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Merck

SML0331

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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About This Item

Fórmula empírica (notación de Hill):
C20H20FNO3S
Número CAS:
150322-43-3
Peso molecular:
373.44
NACRES:
NA.77
PubChem Substance ID:
329825336
UNSPSC Code:
12352200
MDL number:
MFCD09954140

Nombre del producto

Prasugrel, ≥98% (HPLC)

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

SMILES string

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

InChI key

DTGLZDAWLRGWQN-UHFFFAOYSA-N

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: >5 mg/mL (warmed at 60 °C)

storage temp.

2-8°C

Quality Level

100

Gene Information

human ... P2RY12(64805)

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Biochem/physiol Actions

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. Prasugrel is less dependent on the CYP (cytochrome P450) enzymes for its conversion to active metabolite.

Features and Benefits

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.

Clase de almacenamiento

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificados de análisis (COA)

Lot/Batch Number
0000174550
0000174549
0000152498
0000152498
0000150340

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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
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
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
Oxford Textbook of Interventional Cardiology, 383-383 (2010)
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
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