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Merck
CN

PZ0366

PD166326

≥98% (HPLC)

别名:

6-(2,6-Dichlorophenyl)-2-[[3-(hydroxymethyl)phenyl]amino]-8-methyl-pyrido[2,3-d]pyrimidin-7(8H)-one, PD 166326

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关于此项目

经验公式(希尔记法):
C21H16Cl2N4O2
化学文摘社编号:
分子量:
427.28
NACRES:
NA.77
UNSPSC Code:
41105101
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
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InChI

1S/C21H16Cl2N4O2/c1-27-19-13(9-15(20(27)29)18-16(22)6-3-7-17(18)23)10-24-21(26-19)25-14-5-2-4-12(8-14)11-28/h2-10,28H,11H2,1H3,(H,24,25,26)

InChI key

ZIQFYVPVJZEOFS-UHFFFAOYSA-N

SMILES string

O=C1N(C)C2=C(C=NC(NC3=CC=CC(CO)=C3)=N2)C=C1C4=C(Cl)C=CC=C4Cl

assay

≥98% (HPLC)

form

powder

color

white to light brown

solubility

DMSO: 2 mg/mL, clear

storage temp.

room temp

Quality Level

Biochem/physiol Actions

PD166326 is an ATP-competitive dual BCR-ABL and Src kinase inhibitor. In some studies it has been found to be more potent than imatinib with inhibition of cancer growth in the low nanomolar range or even picomolar range in various biological systems.

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

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分析证书(COA)

Lot/Batch Number

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Nicholas C Wolff et al.
Blood, 105(10), 3995-4003 (2005-01-20)
Imatinib mesylate is highly effective in newly diagnosed chronic myeloid leukemia (CML), but BCR/ABL (breakpoint cluster region/abelson murine leukemia)-positive progenitors persist in most patients with CML treated with imatinib mesylate, indicating the need for novel therapeutic approaches. In this study
Sapan J Patel et al.
American journal of translational research, 8(9), 3614-3629 (2016-10-12)
Tumors contain heterogeneous cell populations and achieve dominance by functioning as collective systems. The mechanisms underlying the aberrant growth and interactions between cells are not very well understood. The pre-B acute lymphoblastic leukemia cells we studied were obtained directly from
John Badger et al.
Biochemistry, 55(23), 3251-3260 (2016-05-12)
Protein tyrosine kinases of the Abl family have diverse roles in normal cellular regulation and drive several forms of leukemia as oncogenic fusion proteins. In the crystal structure of the inactive c-Abl kinase core, the SH2 and SH3 domains dock

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