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Merck
CN

PZ0150

SU5614

≥98% (HPLC)

Synonym(s):

(3Z)-5-Chloro-3-[(3,5-dimethyl-1H-pyrrol-2-yl)methylene]-1,3-dihydro-2H-indol-2-one

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About This Item

Empirical Formula (Hill Notation):
C15H13ClN2O
CAS Number:
Molecular Weight:
272.73
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
51111800
MDL number:
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InChI

1S/C15H13ClN2O/c1-8-5-9(2)17-14(8)7-12-11-6-10(16)3-4-13(11)18-15(12)19/h3-7,17H,1-2H3,(H,18,19)/b12-7-

SMILES string

Cc1cc(C)c(\C=C2/C(=O)Nc3ccc(Cl)cc23)[nH]1

InChI key

XLBQNZICMYZIQT-GHXNOFRVSA-N

assay

≥98% (HPLC)

form

powder

color

orange

solubility

DMSO: ≥20 mg/mL

storage temp.

2-8°C

Quality Level

Biochem/physiol Actions

SU5614 is a FMS-like tyrosine kinase 3 (FLT3) inhibitor.
SU5614 is a FMS-like tyrosine kinase 3 (FLT3) inhibitor; selective inhibitor of VEGF and PDGF receptor tyrosine kinases.

Features and Benefits

This compound is featured on the PDGFR page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

hcodes

Hazard Classifications

Aquatic Chronic 4

Storage Class

11 - Combustible Solids

flash_point_f

Not applicable

flash_point_c

Not applicable


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Shoko Matsushima et al.
Scientific reports, 10(1), 188-188 (2020-01-15)
Anosmin-1 is a secreted glycoprotein encoded by the ANOS1 gene, and its loss of function causes Kallmann syndrome (KS), which is characterized by anosmia and hypogonadism due to olfactory bulb (OB) dysfunction. However, the physiological function of anosmin-1 remains to
Manja Wobus et al.
Oncotarget, 6(36), 38804-38815 (2015-10-16)
Internal tandem duplications within the juxtamembrane region of the FMS-like tyrosine kinase receptor FLT3 (FLT3-ITD) represents one of the most common mutations in patients with acute myeloid leukemia (AML) which results in constitutive aberrant activation, increased proliferation of leukemic progenitors
Ayumi Yoshida et al.
Biology open, 4(9), 1063-1076 (2015-07-26)
Neuropilin-1 (NRP1) has been identified as a VEGF-A receptor. DJM-1, a human skin cancer cell line, expresses endogenous VEGF-A and NRP1. In the present study, the RNA interference of VEGF-A or NRP1 suppressed DJM-1 cell proliferation. Furthermore, the overexpression of

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