Prasugrel

• CAT Number: I001860
• CAS Number: 150322-43-3
• Molecular Formula: C₂₀H₂₀FNO₃S
• Molecular Weight: 373.44
• Purity: ≥95%
• Target: P2Y12 receptor
• Solubility: DMSO ≥28mg/mL Water <1.2mg/mL Ethanol ≥6.6mg/mL
• Storage: <label class=
• IC50: 1.8 μm
• InChI: 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
• InChIKey: DTGLZDAWLRGWQN-UHFFFAOYSA-N
• SMILES: CC(=O)OC1=CC2=C(S1)CCN(C2)C(C3=CC=CC=C3F)C(=O)C4CC4

Prasugrel(CAT: I001860) is an antiplatelet medication that is used to prevent blood clots in patients with acute coronary syndrome (ACS) who are undergoing percutaneous coronary intervention (PCI). It works by irreversibly inhibiting the P2Y12 receptor on platelets, thereby preventing them from aggregating and forming clots. Prasugrel is a prodrug that is converted into its active form by the liver, and its effects can last for up to five days. Common side effects of prasugrel include bleeding, bruising, and shortness of breath. Prasugrel should not be used in patients with a history of stroke or transient ischemic attack, as it can increase the risk of bleeding.

Reference

1. Cardiovasc Drug Rev. 2007 Winter;25(4):357-74.

Prasugrel: a novel thienopyridine antiplatelet agent. A review of preclinical and
clinical studies and the mechanistic basis for its distinct antiplatelet profile.

Jakubowski JA(1), Winters KJ, Naganuma H, Wallentin L.

Author information:
(1)Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285,
USA.

Prasugrel (CS-747, LY640315) is a novel member of the thienopyridine class of
oral antiplatelet agents that includes ticlopidine and clopidogrel. Like other
thienopyridines, prasugrel is a prodrug that is inactive in vitro. Prasugrel/’s
distinct chemical structure permits efficient conversion to its active metabolite
with a less rigorous dependence on specific cytochrome P-450 enzymes. Prasugrel
is rapidly converted in vivo to an active metabolite (R-138727) that binds
specifically and irreversibly to the platelet P2Y 12 purinergic receptor
inhibiting ADP-mediated platelet activation and aggregation. Preclinical studies
indicated that prasugrel is approximately 10- and 100-fold more potent at
inhibiting ex vivo platelet aggregation and in vivo thrombus formation than
clopidogrel and ticlopidine, respectively. Early clinical data in healthy
subjects confirmed the greater platelet inhibition and consistency with prasugrel
compared to clopidogrel. While the active metabolites of prasugrel and
clopidogrel resulted in similar levels of platelet inhibition in vitro, the
amount of each active metabolite generated in vivo was quite different-prasugrel
(60 mg) resulting in an approximately 12-fold greater exposure to its active
metabolite compared with clopidogrel (300 mg). This observation provides a
mechanistic basis for the faster, greater, and more consistent inhibition of
platelet aggregation observed with prasugrel. Clinical studies in patients with
cardiovascular disease confirmed the potent antiplatelet effect of prasugrel
compared with clopidogrel. Collectively, these phase 1/1b studies and a phase 2
study (JUMBO-TIMI 26) aided in dose selection for the recently completed phase 3
trial (TRITON-TIMI 38) in patients with acute coronary syndrome undergoing
percutaneous coronary intervention.

2. Semin Thromb Hemost. 2005 Apr;31(2):184-94.

Pharmacology of CS-747 (prasugrel, LY640315), a novel, potent antiplatelet agent
with in vivo P2Y12 receptor antagonist activity.

Niitsu Y(1), Jakubowski JA, Sugidachi A, Asai F.

Author information:
(1)Pharmacology and Molecular Biology Research Laboratories, Sankyo Co. Ltd.,
1-2-58 Hiromachi, Shinagawa-ku, Tokyo 140-8710, Japan.

CS-747 (prasugrel, LY640315) is a member of the thienopyridine class of oral
platelet aggregation inhibitors that includes ticlopidine and clopidogrel. A
single oral administration of CS-747 produced a dose-related inhibition of
platelet aggregation in rats that was approximately 10- and 100-fold more potent
than that of clopidogrel and ticlopidine, respectively. The antiaggregatory
effect of CS-747 was evident at 30 minutes and lasted until 72 hours after
dosing, indicating fast onset and long duration of action. CS-747 showed more
potent antithrombotic activity compared with clopidogrel and ticlopidine with the
same rank order as the antiaggregatory potencies. Combined administration of
CS-747 with aspirin to rats produced substantially greater inhibition of both
platelet aggregation and thrombus formation compared with each agent alone. The
antiplatelet action of CS-747 is due to irreversible and selective blockade of
platelet P2Y (12) adenosine diphosphate (ADP) receptors by its active metabolite
R-138727. In phase I studies, a single oral dose of CS-747 (30 and 75 mg)
produced > 50% inhibition of ADP-induced platelet aggregation, with rapid onset
(1 hour) and long duration (> 48 hours) of action. In healthy volunteers,
once-daily administration of 10 mg CS-747 for 10 days showed significant
cumulative inhibition of platelet aggregation from 2 days after the first dose
until at least 2 days after the final dose. Studies conducted to date indicate
that CS-747 is a highly effective antiplatelet and antithrombotic agent and is
anticipated to be effective in the treatment of atherothrombotic and other
ischemic vascular diseases.