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PubMedDate not supplied

[Mechanism of action of platelet aggregation inhibitors].

The antiaggregant drugs class is registering in the last few years an increased dynamics. The action mechanism relies either on the platelet activator pathway inhibition, or on the natural inhibitory pathway stimulation. The most frequently implied action mechanisms are COX inhibition, the cyclic nucleotides synthesis inhibition, ADP receptor's inhibition, TxA2 synthesis/action's inhibition, the fibrinogen receptor's blocking. The foreseen introduction of new antiaggregant drugs does have in view the von Willebrand factor-GP I interaction's inhibition, NO releasing, the platelet activation's inhibition using thrombin, the collagen--platelet interaction's inhibition. The widening of this drugs class, established by the constant creation of new antiaggregants, is leading to a doubtless result, meaning the prognosis improvement of certain diseases, in which the platelet activation is a key link of the pathogenic mechanism.

Cardiovascular Diseases↗
PubMedDate not supplied

Pseudosemiglabrin, a platelet aggregation inhibitor from tephrosia semiglabra.

Following bioassay-directed fractionation procedures, two 7-oxygenated-8-prenylflavones, (-)-pseudosemiglabrin [1] and (-)-semiglabrin [2], were isolated from an MeOH extract of Tephrosia semiglabra. (-)-Pseudosemiglabrin [1] displayed in vitro inhibitory effects on human platelet aggregation.

Flavonoids↗
PubMed1994

[An experimental study of the efficacy of platelet aggregating inhibitor on hepatic metastasis].

To investigate whether OKY-046 (an inhibitor of thromboxane A2 synthetase) and TCV-309 (an antagonist of platelet activating factor) can inhibit VX-2 tumor metastasis, the following studies were performed. Study 1 animal experiment: VX-2 tumors were inoculated and OKY-046 or TCV-309 was administered into the portal vein with or without combination of adriamycin (ADR). The number of tumor nodules on the whole liver surface were counted at three weeks after tumor cells inoculation. The combination of OKY-046 and ADR significantly reduced the number of tumor nodules compared to control and TCV-309. Study 2 in vitro experiment: Human breast cancer cells (MCF-7) overlayed confluently cultured human endothelial cells (HUVEC) in vitro with or without OKY-046 and TCV-309 for 3 days; MCF-7 cells invaded the endothelial cells and built-up colonies. The number of colonies built up were counted. OKY-046 significantly decreased the number of colony formations, but TCV-309 did not. These results suggest that OKY-046 has an inhibitory effect on extravasation of tumor cells.

Animals↗
PubMed2001

Rationale for the use of platelet aggregation inhibitors in PAD patients.

Peripheral arterial disease (PAD) is a major risk marker for systemic ischaemic events. The understanding of PAD has moved from PAD as an organ-specific disease to PAD as the lower-limb localization of a multifocal disease, i.e. atherothrombosis. Blood platelet activation and aggregation is a common denominator in atherothrombotic events, and use of antiplatelet agents in patients with PAD can inhibit thrombus formation and reduce the occurrence of myocardial infarction (MI), ischaemic stroke (IS) and vascular death. Many studies have investigated various antiplatelet regimens for preventing acute cardiovascular events in patients with a prior ischaemic event, although many of these studies had a number of limitations. The Antiplatelet Trialists' Collaboration performed a meta-analysis of 23 stroke trials and found an average odds risk reduction of 25% for a combined endpoint of stroke, MI or vascular death. The concept of atherothrombosis as a multifocal disease was challenged by the Clopidogrel versus Aspirin in Patients at Risk of Ischaemic Events (CAPRIE) trial. This study showed an 8.7% decrease in the relative risk reduction for further atherothrombotic events with clopidogrel over aspirin (p = 0.043) for the overall population, in terms of the combined endpoint of IS, Ml or vascular death.

Aspirin↗
PubMed1999

Novel arylpyrazino[2,3-c][1,2,6]thiadiazine 2,2-dioxides as platelet aggregation inhibitors. 2. Optimization by quantitative structure-activity relationships.

In the previous paper (Part 1), we described the synthesis and antiplatelet activity of a series of phenyl- and heteroarylpyrazino[2,3-c][1,2,6]thiadiazine 2,2-dioxides. In this paper, we report the optimization of the platelet aggregation inhibitory activity by an iterative sequence of quantitative structure-activity relationship studies which encompassed synthesis and evaluation of the effects of structure variations at the 1-, 6-, and 7-positions of the heterocyclic system. A model has been established that correctly correlates antiplatelet activity in this series with the partial atomic charges calculated by a local density functional ab initio method. As a result of this study, the experimental platelet aggregation inhibitory activity of the lead compound was improved 300-fold.

Animals↗
PubMed1998

Characterization of fetal serum 5'-nucleotide phosphodiesterase: a novel function as a platelet aggregation inhibitor in fetal circulation.

The study was performed to indicate the ADPase activity of 5'-nucleotide phosphodiesterase (PDEase) from human umbilical cord blood serum and demonstrates the effect of this enzyme on ADP-induced platelet aggregation. The PDEase was purified by using p-nitrophenyl-5'-TMP as a substrate. The PDEase had a molecular weight of 128,000 daltons, and activity of 103 nmol/min/mg protein. The PDEase activity was inhibited by 5'-AMP, ADP, ATP. But 2'-AMP, 3'-AMP, 3':5' cAMP, and adenosine had no inhibiting effects. Kinetic analysis indicated that ADP was a competitive inhibitor with a Ki value of 4.05x10(-5) M. The enzyme was markedly inhibited by 1 mM EDTA. The ADPase activity of the PDEase was 7.79 nmol/min/mg protein. The hydrolized products of ADP by the PDE ase were AMP and phosphoric acid. The platelet aggregation by ADP was inhibited by the addition of the PDEase in the platelet-rich plasma.

Adenosine Diphosphate↗
PubMed1996

Herquline B, a new platelet aggregation inhibitor produced by Penicillium herquei Fg-372.

A new herquline analog, herquline B was isolated from the culture broth of Penicillium herquei Fg372. Herquline B contains one piperazine and two cyclohexenones. The pyrrolidine ring of herquline A was cleaved to yield herquline B. The IC50 value of herquline B against platelet aggregation induced by ADP and platelet-activating factor were 1.6 and 5.0 microM, respectively.

Alkaloids↗