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Safety Information

SML3799

Sigma-Aldrich

Nilotinib

≥98% (HPLC)

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Synonym(s):
4-Methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]-N-[5-(4-methyl-1H-imidazol-1-yl)-3-(trifluoromethyl)phenyl]benzamide, 4-Methyl-N-[3-(4-methyl-1H-imidazol-1-yl)-5-(trifluoromethyl)phenyl]-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]-benzamide, AMN 107, AMN107
Empirical Formula (Hill Notation):
C28H22F3N7O
CAS Number:
Molecular Weight:
529.52
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.21

Quality Level

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear (Warmed)

storage temp.

2-8°C

Biochem/physiol Actions

Nilotinib (AMN107) is an orally available, selective and potent ATP-competitive wild-type and mutant Bcr-Abl kinase inhibitor that is 10-30-fold more potent than imatinib. Nilotinib is used to treat Philadelphia chromosome (Ph+)-positive chronic myelogenous leukemia (CML). Nilotinib reduces midbrain Bcr-Abl autophosphorylation, amyloid-β levels, and neuronal loss, as well as improves autophagosome clearance and reverses cognitive deficits in the Tg2576 transgenic mouse model of Alzheimer’s disease.

Pictograms

Health hazard

Signal Word

Danger

Hazard Statements

Hazard Classifications

Aquatic Chronic 4 - STOT RE 1

Target Organs

Liver,Kidney,gallbladder

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl
Cancer Cell, 7(2), 129-141 (2005)
Tomer Meirson et al.
Oncotarget, 9(31), 22158-22183 (2018-05-19)
Metastatic dissemination of cancer cells from the primary tumor and their spread to distant sites in the body is the leading cause of mortality in breast cancer patients. While researchers have identified treatments that shrink or slow metastatic tumors, no
Livia La Barbera et al.
Progress in neurobiology, 202, 102031-102031 (2021-03-09)
What happens precociously to the brain destined to develop Alzheimer's Disease (AD) still remains to be elucidated and this is one reason why effective AD treatments are missing. Recent experimental and clinical studies indicate that the degeneration of the dopaminergic

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