Randomized, open-label, single dose, two-period, two-treatment, cross-over bioequivalence study comparing test product Rivaroxaban/Acetylsalicylic acid, tablet, 2.5 mg/50 mg (given as two tablets) to reference product Xarelto 2.5 mg film-coated tablets (given as two tablets) and Aspirin® N 100 mg tablet in healthy male and female subjects under fasting conditions.

开始日期2024-07-29

申办/合作机构-

CTR20242554 / CompletedN/A

氯吡格雷阿司匹林片在健康人群中的生物等效性试验

研究空腹和餐后状态下单次口服受试制剂氯吡格雷阿司匹林片（北京福元医药股份有限公司生产）与参比制剂氯吡格雷阿司匹林片（商品名：多立维，Sanofi K.K.持证，Sanofi Winthrop Industrie, Ambares Plant生产）后在健康受试者体内的药代动力学，评价空腹和餐后状态下口服两种制剂的生物等效性。观察受试制剂氯吡格雷阿司匹林片和参比制剂氯吡格雷阿司匹林片在中国健康受试者中的安全性。

开始日期2024-07-23

申办/合作机构

北京福元医药股份有限公司

CTR20241875 / CompletedN/A

氯吡格雷阿司匹林片在健康人群中的生物等效性试验

空腹和餐后状态下单次口服受试制剂氯吡格雷阿司匹林片（北京福元医药股份有限公司生产）与参比制剂氯吡格雷阿司匹林片（Sanofi K.K.持证，Sanofi Winthrop Industrie, Ambares Plant生产）后，研究受试制剂和参比制剂的吸收速度和吸收程度，初步评估受试制剂和参比制剂是否具有生物等效性，估算参比制剂的个体内变异，为后续研究提供数据参考。观察受试制剂氯吡格雷阿司匹林片和参比制剂氯吡格雷阿司匹林片在中国健康受试者中的安全性。

开始日期2024-05-27

申办/合作机构

北京福元医药股份有限公司

100 项与 P2Y12 receptor x COX 相关的临床结果

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100 项与 P2Y12 receptor x COX 相关的转化医学

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0 项与 P2Y12 receptor x COX 相关的专利（医药）

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项与 P2Y12 receptor x COX 相关的文献（医药）

2023-03-01·Seminars in Nuclear Medicine

Positron Emission Tomography of Neuroimmune Responses in Humans: Insights and Intricacies

Review

作者: Raval, Nakul R ; Dubroff, Jacob G ; Hillmer, Ansel T ; Wetherill, Reagan R ; Wiers, Corinde E

The brain's immune system plays a critical role in responding to immune challenges and maintaining homeostasis. However, dysregulated neuroimmune function contributes to neurodegenerative disease and neuropsychiatric conditions. In vivo positron emission tomography (PET) imaging of the neuroimmune system has facilitated a greater understanding of its physiology and the pathology of some neuropsychiatric conditions. This review presents an in-depth look at PET findings from human neuroimmune function studies, highlighting their importance in current neuropsychiatric research. Although the majority of human PET studies feature radiotracers targeting the translocator protein 18 kDa (TSPO), this review also considers studies with other neuroimmune targets, including monoamine oxidase B, cyclooxygenase-1 and cyclooxygenase-2, nitric oxide synthase, and the purinergic P2X7 receptor. Promising new targets, such as colony-stimulating factor 1, Sphingosine-1-phosphate receptor 1, and the purinergic P2Y12 receptor, are also discussed. The significance of validating neuroimmune targets and understanding their function and expression is emphasized in this review to better identify and interpret PET results.

2023-02-01·Thrombosis and Haemostasis

P2Y12 Inhibition Suppresses Proinflammatory Platelet–Monocyte Interactions

Article

作者: El Bannoudi, Hanane ; Wang, Tricia T. ; Buyon, Jill ; Myndzar, Khrystyna ; Schwartz, Tamar ; Barrett, Tessa J. ; Cornwell, MacIntosh ; Berger, Jeffrey S. ; Sowa, Marcin A. ; Rolling, Christina C.

