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Merck
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重要文件

SML3799

Sigma-Aldrich

Nilotinib

≥98% (HPLC)

同義詞:

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

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About This Item

經驗公式(希爾表示法):
C28H22F3N7O
CAS號碼:
分子量::
529.52
MDL號碼:
分類程式碼代碼:
12352200
NACRES:
NA.21

品質等級

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear (Warmed)

儲存溫度

2-8°C

SMILES 字串

FC(F)(F)c1cc(cc(c1)NC(=O)c3cc(c(cc3)C)Nc4nc(ccn4)c5cnccc5)[n]2cnc(c2)C

InChI

1S/C28H22F3N7O/c1-17-5-6-19(10-25(17)37-27-33-9-7-24(36-27)20-4-3-8-32-14-20)26(39)35-22-11-21(28(29,30)31)12-23(13-22)38-15-18(2)34-16-38/h3-16H,1-2H3,(H,35,39)(H,33,36,37)

InChI 密鑰

HHZIURLSWUIHRB-UHFFFAOYSA-N

生化/生理作用

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.
Orally available, selective and potent ATP-competitive wild-type and mutant Bcr-Abl kinase inhibitor

象形圖

Health hazard

訊號詞

Danger

危險聲明

危險分類

Aquatic Chronic 4 - STOT RE 1

標靶器官

Liver,Kidney,gallbladder

儲存類別代碼

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

水污染物質分類(WGK)

WGK 2

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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分析證明 (COA)

Lot/Batch Number

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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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