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Merck
모든 사진(1)

문서

PZ0366

Sigma-Aldrich

PD166326

≥98% (HPLC)

동의어(들):

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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About This Item

실험식(Hill 표기법):
C21H16Cl2N4O2
CAS Number:
Molecular Weight:
427.28
UNSPSC 코드:
41105101
NACRES:
NA.77

Quality Level

분석

≥98% (HPLC)

형태

powder

색상

white to light brown

solubility

DMSO: 2 mg/mL, clear

저장 온도

room temp

SMILES string

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

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

생화학적/생리학적 작용

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.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

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문서 라이브러리 방문

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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