Background Monocyte–platelet aggregates (MPAs) represent the crossroads between thrombosis and inflammation, and targeting this axis may suppress thromboinflammation. While antiplatelet therapy (APT) reduces platelet–platelet aggregation and thrombosis, its effects on MPA and platelet effector properties on monocytes are uncertain. Objectives To analyze the effect of platelets on monocyte activation and APT on MPA and platelet-induced monocyte activation. Methods Agonist-stimulated whole blood was incubated in the presence of P-selectin, PSGL1, PAR1, P2Y12, GP IIb/IIIa, and COX-1 inhibitors and assessed for platelet and monocyte activity via flow cytometry. RNA-Seq of monocytes incubated with platelets was used to identify platelet-induced monocyte transcripts and was validated by RT-qPCR in monocyte-PR co-incubation ± APT. Results Consistent with a proinflammatory platelet effector role, MPAs were increased in patients with COVID-19. RNA-Seq revealed a thromboinflammatory monocyte transcriptome upon incubation with platelets. Monocytes aggregated to platelets expressed higher CD40 and tissue factor than monocytes without platelets (p < 0.05 for each). Inhibition with P-selectin (85% reduction) and PSGL1 (87% reduction) led to a robust decrease in MPA. P2Y12 and PAR1 inhibition lowered MPA formation (30 and 21% reduction, p < 0.05, respectively) and decreased monocyte CD40 and TF expression, while GP IIb/IIIa and COX1 inhibition had no effect. Pretreatment of platelets with P2Y12 inhibitors reduced the expression of platelet-mediated monocyte transcription of proinflammatory SOCS3 and OSM. Conclusions Platelets skew monocytes toward a proinflammatory phenotype. Among traditional APTs, P2Y12 inhibition attenuates platelet-induced monocyte activation.

2023-01-01·Pharmacology

High On-Treatment Platelet Reactivity: Aspirin versus Clopidogrel

Article

作者: M'Pembele, René ; Hohlfeld, Thomas ; Zeus, Tobias ; Petzold, Tobias ; Polzin, Amin ; Mourikis, Philipp ; Zako, Saif ; Huhn, Ragnar ; Trojovsky, Kajetan ; Dannenberg, Lisa ; Ahlbrecht, Samantha ; Kelm, Malte ; Helten, Carolin ; Naguib, David

Background: Antithrombotic regimen in patients on oral anticoagulation (OAC) post-percutaneous coronary intervention (PCI) is challenging. At least, one antiplatelet agent in combination with OAC is recommended after PCI for 6–12 months. Clopidogrel is used most frequently in this setting. However, data comparing P2Y12 inhibition with clopidogrel versus cyclooxygenase inhibition by acetylsalicylic acid (ASA, aspirin) is missing. It is well known that the antiplatelet effects of ASA and clopidogrel are frequently impaired (high on-treatment platelet reactivity [HTPR]). In this pilot investigation, we compared the antiplatelet effects of clopidogrel versus ASA. Methods: In this retrospective single-center database analysis, we investigated platelet reactivity by light transmission aggregometry in patients under different antiplatelet regimes. Results were presented as maximum of aggregation (MoA). HTPR to ASA and to clopidogrel were assessed. Results: 755 patients were enrolled. 677 were on ASA, 521 were on clopidogrel, and 198 had OAC. Overall mean age was 73 ± 13.4 years, and 458 (60.7%) were male. HTPR to ASA occurred in 94/677 patients (13.9%), and mean arachidonic acid-induced MoA was 14.15 ± 19.04%. HTPR to clopidogrel occurred in 241/521 patients (46.3%), and mean adenosine diphosphate-induced MoA was 50.06 ± 20.42%. HTPR to clopidogrel was significantly more frequent than HTPR to ASA; single antiplatelet therapy (SAPT)-mono ASA: 27/199 (13.6%) versus mono clopidogrel: 6/18 (33.3%); p = 0.037; SAPT with OAC-OAC with ASA: 8/35 (22.9%) versus OAC with clopidogrel: 27/60 (45%); p = 0.046. Same difference in HTPR contingency could be shown in subgroups of dual antiplatelet therapy and ASA + clopidogrel + OAC therapy. Conclusion: Impaired pharmacodynamic response to clopidogrel was more frequent as HTPR to ASA. Hence, ASA should be tested in combination with OAC post-PCI.