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CDS022173

Sigma-Aldrich

Imatinib

Synonyme(s) :

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

Formule empirique (notation de Hill):
C29H31N7O
Numéro CAS:
152459-95-5
Poids moléculaire :
493.60
Numéro MDL:
MFCD05662257
Code UNSPSC :
12352200
ID de substance PubChem :
329795436

Description

AldrichCPR

Forme

solid

Chaîne SMILES 

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

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)

Clé InChI

KTUFNOKKBVMGRW-UHFFFAOYSA-N

Informations sur le gène

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

Description générale

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.

Autres remarques

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.

Pictogrammes

Health hazard
GHS08

Mention d'avertissement

Danger

Mentions de danger

H341,H351,H360D,H362

Classification des risques

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

Code de la classe de stockage

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

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

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
Doing evidence-based medicine? How NHS managers ration high-cost drugs.
David Hughes et al.
Social science & medicine (1982), 235, 112304-112304 (2019-07-16)
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
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
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