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Letteratura scientifica selezionata sul tema "Glenzocimab"

Autore: Grafiati

Pubblicato: 9 novembre 2024

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Articoli di riviste sul tema "Glenzocimab"

Pottecher, Julien, Francois Raffi, Martine Jandrot-Perrus, Sophie Binay, Andrea Comenducci, Violaine Desort-Henin, Déborah François et al. "Targeting GPVI with glenzocimab in COVID-19 patients: Results from a randomized clinical trial". PLOS ONE 19, n. 6 (17 giugno 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 for 40 days. Primary efficacy endpoint was clinical progression at Day 4. All analyses concerned the intention-to-treat population. Results Between December 2020 and August 2021, 61 patients received at least one dose (30 glenzocimab vs 32 placebo) and 58 completed the study (29 vs 29). Clinical progression of COVID-19 ARDS was not statistically different between glenzocimab and placebo arms (43.3% and 29.0%, respectively; p = 0.245). Decrease in the NEWS-2 category at D4 was statistically significant (p = 0.0290) in the glenzocimab arm vs placebo. No Serious Adverse Event (SAE) was deemed related to study drug; bleeding related events were reported in 6 patients (7 events) and 4 patients (4 events) in glenzocimab and placebo arms, respectively. Conclusions Therapeutic GPVI inhibition assessment during COVID-19 was conducted in response to a Public Health emergency. Glenzocimab in coagulopathic patients under therapeutic heparin was neither associated with increased bleeding, nor SAE. Clinical impact of glenzocimab on COVID-19 ARDS was not demonstrated. A potential role for GPVI inhibition in other types of ARDS deserves further experimentation. Glenzocimab is currently studied in stroke (ACTISAVE: NCT05070260) and cardiovascular indications.

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Renaud, Lionel, Kristell Lebozec, Christine Voors‐Pette, Peter Dogterom, Philippe Billiald, Martine Jandrot Perrus, Yannick Pletan e Matthias Machacek. "Population Pharmacokinetic/Pharmacodynamic Modeling of Glenzocimab (ACT017) a Glycoprotein VI Inhibitor of Collagen‐Induced Platelet Aggregation". Journal of Clinical Pharmacology 60, n. 9 (4 giugno 2020): 1198–208. http://dx.doi.org/10.1002/jcph.1616.

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Jandrot-Perrus, M., J. Pottecher, E. Toledano, A. Commenducci, A. Meilhoc, S. Gharakhanian, G. Avenard, Y. Pletan, S. Binay e M. Mazighi. "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 (ottobre 2023): 101499. http://dx.doi.org/10.1016/j.rpth.2023.101499.

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Comenducci, Andrea, Adeline Meilhoc, Yannick Pletan, Sophie Binay, Gilles Avenard, Alistair Perry, Rafael Namias 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 (febbraio 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 and MRI at 7 days for safety and efficacy analysis. Baseline and follow up imaging were processed as post-hoc analysis using AI core lab software (Brainomix, Oxford, UK). Automated output was reviewed for accuracy by an expert clinician (DC) blinded to treatment allocation. Results and Conclusions: Follow up imaging data were available from 103/106 patients (51 glenzocimab, 52 placebo) at 24 hours. Of these, 54 underwent mechanical thrombectomy (MT, 27 glenzocimab, 27 placebo). Day-7 imaging was available for 9 fewer placebo patients and 1 glenzocimab patient. All except 2 patients (1 placebo, 1 glenzocimab) with missing data at Day-7 died during the study. Preliminary analysis showed smaller volume of hemorrhagic transformation (HT) in the glenzocimab group at 24 hours compared to placebo and a trend towards smaller volume of ischemic injury. Exploratory analysis also highlighted an interaction effect between risk of HT following MT and glenzocimab (lower risk in patients treated with glenzocimab). The full results of the imaging sub-analysis of the ACTIMIS study will be presented at the conference and discussed in the context of current literature.

