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Artykuły w czasopismach na temat „Glenzocimab”

Autor: Grafiati
Data publikacji: 9 listopada 2024
Data aktualizacji: 31 lipca 2025

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Sprawdź 17 najlepszych artykułów w czasopismach naukowych na temat „Glenzocimab”.

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1

Pottecher, Julien, Francois Raffi, Martine Jandrot-Perrus, et al. "Targeting GPVI with glenzocimab in COVID-19 patients: Results from a randomized clinical trial." PLOS ONE 19, no. 6 (2024): e0302897. http://dx.doi.org/10.1371/journal.pone.0302897.

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Background Glenzocimab is a novel antithrombotic agent which targets platelet glycoprotein VI (GPVI) and does not induce haemorrhage. SARS-CoV-2 triggers a prothrombotic state and lung injury whose mechanisms include coagulopathy, endothelial dysfunction, and inflammation with dysregulated platelets. Methods and patients GARDEN was a randomised double-blind, exploratory phase II study of glenzocimab in SARS-CoV-2 respiratory failure (NCT04659109). PCR+ adults in Brazil and France (7 centres) were randomized to standard-of-care (SOC) plus glenzocimab (1000 mg/dayx3 days) or placebo, followed fo
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2

Renaud, Lionel, Kristell Lebozec, Christine Voors‐Pette, et al. "Population Pharmacokinetic/Pharmacodynamic Modeling of Glenzocimab (ACT017) a Glycoprotein VI Inhibitor of Collagen‐Induced Platelet Aggregation." Journal of Clinical Pharmacology 60, no. 9 (2020): 1198–208. http://dx.doi.org/10.1002/jcph.1616.

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3

Jandrot-Perrus, M., J. Pottecher, E. Toledano, et al. "PB0364 Glycoprotein VI-Targeted Antiplatelet Therapy with Glenzocimab is Safe in Patients Exposed to Current Antithrombotic and Fibrinolytic Drugs." Research and Practice in Thrombosis and Haemostasis 7 (October 2023): 101499. http://dx.doi.org/10.1016/j.rpth.2023.101499.

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4

Comenducci, Andrea, Adeline Meilhoc, Yannick Pletan, et al. "Abstract 28: Patients Randomised to Glenzocimab Suffered Less Haemorrhagic Transformation at 24 Hours Compared to Placebo: AI-Imaging Sub-Analysis of the ACTIMIS Trial." Stroke 55, Suppl_1 (2024). http://dx.doi.org/10.1161/str.55.suppl_1.28.

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Introduction: ACTIMIS (NCT03803007) was a randomized phase 1b/2a clinical trial evaluating glenzocimab, a monoclonal antibody fragment targeting platelet receptor glycoprotein VI in patients with acute ischemic stroke treated by thrombolysis. Primary analysis demonstrated a reduction in intracranial hemorrhage occurrence stroke-related mortality. In this sub-analysis, volumetric imaging biomarkers were used to assess efficacy of glenzocimab. Methods: In the phase 2a study, patients were randomized (1:1) with 1000mg glenzocimab or placebo. CT or MRI was acquired at baseline with CT at 24 hours
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5

Comenducci, Andrea, Adeline Meilhoc, Yannick Pletan, et al. "Abstract 006: Glenzocimab Is Associated With Less Haemorrhagic Transformation Using Artificial Intelligence Imaging In Mechanical Thrombectomy Patients." Stroke: Vascular and Interventional Neurology 3, S2 (2023). http://dx.doi.org/10.1161/svin.03.suppl_2.006.

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Introduction Lesion volume measurement provides an objective and quantitative assessment of stroke severity and it is often used as a surrogate endpoint of clinical outcome in therapeutic trials. ACTIMIS (NCT03803007) was a randomized phase 1b/2a clinical trial evaluating glenzocimab, a monoclonal antibody fragment targeting platelet receptor glycoprotein VI, versus placebo in patients with acute ischemic stroke treated by thrombolysis alone or associated with mechanical thrombectomy (MT), both subgroups being well balanced. Primary analysis demonstrated a significant reduction in intracranial
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6

Wichaiyo, Surasak, Warisara Parichatikanond, and Wipharak Rattanavipanon. "Glenzocimab: A GPVI (Glycoprotein VI)-Targeted Potential Antiplatelet Agent for the Treatment of Acute Ischemic Stroke." Stroke, September 21, 2022. http://dx.doi.org/10.1161/strokeaha.122.039790.

