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Merck

SML2852

Sigma-Aldrich

Capadenoson

≥98% (HPLC)

别名:

2-Amino-6-[[[2-(4-chlorophenyl)-1,3-thiazol-4-yl]methyl]sulfanyl]-4-[4-(2-hydroxyethoxy)phenyl]pyridine-3,5-dicarbonitrile, 2-Amino-6-[[[2-(4-chlorophenyl)-4-thiazolyl]methyl]thio]-4-[4-(2-hydroxyethoxy)phenyl]-3,5-pyridinedicarbonitrile, BAY 68-4986, BAY-68-4986, BAY68-4986

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About This Item

经验公式(希尔记法):
C25H18ClN5O2S2
分子量:
520.03
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: 2 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

N#CC1=C(C2=CC=C(OCCO)C=C2)C(C#N)=C(N)N=C1SCC3=CSC(C4=CC=C(Cl)C=C4)=N3

InChI

1S/C25H18ClN5O2S2/c26-17-5-1-16(2-6-17)24-30-18(13-34-24)14-35-25-21(12-28)22(20(11-27)23(29)31-25)15-3-7-19(8-4-15)33-10-9-32/h1-8,13,32H,9-10,14H2,(H2,29,31)

InChI 密鑰

CITWCLNVRIKQAF-UHFFFAOYSA-N

生化/生理作用

Capadenoson (BAY 68-4986) is an adenosine receptor A1 (A1AR) partial agonist (GTPγS binding EC50/Emax = 0.1 nM/74% vs. 0.3 nM/100% with CCPA; human cortex membranes) that exerts additional biased A2BAR agonism toward cAMP signal transduction (pEC50 = 8.94/cAMP, 6.20/Ca+2, 6.12/pERK, 5.03/IP1), while exhibiting weak A2A & A3 potency. Capadenoson offers cardioprotection efficacy in an ischemia-reperfusion injury rat model in vivo (25/28% infarct size reduction with 0.1/0.3 mg/kg iv.) without the risk of a full atrioventricular (AV) block (isolated perfused rat heart rate = 100% up to 10 nM, 90% at ≥10 μM) seen with the full A1 agonist CCPA.
Partial adenosine receptor A1 and cAMP-biased A2B agonist with in vivo cardioprotection efficacy without the risk of a full atrioventricular block.

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


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Daniel Meibom et al.
ChemMedChem, 12(10), 728-737 (2017-05-11)
Adenosine is known to be released under a variety of physiological and pathophysiological conditions to facilitate the protection and regeneration of injured ischemic tissues. The activation of myocardial adenosine A1 receptors (A1 Rs) has been shown to inhibit myocardial pathologies associated

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