background | In the nervous system, NMDA receptors (NMDARs) participate in neurotransmission and modulate the viability of neurons. In contrast, little is known about the role of NMDARs in pancreatic islets and the insulin-secreting beta cells whose functional impairment contributes to diabetes mellitus. Here we found that inhibition of NMDARs in mouse and human islets enhanced their glucose-stimulated insulin secretion (GSIS) and survival of islet cells. Further, NMDAR inhibition prolonged the amount of time that glucose-stimulated beta cells spent in a depolarized state with high cytosolic Ca2+ concentrations. |
Link | https://www.nature.com/ |
Document Type | Publication |
Platelet function recovery following exposure to triple anti-platelet inhibitors using an in vitro transfusion model
Publication Source | Thrombosis research vol. 136,6 (2015): 1216-23 |
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Abstract | Dual anti-platelet therapy (DAPT) with aspirin and a P2Y 12 antagonist is standard of care to reduce risk of thrombosis, but does not directly target thrombin-dependent platelet activation. Therefore, PAR-1 antagonist addition to DAPT (i.e., triple anti-platelet therapy; TAPT) may improve the efficacy of treatment, though at the expense of an increase in bleeding risk. Using an in vitro transfusion model, we evaluated if platelet function loss associated with TAPT can be remedied by the addition of drug-naïve platelets. |
Link | https://www.thrombosisresearch.com/ |
Document Type | Publication |
2014
FDA Raises the Bar in Bioanalytical Method Validation
Publication Source | Journal for Clinical Studies, Regulatory V6 13, Volume 6, Issue 3, 2014 |
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Background | This paper on the new FDA draft validation guidelines is the second from MLM.For many years, the FDA guidance on bioanalytical method validation (BMV) issued by the CDER in 20011, has been the Holy Grail for laboratories which deal with the pharmacokinetic analysis of drugs and their metabolites in clinical trials. A revised version has been expected at least since the EMA issued its guideline on BMV in 20122, which is much more explicit and detailed in its requirements compared to the FDA guidance from 2001. The new FDA draft guidance is summarised in this editorial, and its implications for clinical studies are discussed. |
Link | Journal for Clinical Studies |
Document Type | Publication |
PAR1 antagonists inhibit thrombin-induced platelet activation whilst leaving the PAR4-mediated response intact
Publication Source | Platelets vol. 26,3 (2015): 236-42. |
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Abstract | Thrombin-induced platelet activation is initiated by PAR1 and PAR4 receptors. Vorapaxar, a PAR1 antagonist, has been assessed in patients with acute coronary syndromes (ACS) and stable atherosclerotic disease in addition to standard-of-care treatment. In clinical trials, vorapaxar has been observed to reduce the frequency of ischaemic events in some subgroups though in others has increased the frequency of bleeding events. Among patients undergoing CABG surgery, which is associated with excess thrombin generation, bleeding was not increased. The aim of these studies was to investigate the effects of selective PAR1 antagonism on thrombin-induced platelet activation in patients receiving vorapaxar or placebo in the TRACER trial and to explore the roles of PAR1 and PAR4 in thrombin-induced platelet activation in healthy volunteers. |
Link | https://www.tandfonline.com/ |
Document Type | Publication |
Tetraspanin CD9 Regulates Cell Contraction and Actin Arrangement via RhoA in Human Vascular Smooth Muscle Cells
Publication Source | PloS one vol. 9,9 e106999. 3 Sep. 2014, |
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Abstract | The most prevalent cardiovascular diseases arise from alterations in vascular smooth muscle cell (VSMC) morphology and function. Tetraspanin CD9 has been previously implicated in regulating vascular pathologies; however, insight into how CD9 may regulate adverse VSMC phenotypes has not been provided. We utilized a human model of aortic smooth muscle cells to understand the consequences of CD9 deficiency on VSMC phenotypes. Upon knocking down CD9, the cells developed an abnormally small and rounded morphology. We determined that this morphological change was due to a lack of typical parallel actin arrangement. We also found similar total RhoA but decreased GTP-bound (active) RhoA levels in CD9 deficient cells. |
Link | https://journals.plos.org/ |
Document Type | Publication |
Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes
Publication Source | Thromb Haemost 2014; 111(05): 883-891 |
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Summary | Vorapaxar is an antagonist of the protease activated receptor-1 (PAR-1), the principal platelet thrombin receptor. The Thrombin Receptor Antagonist for Clinical Event Reduction (TRACER) trial evaluated vorapaxar compared to placebo in non-ST-elevation (NSTE)-acute coronary syndrome (ACS) patients. It was the study′s objective to assess the pharmacodynamic effects of vorapaxar versus placebo that included aspirin or a thienopyridine or, frequently, a combination of both agents in NSTE-ACS patients. In a substudy involving 249 patients, platelet aggregation was assessed by light transmittance aggregometry (LTA) in 85 subjects (41 placebo, 44 vorapaxar) using the agonists thrombin receptor activating peptide (TRAP, 15 μM), adenosine diphosphate (ADP, 20 μM), and the combination of collagen-related peptide (2.5 μg/ml) + ADP (5 μM) + TRAP (15 μM) (CAT). VerifyNow® IIb/IIIa and vasodilator-stimulated phosphoprotein (VASP) phosphorylation assays were performed, and platelet PAR-1 expression, plasma platelet/endothelial and inflammatory biomarkers were determined before and during treatment. |
Link | https://www.thieme-connect.com/ |
Document Type | Publication |
2013
Choosing the Right Lab: Big is Not Always Beautiful
(Kopie 1)
Publication Source | Journal of American Heart Association, Vol. 9, No.8 |
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Background | Vorapaxar as an adjunct to dual antiplatelet therapy (DAPT) reduces thrombotic events in patients with prior myocardial infarction at the expense of increased bleeding. Withdrawal of aspirin has emerged as a bleeding reduction strategy. The pharmacodynamic effects of vorapaxar with potent P2Y12 inhibitors as well as the impact of dropping aspirin is unexplored and represented the aim of the VORA‐PRATIC (Vorapaxar Therapy in Patients With Prior Myocardial Infarction Treated With Newer Generation P2Y12 Receptor Inhibitors Prasugrel and Ticagrelor) study. |
Link | https://www.ahajournals.org |
Document Type | Publication |
Association of Aspirin Dose and Vorapaxar Safety and Efficacy in Patients With Non–ST-Segment Elevation Acute Coronary Syndrome (from the TRACER Trial)
Publication Source | Journal for Clinical Studies, Market Report V5 15, Volume 5, Issue 5, 2013 |
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Summary | This paper will discuss the different categories of laboratories involved in clinical labs and may be used as a brief guide to a good match between study design and laboratory services. |
Link | Journal for Clinical Studies |
Document Type | Publication |
2012
Thrombin-Receptor Antagonist Vorapaxar in Acute Coronary Syndromes
Publication Source | N Engl J Med 2012; 366:20-33 |
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Background | Vorapaxar is a new oral protease-activated–receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation. |
Link | https://www.nejm.org/ |
Document Type | Publication |