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Key Documents

SML3780

Sigma-Aldrich

Nintedanib ethanesulphonate

≥98% (HPLC)

Synonyme(s) :

(3Z)-2,3-Dihydro-3-[[[4-[methyl[2-(4-methyl-1-piperazinyl)acetyl]amino]phenyl]amino]phenylmethylene]-2-oxo-1H-indole-6-carboxylic acid methyl ester, monoethanesulphonate salt, (Z)-3-[(4-{Methyl-[2-(4-methylpiperazin-1-yl)acetyl]amino}phenylamino)methylene]-2-oxo-2,3-dihydro-1H-indole-6-carboxylic acid methyl ester, monoethanesulphonate salt, BIBF 1120 esylat, BIBF-1120 esylate, BIBF1120 esylate, Methyl (Z)-3-(((4-(N-methyl-2-(4-methylpiperazin-1-yl)acetamido)phenyl)amino)(phenyl)methylene)-2-oxoindoline-6-carboxylate, monoethanesulphonate salt, Nintedanib monoethanesulphonate salt

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About This Item

Formule empirique (notation de Hill):
C31H33N5O4·C2H6O3S
Numéro CAS:
Poids moléculaire :
649.76
Numéro MDL:
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.21

Niveau de qualité

Pureté

≥98% (HPLC)

Forme

powder

Conditions de stockage

desiccated

Couleur

white to beige

Solubilité

DMSO: 2 mg/mL, clear (Warmed)

Température de stockage

-10 to -25°C

Actions biochimiques/physiologiques

Nintedanib (BIBF1120) is an orally active, potent ATP-competitive inhibitor against angiokinases VEGFR-1/2/3 (IC50 = 34/21/13 nM), FGFR-1/2/3/4 (IC50 = 69/37/108/610 nM), PDGFRα/β (IC50 = 59/65 nM), as well as Flt-3, Lck, Lyn, and Src (IC50 = 26, 16, 195, 156 nM, repectively), but not 33 other kinases. Nintedanib exhibits antiangiogenic and antifibrotic efficacy in cultures and in animal models of cancers and pulmonary fibrosis in vivo.

Attention

Hygroscopic

Pictogrammes

Health hazardEnvironment

Mention d'avertissement

Danger

Mentions de danger

Classification des risques

Aquatic Chronic 2 - Repr. 1B - STOT RE 1

Organes cibles

Liver,Gastro-intestinal system

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


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Consulter la Bibliothèque de documents

Gerald J Roth et al.
Journal of medicinal chemistry, 52(14), 4466-4480 (2009-06-16)
Inhibition of tumor angiogenesis through blockade of the vascular endothelial growth factor (VEGF) signaling pathway is a new treatment modality in oncology. Preclinical findings suggest that blockade of additional pro-angiogenic kinases, such as fibroblast and platelet-derived growth factor receptors (FGFR
Raquel Frenedoso da Silva et al.
Cell and tissue research, 379(2), 407-420 (2019-09-02)
The antiangiogenic therapy for prostate cancer with Nintedanib, a potent inhibitor of important growth factor receptors, has been proven to delay tumor progression and arrest tumor growth; thus, the aim herein is to evaluate Nintedanib effects on tumor cells, besides angiogenesis
Frank Hilberg et al.
Cancer research, 68(12), 4774-4782 (2008-06-19)
Inhibition of tumor angiogenesis through blockade of the vascular endothelial growth factor (VEGF) signaling pathway is a novel treatment modality in oncology. Preclinical findings suggest that long-term clinical outcomes may improve with blockade of additional proangiogenic receptor tyrosine kinases: platelet-derived
Roman C Brands et al.
Oncology letters, 18(3), 2220-2231 (2019-08-28)
Multidrug resistance (MDR) remains one of the major causes of suboptimal outcome following therapy in head and neck squamous cell carcinoma (HNSCC). ATP-binding cassette (ABC) transporters are overexpressed in HNSCC, which contributes to the limited effect of chemotherapeutic treatment. In
Emma Kulimova et al.
Molecular cancer therapeutics, 5(12), 3105-3112 (2006-12-19)
In acute myeloid leukemia (AML), receptor tyrosine kinase ligands promote growth and survival and contribute to AML-associated marrow neoangiogenesis. We have tested simultaneous inhibition of vascular endothelial growth factor, fibroblast growth factor, and platelet-derived growth factor receptor signaling by novel

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