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Merck

SML0331

Sigma-Aldrich

Prasugrel

≥98% (HPLC)

Sinónimos:

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

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10 MG
MXP 2,379.00
50 MG
MXP 9,245.00

MXP 2,379.00


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10 MG
MXP 2,379.00
50 MG
MXP 9,245.00

About This Item

Fórmula empírica (notación de Hill):
C20H20FNO3S
Número de CAS:
Peso molecular:
373.44
Número MDL:
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
NACRES:
NA.77

MXP 2,379.00


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Nivel de calidad

Ensayo

≥98% (HPLC)

Formulario

powder

color

white to beige

solubilidad

DMSO: >5 mg/mL (warmed at 60 °C)

temp. de almacenamiento

2-8°C

cadena SMILES

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

Clave InChI

DTGLZDAWLRGWQN-UHFFFAOYSA-N

Información sobre el gen

human ... P2RY12(64805)

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Acciones bioquímicas o fisiológicas

Prasugrel is a platelet inhibitor that reduces the aggregation of platelets by irreversible binding to P2Y12 receptors.
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.[1] Prasugrel is less dependent on the CYP (cytochrome P450) enzymes for its conversion to active metabolite.[2]

Características y beneficios

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.

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


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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
Platelets, 1125-1125 (2013)
T Yetgin et al.
Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation (2018-06-23)
To investigate 1‑year outcomes with routine prasugrel treatment after acute coronary syndrome (ACS) in a large-scale registry. The Rijnmond Collective Cardiology Research registry is a prospective, observational study that enrolled 4,258 consecutive ACS patients treated with percutaneous coronary intervention (PCI) with 1‑year
Cynthia Larmore et al.
Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions, 88(4), 535-544 (2016-10-21)
The 30-day clinical outcomes with prasugrel or ticagrelor were compared using a US payer database in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). Prasugrel and ticagrelor demonstrated superior efficacy with increased non-coronary artery bypass graft major
Martina Rothenbühler et al.
European heart journal, 40(15), 1226-1232 (2019-01-29)
In the Minimizing Adverse Haemorrhagic Events by TRansradial Access Site and Systemic Implementation of angioX (MATRIX) trial, adults with acute coronary syndrome undergoing coronary intervention who were allocated to radial access had a lower risk of bleeding, acute kidney injury

Artículos

Surface receptors for extracellular nucleotides are called P2 receptors. Learn more about P2Y G protein-coupled receptors, GPCRs, and ionotropic P2 receptors (P2X ligand-gated ion channels, LGICs).

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