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Merck

CDS022173

Imatinib

Sinónimos:

4-(4-Methylpiperazin-1-ylmethyl)-N-[4-methyl-3-[[4-(pyridin-3-yl)pyrimidin-2-yl]amino]phenyl]benzamide, 4-[(4-Methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]benzamide, CGP 57148, Genfatinib, N-(4-Methyl-3-((4-(pyridin-3-yl)pyrimidin-2-yl)amino)phenyl)-4-((4-methylpiperazin-1-yl)methyl)benzamide

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About This Item

Fórmula empírica (notación de Hill):
C29H31N7O
Número CAS:
152459-95-5
Peso molecular:
493.60
UNSPSC Code:
12352200
PubChem Substance ID:
329795436
MDL number:
MFCD05662257
NACRES:
NA.21

InChI

1S/C29H31N7O/c1-21-5-10-25(18-27(21)34-29-31-13-11-26(33-29)24-4-3-12-30-19-24)32-28(37)23-8-6-22(7-9-23)20-36-16-14-35(2)15-17-36/h3-13,18-19H,14-17,20H2,1-2H3,(H,32,37)(H,31,33,34)

SMILES string

O=C(C(C=C1)=CC=C1CN2CCN(C)CC2)NC3=CC(NC4=NC(C5=CN=CC=C5)=CC=N4)=C(C)C=C3

InChI key

KTUFNOKKBVMGRW-UHFFFAOYSA-N

description

AldrichCPR

form

solid

Gene Information

human ... ABL1(25), KIT(3815), PDGFRB(5159)

General description

Imatinib is a benzamide derivative used as a is specific tyrosine kinase receptor inhibitor. It is designed to inhibit the breakpoint cluster region (BCR)-Abelson (ABL) fusion protein, which is caused by the Philadelphia chromosome abnormalities. Imatinib is also used as a potent apoptosis inducer and an antineoplastic agent.

Other Notes

Please note that Sigma-Aldrich provides this product to early discovery researchers as part of a collection of unique chemicals. Sigma-Aldrich does not collect analytical data for this product. Buyer assumes responsibility to confirm product identity and/or purity. All sales are final.

NOTWITHSTANDING ANY CONTRARY PROVISION CONTAINED IN SIGMA-ALDRICH′S STANDARD TERMS AND CONDITIONS OF SALE OR AN AGREEMENT BETWEEN SIGMA-ALDRICH AND BUYER, SIGMA-ALDRICH SELLS THIS PRODUCT "AS-IS" AND MAKES NO REPRESENTATION OR WARRANTY WHATSOEVER WITH RESPECT TO THIS PRODUCT, INCLUDING ANY (A) WARRANTY OF MERCHANTABILITY, (B) WARRANTY OF FITNESS FOR A PARTICULAR PURPOSE, OR (C) WARRANTY AGAINST INFRINGEMENT OF INTELLECTUAL PROPERTY RIGHTS OF A THIRD PARTY, WHETHER ARISING BY LAW, COURSE OF DEALING, COURSE OF PERFORMANCE, USAGE OF TRADE OR OTHERWISE.

pictograms

Health hazard
GHS08

signalword

Danger

Hazard Classifications

Carc. 2 - Lact. - Muta. 2 - Repr. 1B

Clase de almacenamiento

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Xiaohui Si et al.
Oncotarget, 7(47), 78095-78109 (2016-11-02)
Leukemia stem cells (LSCs) can resist available treatments that results in disease progression and/or relapse. To dissect the microRNA (miRNA) expression signature of relapse in acute myeloid leukemia (AML), miRNA array analysis was performed using enriched LSCs from paired bone
Laurent L Reber et al.
PloS one, 12(10), e0185704-e0185704 (2017-10-06)
Gouty arthritis is caused by the deposition of monosodium urate (MSU) crystals in joints. Despite many treatment options for gout, there is a substantial need for alternative treatments for patients unresponsive to current therapies. Tyrosine kinase inhibitors have demonstrated therapeutic
Kateřina Kuželová et al.
Journal of cellular biochemistry, 112(11), 3334-3342 (2011-07-14)
The effects of the pan-caspase inhibitor Q-VD-OPh on caspase activity, DNA fragmentation, PARP cleavage, 7A6 exposition, and cellular adhesivity to fibronectin were analyzed in detail in three different apoptotic systems involving two cell lines (JURL-MK1 and HL60) and two apoptosis
Fengling Wang et al.
Anti-cancer drugs, 30(2), 159-166 (2018-11-14)
The Bcr/Abl kinase is an oncogenic fusion protein that plays a central role in the pathogenesis of chronic myeloid leukemia (CML). Some small-molecule kinase inhibitors such as imatinib were developed in the treatment of CML; however, resistant to imatinib is
Mahnoush Bahjat et al.
Cell cycle (Georgetown, Tex.), 18(18), 2307-2322 (2019-07-28)
The BCR-ABL1 fusion gene is the driver oncogene in chronic myeloid leukemia (CML) and Philadelphia-chromosome positive (Ph+) acute lymphoblastic leukemia (ALL). The introduction of tyrosine kinase inhibitors (TKIs) targeting the ABL kinase (such as imatinib) has dramatically improved survival of
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