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Comenducci, Andrea, Adeline Meilhoc, Yannick Pletan, Sophie Binay, Gilles Avenard, Davide Carone, Alistair Perry 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 (novembre 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 hemorrhage occurrence stroke‐related mortality and a trend towards reduction in severe disability. In this sub‐analysis, Artificial Intelligence (AI) imaging biomarkers were used to assess efficacy of glenzocimab in the subgroup undergoing MT in the pooled phase 1b (dose escalation) and phase 2a (dose confirmation) studies. Methods In the phase 1b study, patients were randomized to an escalating dose of glenzocimab or placebo (4:1, n=12 per group, 125mg, 250mg, 500mg, 1000mg). In the phase 2 dose confirmation study, patients were randomized (1:1) with 1000mg glenzocimab or placebo. CT scan or MRI was acquired at baseline with CT at 24 hours and MRI at 7 days (CT if MRI not available) for safety and efficacy analysis, respectively. Baseline and follow up imaging were processed using Brainomix software (Oxford, UK). AI output was reviewed for accuracy by an expert clinician (DC) blinded to treatment allocation. Results Of 166 patients in the trial, 81 patients underwent MT and had follow up non‐contrast CT imaging available at 24 hours (48 glenzocimab, 33 placebo) and 72 had Day‐7 imaging (47 glenzocimab, 25 placebo). Day‐7 imaging was available for 8 fewer placebo patients and 1 glenzocimab patient than at 24 hours. All except 2 patients (1 placebo, 1 glenzocimab) with missing data at Day‐7 died during the study. Multivariate regression modelling showed a significant interaction between patients undergoing MT and receiving glenzocimab. Glenzocimab had a greater effect on reducing the risk of haemorrhagic transformation in the MT subgroup (exploratory p=0.001). Presenting acute infarct volume was similar between glenzocimab and placebo arms (mean [SD]; 16.27mL [30.2] vs. 19.62mL [28.98], non‐significant). There was a significantly smaller volume of haemorrhagic transformation in the glenzocimab group at 24 hours compared to placebo (1.83mL [6.59] vs 33.46mL [75.07], exploratory p<0.01) and a trend towards smaller volume of ischemic injury in the glenzocimab group (52.32mL [82.07] vs 62.93mL [79.4]). Similar significant trend at Day‐7 for haemorrhagic transformation was seen but less marked due to the unbalanced loss to follow up at Day‐7 (2.99mL [12.35] vs 4.19mL [10.83], exploratory p<0.05). Conclusion Glenzocimab reduces likelihood of haemorrhagic transformation in patients undergoing MT. Haemorrhage volumes were smaller in the glenzocimab group and encouragingly there was a trend to smaller volumes of ischemic injury. There was a greater drop‐out rate in the placebo group between 24 hours and Day‐7, which resulted in a smaller difference in haemorrhagic volumes at Day‐7. Those results, which are to be further analysed in ACTIMIS overall population of AIS patients, could highlight glenzocimab mechanism in the reperfusion injury mitigation.

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Wichaiyo, Surasak, Warisara Parichatikanond e Wipharak Rattanavipanon. "Glenzocimab: A GPVI (Glycoprotein VI)-Targeted Potential Antiplatelet Agent for the Treatment of Acute Ischemic Stroke". Stroke, 21 settembre 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 middle cerebral artery occlusion, a model of ischemic stroke, with no or minor bleeding tendency. Intravenous injection of glenzocimab in nonhuman primates produced rapid inhibition of ex vivo platelet aggregation induced by collagen (a GPVI ligand). Complete platelet inhibition is observed at 30 minutes following administration without increasing the risk of bleeding. In humans, glenzocimab is well tolerated and produces dose-dependent antiplatelet activity. More importantly, glenzocimab (125–1000 mg) was safe when administered as soon as possible (<3 hours) following reperfusion with the r-tPA (recombinant tissue-type plasminogen activator) in patients with acute ischemic stroke. Although glenzocimab 1000 mg (a selected dose) did not demonstrate a significant improvement in overall clinical outcomes, it appeared to provide benefits in severe cases and in patients who required thrombectomy. This promising efficacy together with a good safety profile of glenzocimab warrant further investigation in phase III (ACTISAVE [Adaptive Efficacy and Safety Study of Glenzocimab Used as an Add-On Therapy on Top of Standard of Care in the 4.5 Hours Following an Acute Ischemic Stroke]) clinical study.

