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安全信息

SML0331

Sigma-Aldrich

Prasugrel

≥98% (HPLC)

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别名:
5-[2-Cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4,5,6,7-tetrahydrothieno[3,2-c]pyridin-2-yl acetate, CS 747, CS-747, Effient, Efient, LY640315
经验公式（希尔记法）:
C20H20FNO3S
CAS号:
150322-43-3
分子量:
373.44
MDL编号:
MFCD09954140
PubChem化学物质编号:
329825336
NACRES:
NA.77

质量水平

100

检测方案

≥98% (HPLC)

形式

powder

颜色

white to beige

溶解性

DMSO: >5 mg/mL (warmed at 60 °C)

储存温度

2-8°C

SMILES字符串

CC(=O)Oc1cc2CN(CCc2s1)C(C(=O)C3CC3)c4ccccc4F

InChI

1S/C20H20FNO3S/c1-12(23)25-18-10-14-11-22(9-8-17(14)26-18)19(20(24)13-6-7-13)15-4-2-3-5-16(15)21/h2-5,10,13,19H,6-9,11H2,1H3

InChI key

DTGLZDAWLRGWQN-UHFFFAOYSA-N

基因信息

human ... P2RY12(64805)

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生化/生理作用

Prasugrel is a platelet inhibitor that reduces the aggregation of platelets by irreversible binding to P2Y12 receptors. Prasugrel interacts in an irreversible manner with the residues Cys97 and Cys175 of the human P2Y12-receptor.
Prasugrel is a thienopyridine prodrug and is considered to be more potent than clopidogrel. It shows a faster generation and also reduces thrombotic events. Prasugrel is less dependent on the CYP (cytochrome P450) enzymes for its conversion to active metabolite.

特点和优势

This compound is featured on the P2 Receptors: P2Y G-Protein Family page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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Shigeru Saito et al.
Circulation journal : official journal of the Japanese Circulation Society, 78(7), 1684-1692 (2014-04-25)
Prasugrel is an antiplatelet agent that shows more prompt, potent, and consistent platelet inhibition than clopidogrel. The objective of this study was to confirm the efficacy and safety of prasugrel at loading/maintenance doses of 20/3.75 mg. Japanese patients (n=1,363) with
Antonio Tello-Montoliu et al.
Platelets, 27(8), 777-783 (2016-06-04)
Everolimus-eluting bioabsorbable scaffolds (BVSs) have exhibited similar long-term clinical outcomes compared to its everolimus-eluting metallic counterparts. However, reports from earlier studies have shown a signal for an increased rate of stent thrombosis. The aim of the current investigation is to
Jeffrey A Bakal et al.
European heart journal, 36(6), 385-92a-385-92a (2014-07-12)
Several methods provide new insights into understanding clinical trial composite endpoints, using both conventional and novel methods. The TRILOGY ACS trial is used as a contemporary example to prospectively compare these methods side by side. The traditional time-to-first-event, Andersen-Gill recurrent
Matti K Itkonen et al.
Clinical pharmacology and therapeutics, 104(3), 495-504 (2017-11-25)
The oxidation of montelukast is mainly mediated by cytochrome P450 (CYP) 2C8, but other mechanisms may contribute to its disposition. In healthy volunteers, we investigated the effects of two widely used P2Y12 inhibitors on montelukast pharmacokinetics. Clopidogrel (300 mg on day
Yochai Birnbaum et al.
Cardiovascular drugs and therapy, 30(6), 539-550 (2016-11-11)
Ticagrelor inhibits the equilibrative-nucleoside-transporter-1 and thereby, adenosine cell re-uptake. Ticagrelor limits infarct size (IS) in non-diabetic rats and the effect is adenosine-dependent. Statins, via ecto-5'-nucleotidase activation, also increase adenosine levels and limit IS. Ticagrelor and rosuvastatin have additive effects on
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