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Merck

SML3780

Nintedanib ethanesulphonate

≥98% (HPLC), angiokinases VEGFR-1/2/3 inhibitor, powder

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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A propos de cet article

Formule empirique (notation de Hill) :
C31H33N5O4·C2H6O3S
Numéro CAS:
656247-18-6
Poids moléculaire :
649.76
UNSPSC Code:
12352200
NACRES:
NA.21
MDL number:
MFCD26142360
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
100
Storage condition:
desiccated

Principaux documents

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Nom du produit

Nintedanib ethanesulphonate, ≥98% (HPLC)

Quality Level

100

assay

≥98% (HPLC)

form

powder

storage condition

desiccated

color

white to beige

solubility

DMSO: 2 mg/mL, clear (Warmed)

storage temp.

-10 to -25°C

SMILES string

[S](=O)(=O)(O)CC.N5(CCN(CC5)C)CC(=O)N(C)c1ccc(cc1)N\C(=C3\c4c(cc(cc4)C(=O)OC)NC\3=O)\c2ccccc2

InChI

1S/C31H33N5O4.C2H6O3S/c1-34-15-17-36(18-16-34)20-27(37)35(2)24-12-10-23(11-13-24)32-29(21-7-5-4-6-8-21)28-25-14-9-22(31(39)40-3)19-26(25)33-30(28)38;1-2-6(3,4)5/h4-14,19,32H,15-18,20H2,1-3H3,(H,33,38);2H2,1H3,(H,3,4,5)/b29-28-;

InChI key

MMMVNAGRWOJNMW-FJBFXRHMSA-N

Catégories apparentées

Biochem/physiol Actions

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.
Orally active, potent ATP-competitive VEGFR, FGFR, PDGFR, Flt3, Lck, Lyn, Src inhibitor with in vivo antiangiogenic and antifibrotic efficacy.

Disclaimer

Hygroscopic

pictograms

Health hazardEnvironment
GHS08,GHS09

signalword

Danger

Hazard Classifications

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

target_organs

Liver,Gastro-intestinal system

Classe de stockage

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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Certificats d'analyse (COA)

Lot/Batch Number
0000425709
0000425709
0000395484
0000395484
0000254981

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Consulter la Bibliothèque de documents

Elaine Reguera-Nuñez et al.
Angiogenesis, 22(4), 535-546 (2019-08-30)
In contrast to VEGF pathway-targeting antibodies, antiangiogenic tyrosine kinase inhibitors (TKIs) have failed to meet primary endpoints in almost all phase III clinical trials when combined with conventional chemotherapy. One exception is the combination of nintedanib and docetaxel as a
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
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
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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