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Alenazy, F. O., M. H. Harbi, D. P. Kavanagh, J. Price, P. Brady, O. Hargreaves, P. H. Harrison 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 (1 ottobre 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 novel platelet GPVI inhibitor, glenzocimab (a Fab fragment of a monoclonal antibody), on platelet activation and thrombus formation when combined with aspirin and ticagrelor. Methods We used intravital microscopy in a murine model of ST-elevation myocardial infarction and ischaemia-reperfusion injury to investigate microvascular thrombosis. We investigated the antithrombotic effects of adding glenzocimab (previously known as ACT017) to blood from healthy donors and 20 patients with ACS treated with aspirin and ticagrelor. We compared the effect of glenzocimab with the GPIIb/IIIa inhibitor eptifibatide ex-vivo. We stimulated platelets with collagen and atherosclerotic plaque material that was sourced from patients undergoing carotid endarterectomy. We investigated effects on platelet aggregation, spreading, signalling, adhesion, thrombin generation, thrombus formation and clot stability ex vivo. Results Genetic depletion of GPVI in an animal model of myocardial infarction reduced microvascular thrombosis. Ex vivo, aspirin and ticagrelor partially inhibited atherosclerotic plaque-induced platelet aggregation (assessed by multiple electrode aggregometry) by 48% compared to control (34±3 vs. 65±4 U; P<0.001; Figure 1). Atherosclerotic plaque-induced platelet aggregation, adhesion, secretion and activation were critically dependent on platelet GPVI activation and were potently inhibited by glenzocimab. Glenzocimab alone reduced atherosclerotic plaque-induced platelet aggregation by 75% compared to control (16±4 vs. 65±4 U; P<0.001; Figure 1) and by over 95% when combined with aspirin and ticagrelor (3±1 vs 65±4 U; P<0.001; Figure 1). Furthermore, glenzocimab provided multiple synergistic antithrombotic effects when added to the blood of aspirin and ticagrelor-treated patients with ACS ex vivo. Glenzocimab and the GPIIb/IIIa inhibitor, eptifibatide, had many similar antithrombotic effects but glenzocimab had less effect on mechanisms of general haemostasis compared to eptifibatide, as assessed by ROTEM (Figure 2). Conclusions The addition of glenzocimab to aspirin and ticagrelor provides synergistic inhibition of multiple critical mechanisms of atherothrombosis. Glenzocimab and the GPIIb/IIIa inhibitor, eptifibatide, share many similar antithrombotic effects, although glenzocimab has less impact on mechanisms involved in haemostasis compared to eptifibatide. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Academy of Medical Sciences UK Clinical Lecturer Starter GrantRoyal Embassy of Saudi Arabia

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Billiald, Philippe, Alexandre Slater, Martin Welin, Joanne C. Clark, Loyau Stéphane, Martine Pugnière, Isabella Gizzi Jiacomini et al. "Targeting platelet GPVI with glenzocimab: a novel mechanism for inhibition". Blood Advances, 14 novembre 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 was obtained and its structure determined to a resolution of 1.9 Å. The data revealed that (i) glenzocimab binds to the D2 domain of GPVI; GPVI dimerisation was not observed in the crystal structure because glenzocimab prevented D2 homotypic interactions and the formation of dimers which have a high affinity for collagen and fibrin; (ii) the light variable (VL) domain of the GPVI-bound Fab causes steric hindrance that is predicted to prevent the collagen-related peptide (CRP)/collagen fibers from extending out of their binding site and preclude GPVI clustering and downstream signaling. Glenzocimab did not bind to a truncated GPVI missing loop residues 129-136, thus validating the epitope identified in the crystal structure. Overall, these findings demonstrate that the binding of glenzocimab to the D2 domain of GPVI induces steric hindrance and structural modifications that drive the inhibition of GPVI interactions with its major ligands.