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It has previously been shown in several animal experiments that platelet GPVI (glycoprotein VI) contributes to thrombosis, particularly in ischemic stroke. Moreover, GPVI levels are upregulated in stroke patients. This review describes the therapeutic roles of anti-GPVI antibody in preclinical models of ischemic stroke and provides the current evidence for potential benefits of glenzocimab, a Fab fragment of humanized anti-GPVI monoclonal antibody, in stroke patients. Anti-GPVI antibody, JAQ1, significantly decreased infarct volume and improved neurological function in mice with transient midd
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7

Alenazy, F. O., M. H. Harbi, D. P. Kavanagh, et al. "GPVI inhibition by glenzocimab synergistically inhibits atherosclerotic plaque-induced platelet activation when combined with conventional dual antiplatelet therapy." European Heart Journal 42, Supplement_1 (2021). http://dx.doi.org/10.1093/eurheartj/ehab724.1425.

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Abstract Introduction Aspirin and a potent platelet P2Y12 inhibitor, such as prasugrel or ticagrelor, are not always sufficient to prevent thrombus formation in patients with ST-elevation MI (STEMI), leading to “slow flow” or “no reflow” effects after stenting. GPIIb/IIIa inhibitors, such as eptifibatide, may help in this setting, but are not used routinely due to their bleeding risk. GPVI has critical roles in thrombosis and a minimal role in haemostasis. Here we tested whether depletion of GPVI has effects on thrombus formation after MI in an animal model and investigated the effects of a no
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8

Billiald, Philippe, Alexandre Slater, Martin Welin, et al. "Targeting platelet GPVI with glenzocimab: a novel mechanism for inhibition." Blood Advances, November 14, 2022. http://dx.doi.org/10.1182/bloodadvances.2022007863.

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Platelet glycoprotein VI (GPVI) is attracting interest as a potential target for the development of new antiplatelet molecules with a low bleeding risk. GPVI binding to vascular collagen initiates thrombus formation and GPVI interactions with fibrin promote the growth and stability of the thrombus. In the present study we show that glenzocimab, a clinical stage humanized antibody fragment (Fab) with high affinity for GPVI, blocks binding of both ligands through a combination of steric hindrance and structural change. A co-crystal of glenzocimab with an extracellular domain of monomeric GPVI wa
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9

Dupont, Sébastien, Héloïse Lebas, Sabrina Mavouna, et al. "Comparative Effects of Glenzocimab and Eptifibatide on Bleeding Severity in 2 Mouse Models of Intracranial Hemorrhage." Journal of the American Heart Association, January 17, 2025. https://doi.org/10.1161/jaha.123.034207.

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Background Antiplatelet drugs represent potential candidates for protecting the penumbral microcirculation during cerebral ischemia and improving the benefits of arterial recanalization in ischemic stroke. Yet while the efficacy of such adjuvant strategies has been shown to be highly time dependent, antiplatelet therapy at the acute phase of ischemic stroke cannot be envisioned until the diagnosis of stroke and its ischemic nature have been confirmed because of the presumed risk of worsening bleeding in case of intracranial hemorrhage (ICH). Here, we investigated this risk for 2 antiplatelet d
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10

Jadoui, Soumaya, Ophélie Le Chapelain, Véronique Ollivier, et al. "Glenzocimab does not impact glycoprotein VI-dependent inflammatory haemostasis." Haematologica, December 30, 2020. http://dx.doi.org/10.3324/haematol.2020.270439.

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11

Mangin, Pierre H., and Martine Jandrot-Perrus. "Glycoprotein VI inhibitors: glenzocimab and EMA601 two inhibitory Fabs." European Heart Journal, April 2, 2025. https://doi.org/10.1093/eurheartj/ehaf160.

