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Merck
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SML2784

Sigma-Aldrich

CMPD101 hydrochloride

≥98% (HPLC)

同義詞:

3-((4-Methyl-5-(pyridin-4-yl)-4H-1,2,4-triazol-3-yl)methylamino)-N-(2-(trifluoromethyl)benzyl)benzamide, 3-[[[4-Methyl-5-(4-pyridinyl)-4H-1,2,4-triazol-3-yl]methyl]amino]-N-[[2-(trifluoromethyl)phenyl]methyl]benzamide hydrochloride, Compound 101 hydrochloride, Cpd101 hydrochloride, Takeda101 hydrochloride

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About This Item

經驗公式（希爾表示法）:
C24H21N6OF3 · HCl
CAS號碼:
1941168-71-3
分子量：:
502.92
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

100

化驗

≥98% (HPLC)

形狀

powder

儲存條件

desiccated

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

CN1C(CNC2=CC=CC(C(NCC3=CC=CC=C3C(F)(F)F)=O)=C2)=NN=C1C4=CC=NC=C4.Cl

生化／生理作用

CMPD101 is an active site-targeting, potent and subtype-selective G protein-coupled receptor kinase GRK2 & GRK3 inhibitor (human GRK2/3 IC50 = 54/32 nM with 3 μM ATP and tubulin dimer as substrate; bovine GRK2 IC50 = 290 nM with 0.5 mM ATP and bROS as substrate; no GRK1/5 inhibition at 125 μM). CMPD101 selectively inhibits GPR39 agonist-induced β-arrestin recruitment (by 94% at 10 μM against 30 μM GPR39-C3/50 μM ZnCl2), but not cAMP pathway desensitization in cultures and prevents β-arrestin2-biased D2R ligand UNC9994(1 μg/side bilateral local injection) from blocking NMDAR antagonist PCP (6 mg/kg i.p.)-induced locomotion (60%/12% blockage without/with 0.5 μg CMPD101 co-injection) in mice in vivo.

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

分析證明 (COA)

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Yuji Shimizu et al.
Biochemical pharmacology, 140, 105-114 (2017-06-18)
GPR39, a G-protein-coupled receptor activated by zinc, reportedly activates multiple intracellular signaling pathways via Gs, Gq, G12/13, and β-arrestin, but little is known about downregulation of the receptor upon its activation. To our knowledge, this is the first report on
Jesse J DiCello et al.
American journal of physiology. Gastrointestinal and liver physiology, 317(2), G79-G89 (2019-05-16)
Endocytosis is a major mechanism through which cellular signaling by G protein-coupled receptors (GPCRs) is terminated. However, recent studies demonstrate that GPCRs are internalized in an active state and continue to signal from within endosomes, resulting in effects on cellular
Alessandro Cannavo et al.
Frontiers in pharmacology, 10, 888-888 (2019-08-27)
Hyperaldosteronism alters cardiac function, inducing adverse left ventricle (LV) remodeling either via increased fibrosis deposition, mitochondrial dysfunction, or both. These harmful effects are due, at least in part, to the activation of the G protein-coupled receptor kinase 2 (GRK2). In

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