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Jadoui, Soumaya, Ophélie Le Chapelain, Véronique Ollivier, Ali Mostefa-Kara, Lucas Di Meglio, Sébastien Dupont, Angèle Gros et al. "Glenzocimab does not impact glycoprotein VI-dependent inflammatory haemostasis". Haematologica, 30 dicembre 2020. http://dx.doi.org/10.3324/haematol.2020.270439.

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

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Tesi sul tema "Glenzocimab"

Kern, Axelle Y. "La thrombose de stent : évaluation de l’importance de la rhéologie dans la thrombogénicité des stents et d’un nouvel agent pharmacologique dirigé contre la GPVI pour prévenir la thrombose de stent". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ027.

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Une complication majeure de la pose d’un stent sur une plaque d’athérosclérose est la thrombose de stent, qui présente un taux de mortalité particulièrement élevé. La bithérapie antiplaquettaire, indiquée dans la prévention de cette complication, entraîne un risque important de saignement et n’est pas toujours efficace. L’objectif de ce travail de thèse a consisté à identifier les mécanismes de la thrombose de stent et à évaluer l’intérêt d’une nouvelle classe d'agents antiplaquettaires capables de la prévenir efficacement avec un risque hémorragique faible. Le développement d’un modèle macrofluidique original a permis de montrer que les stents carotidiens utilisés en clinique possèdent une thrombogénicité intrinsèque d’une part au niveau de la bifurcation, dans la lumière du vaisseau, et d’autre part au niveau des mailles en contact avec la paroi du vaisseau. Le dispositif a également mis en lumière un effet protecteur des mailles du stent sur la thrombose de stent. Enfin, le modèle a montré que le glenzocimab, un agent anti-GPVI, est aussi efficace dans la prévention de la thrombose de stent que les traitements de référence, mais sans risque de saignements
A major complication of stenting in a diseased artery is stent thrombosis, which has a particularly high mortality rate. Dual antiplatelet therapy, indicated to prevent this complication, possesses a high risk of bleeding and is not always effective. The aim of my PhD was to identify the mechanisms of stent thrombosis and to evaluate the interest of a new class of antiplatelet agents to efficiently prevent it with a low bleeding risk. The development of an original macrofluidic model has enabled us to show that the carotid stents used in clinical practice present an intrinsic thrombogenicity evidenced both at the bifurcation of a vessel where the stent meshes lie in the lumen, and around some specific places of the stent struts which are in contact with the vessel wall. The device also helped to identify a protective effect of the stent mesh, which reduces stent thrombosis. Finally, the model showed that glenzocimab, an anti-GPVI agent, is effective in preventing stent thrombosis to a similar extent than reference treatments, but with no bleeding risk

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Atti di convegni sul tema "Glenzocimab"

Pottecher, J., V. A. H. Sato, Y. Plétan, A. Comenducci, V. Desort-Henin, M. Jandrot-Perrus, S. Binay, A. Meilhoc e G. Avenard. "A Novel Anti-Thrombotic, Glenzocimab, in Covid-19 acute respiratory distress syndrome (Cov-ARDS)." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2878.

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Köhrmann, Martin, Elie Toledano, Yannick Plétan, Andrea Comenducci, Adeline Meilhoc, Sophie Binay, Gilles Avenard e James Grotta. "P024 ACTISAVE study: efficacy and safety of glenzocimab on top of thrombolysis and mechanical thrombectomy". In 16th Congress of the European Society of Minimally Invasive Neurological Therapy (ESMINT) 2024, A36.2—A36. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2024. http://dx.doi.org/10.1136/jnis-2024-esmint.61.

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