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Merck

SML1958

Sigma-Aldrich

Bay 60-6583

≥98% (HPLC)

别名:

2-[[6-氨基-3,5-二氰基-4- [4-(环丙基甲氧基)苯基] -2-吡啶基]硫代]-乙酰胺, BAY606583, BR 4887, BR4887, Bay 60-6,583, Bay 606583

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About This Item

经验公式(希尔记法):
C19H17N5O2S
分子量:
379.44
MDL號碼:
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 20 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

NC1=C(C#N)C(C2=CC=C(OCC3CC3)C=C2)=C(C#N)C(SCC(N)=O)=N1

InChI

1S/C19H17N5O2S/c20-7-14-17(12-3-5-13(6-4-12)26-9-11-1-2-11)15(8-21)19(24-18(14)23)27-10-16(22)25/h3-6,11H,1-2,9-10H2,(H2,22,25)(H2,23,24)

InChI 密鑰

ZTYHZMAZUWOXNC-UHFFFAOYSA-N

生化/生理作用

BAY 60-6583是一种有效的腺苷受体A2b(A2bR)的部分激动剂(抑制0.3 nM [3H] PSB-603与人/小鼠/大鼠A2bR结合的Ki = 114/136/100 nM),可在转染后表达人A2bR(EC50〜100 nM)的CHO中选择性诱导cAMP依赖性转录活性,但在表达A1R或A2aR的CHO中无效,其对人/大鼠/小鼠A2aR没有亲和力。BAY 60-6583还显示出对A1R(抑制1 nM [3H]CCPA与人/小鼠/大鼠A1R结合的 Ki= 387/351/514 nM;对100 nM CCPA诱导的hA1R β-抑制蛋白募集过程的抑制IC50 = 7.4 μM)和A3R(抑制10 nM [3H]NECA与人/小鼠/大鼠的A3R结合的 Ki= 223/3920/2750 nM;对30 nM Cl-IB-MECA诱导的hA3R β-抑制蛋白募集过程的抑制IC50 = 6.7 μM)的低亲和性拮抗活性。BAY 60-6583已通过i.p.(0.1-80 mg/kg)或i.v.(0.2-2 mg/kg)广泛应用于动物体内,以研究A2bR介导的生物反应。

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Tobias Eckle et al.
Circulation, 115(12), 1581-1590 (2007-03-14)
Ecto-5'-nucleotidase (CD73)-dependent adenosine generation has been implicated in tissue protection during acute injury. Once generated, adenosine can activate cell-surface adenosine receptors (A1 AR, A2A AR, A2B AR, A3 AR). In the present study, we define the contribution of adenosine to
Atsushi Kuno et al.
Journal of molecular and cellular cardiology, 43(3), 262-271 (2007-07-17)
Although protein kinase C (PKC) plays a key role in ischemic preconditioning (IPC), the actual mechanism of that protection is unknown. We recently found that protection from IPC requires activation of adenosine receptors during early reperfusion. We, therefore, hypothesized that
Mohamad Wessam Alnouri et al.
Purinergic signalling, 11(3), 389-407 (2015-07-02)
Adenosine receptors (ARs) have emerged as new drug targets. The majority of data on affinity/potency and selectivity of AR ligands described in the literature has been obtained for the human species. However, preclinical studies are mostly performed in mouse or

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