チカグレロル 化学特性,用途語,生産方法
効能
血小板凝集抑制薬, P2Y12阻害薬
商品名
ブリリンタ (アストラゼネカ)
説明
In December 2010, the P2Y
12 receptor antagonist ticagrelor (also
known as AZD6140) was approved in Europe for the treatment of acute
coronary syndrome (ACS), a condition that covers several clinical symptoms
with the potential to cause acute myocardial ischemia (MI).
ADP binds to two purinergic receptors, the P2Y1 and P2Y
12 receptors. The
action of ADP binding to the P2Y
12 receptor results in activation of the GP
Ⅱb/Ⅲa (integrin) receptor.GP Ⅱb/Ⅲa initiates and prolongs platelet aggregation,
which in turn results in the cross-linking of platelets through fibrin
and finally thrombus formation. Inhibition of ADP stimulation of the P2Y
12
receptor has been found to be an effective strategy for managing the atherothrombotic
events associated with ACS and potentially resulting from
percutaneous coronary intervention (PCI, stent implantation) .
化学的特性
White Solid
定義
ChEBI: A triazolopyrimidine that is an adenosine isostere; the cyclopentane ring is similar to ribose and the nitrogen-rich [1,2,3]triazolo[4,5-d]pyrimidine moiety resembles the nucleobase adenine. A platelet aggregation inhibitor which is used for p
evention of thromboembolic events in patients with acute coronary syndrome.
臨床応用
Ticagrelor, discovered and developed by AstraZeneca, is a platelet
adenosine diphosphate (ADP) P2Y12 (P2T) reversible receptor
antagonist approved in the E.U. in 2010 and launched in Germany
and the UK in 2011 for the treatment of patients with acute coronary
syndromes (ACS). It was approved in the U.S. and Canada in
2011 following successful clinical trial results in patients with
ACS which showed it to be superior to preexisting drugs for reducing death due to vascular causes. Ticagrelor is an oral drug
indicated for use in combination with acetylsalicylic acid (aspirin)
for the prevention of atherothrombotic events in adult patients
with ACS (unstable angina, non-ST elevation myocardial infarction
(NSTEMI), or ST elevation myocardial infarction (STEMI)). Unlike
its competitors prasugrel and clopidogrel, which require bioactivation,
ticagrelor is not a prodrug and does not require in vivo activation.
It has a rapid onset of action, relatively rapid reversibility,
greater potency, and exhibits consistency in platelet inhibition.
Following dosing, ticagrelor reaches Cmax in about 1.5 h, with formation
of a major metabolite with equipotent intrinsic activity to
the parent compound.
チカグレロル 上流と下流の製品情報
原材料
準備製品
2-[[(3aS,4R,6S,6aR)-4-[7-[[(1R,2S)-2-(3,4-Difluorophenyl)cyclopropyl]amino]-5-(propylthio)-3H-[1,2,3]triazolo[4,5-d]pyrimidin-3-yl]-2,2-dimethyl-tetrahydro-3aH-cyclopenta[d][1,3]dioxol-6-yl]oxy]ethanol