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12

Nieswandt, Bernhard, David Stegner, and Stefano Navarro. "EMA601 and glenzocimab: two glycoprotein VI inhibitory Fabs with different potency." European Heart Journal, April 2, 2025. https://doi.org/10.1093/eurheartj/ehaf162.

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13

Alenazy, Fawaz O., Maan H. Harbi, Dean P. Kavanagh, et al. "Amplified inhibition of atherosclerotic plaque-induced platelet activation by glenzocimab with dual antiplatelet therapy." Journal of Thrombosis and Haemostasis, August 2023. http://dx.doi.org/10.1016/j.jtha.2023.07.018.

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14

Slater, Alexandre, Sophia Khattak, and Mark R. Thomas. "GPVI as an effective antithrombotic target." European Heart Journal - Cardiovascular Pharmacotherapy, March 7, 2024. http://dx.doi.org/10.1093/ehjcvp/pvae018.

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Abstract Glycoprotein (GP) VI plays a major role in thrombosis but not haemostasis, making it a promising antithrombotic target. The primary role of GPVI on the surface of platelets is a signalling receptor for collagen, which is one of the most potent thrombotic sub-endothelial components that is exposed by atherosclerotic plaque rupture. Inhibition of GPVI has therefore been investigated as a strategy for treatment and prevention of atherothrombosis, such as during stroke and acute coronary syndromes. A range of specific GPVI inhibitors have been characterised and 2 of these inhibitors, glen
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15

Jooss, Natalie J., Yvonne M. C. Henskens, Steve P. Watson та ін. "Pharmacological Inhibition of Glycoprotein VI- and Integrin α2β1-Induced Thrombus Formation Modulated by the Collagen Type". Thrombosis and Haemostasis, 17 лютого 2023. http://dx.doi.org/10.1055/s-0043-1761463.

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Background In secondary cardiovascular disease prevention, treatments blocking platelet-derived secondary mediators pose a risk of bleeding. Pharmacological interference of the interaction of platelets with exposed vascular collagens is an attractive alternative, with clinical trials ongoing. Antagonists of the collagen receptors, glycoprotein VI (GPVI), and integrin α2β1, include recombinant GPVI-Fc dimer construct Revacept, 9O12 mAb based on the GPVI-blocking reagent Glenzocimab, Syk tyrosine-kinase inhibitor PRT-060318, and anti-α2β1 mAb 6F1. No direct comparison has been made of the antith
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16

Xu, Rui-Gang, Christian Tiede, Antonio N. Calabrese, et al. "Affimer reagents as tool molecules to modulate platelet GPVI-ligand interactions and specifically bind GPVI dimer." Blood Advances, June 5, 2024. http://dx.doi.org/10.1182/bloodadvances.2024012689.

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Glycoprotein (GP)VI plays a key role in collagen-induced platelet aggregation. Affimers are engineered binding protein alternatives to antibodies. We screened and characterized GPVI-binding Affimers as novel tools to probe GPVI function. Among the positive clones, M17, D22 and D18 bound GPVI with the highest affinities (KD in the nM range). These Affimers inhibited GPVI-CRP-XL/collagen interactions, CRP-XL/collagen induced platelet aggregation and D22 also inhibited in vitro thrombus formation on a collagen surface under flow. D18 bound GPVI dimer but not monomer. GPVI binding was increased fo
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17

Stoll, Guido, Bernhard Nieswandt, and Michael K. Schuhmann. "Ischemia/reperfusion injury in acute human and experimental stroke: focus on thrombo-inflammatory mechanisms and treatments." Neurological Research and Practice 6, no. 1 (2024). http://dx.doi.org/10.1186/s42466-024-00355-y.

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Abstract Background Despite high recanalization rates of > 90% after endovascular thrombectomy (EVT) clinical outcome in around 50% of treated acute ischemic stroke (AIS) patients is still poor. Novel treatments augmenting the beneficial effects of recanalization are eagerly awaited, but this requires mechanistic insights to explain and overcome futile recanalization. Main body At least two mechanisms contribute to futile recanalization after cerebral large vessel occlusions (LVO): (i) the no reflow phenomenon as evidenced by randomly distributed areas without return of blood flow despite r
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