KX2-391

Names

[ Name ]:
KX2-391

[Synonym ]:
KX2-391
N-Benzyl-2-(5-{4-[2-(4-morpholinyl)ethoxy]phenyl}-2-pyridinyl)acetamide
N-benzyl-2-(5-(4-(2-morpholinoethoxy)phenyl)pyridin-2-yl)acetamide
pound not KX2391 pound not KX2 391
UNII-4V9848RS5G
2-(5-(4-(2-morpholinoethoxy)phenyl)pyridin-2-yl)-N-benzylacetamide
2-Pyridineacetamide, 5-[4-[2-(4-morpholinyl)ethoxy]phenyl]-N-(phenylmethyl)-
N-benzyl-2-{5-[4-(2-morpholin-4-ylethoxy)phenyl]pyridin-2-yl}acetamide
cc-266
KX01

Biological Activity

[Description]:

KX2-391 is an inhibitor of Src that targets the peptide substrate site of Src, with GI50 of 9-60 nM in cancer cell lines.

[Related Catalog]:

Signaling Pathways >> Cell Cycle/DNA Damage >> Microtubule/Tubulin

Signaling Pathways >> Cytoskeleton >> Microtubule/Tubulin

Signaling Pathways >> Protein Tyrosine Kinase/RTK >> Src

Research Areas >> Cancer

[Target]

GI50: 9 nM (Src, in HuH7 cells), 13 nM (Src, in PLC/PRF/5 cells), 26 nM (Src, in Hep3B cells), 60 nM (Src, in HepG2 cells)[1]

[In Vitro]

KX2-391 is a Src inhibitor that is directed to the Src substrate pocket. KX2-391 shows steep dose-response curves against Huh7 (GI50=9 nM), PLC/PRF/5 (GI50=13 nM), Hep3B (GI50=26 nM), and HepG2 (GI50=60 nM), four hepatic cell cancer (HCC) cell lines[1]. KX2-391 is found to inhibit certain leukemia cells that are resistant to current commercially available drugs, such as those derived from chronic leukemia cells with the T3151 mutation. KX2-391 is evaluated in engineered Src driven cell growth assays inNIH3T3/c-Src527F and SYF/c-Src527F cells and exhibits GI50 with 23 nM and 39 nM, respectively[2].

[In Vivo]

Orally administered KX2-391 is shown to inhibit primary tumor growth and to suppress metastasis, in pre-clinical animal models of cancer[2].

[Cell Assay]

Liver cell lines including Huh7, PLC/PRF/5, Hep3B, and HepG2 are routinely cultured and maintained in basal medium containing 2% fetal bovine serum (FBS) at 37°C and 5% CO2. Cells are seeded at 4.0×103/190 μL and 8.0×103/190 μL per well of 96-well plate in basal medium containing 1.5% FBS. These are cultured overnight at 37°C and 5% CO2 prior to the addition of KX2-391, at concentrations ranging from 6,564 to 0.012 nM in triplicates. Treated cells are incubated for 3 days. Ten μLs of 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) solution (5 mg/mL) is then added to each well on day 3 and cells incubated for 4 hours. The formazan product is dissolved with 10% SDS in dilute HCl. Optical density at 570 nm is measured. For comparison of activity and potency, parallel experiments are performed using KX2-391. Growth inhibition curves, 50% inhibition concentration (GI50), and 80% inhibition concentration (GI80) are determined using GraphPad Prism 5 statistical software. Data are normalized to represent percentage of maximum response as well as reported in optical density at wavelength of 570 nm (OD570) signal format[1].

[References]

[1]. Lau GM, et al. Expression of Src and FAK in hepatocellular carcinoma and the effect of Src inhibitors on hepatocellular carcinoma in vitro. Dig Dis Sci, 2009, 54(7), 1465-1474.

[2]. Fallah-Tafti A, et al. Thiazolyl N-benzyl-substituted acetamide derivatives: synthesis, Src kinase inhibitory and anticancer activities. Eur J Med Chem, 2011, 46(10), 4853-4858.

[Related Small Molecules]

Chemical & Physical Properties

[ Density]:
1.2±0.1 g/cm3

[ Boiling Point ]:
680.9±55.0 °C at 760 mmHg

[ Molecular Formula ]:
C₂₆H₂₉N₃O₃

[ Molecular Weight ]:
431.527

[ Flash Point ]:
365.6±31.5 °C

[ Exact Mass ]:
431.220886

[ PSA ]:
67.18000

[ LogP ]:
1.97

[ Vapour Pressure ]:
0.0±2.1 mmHg at 25°C

[ Index of Refraction ]:
1.588

[ Storage condition ]:
-20℃

Safety Information

[ Hazard Codes ]:
N

Synthetic Route

Click to get detail synthetic route

Precursor & DownStream

Precursor

DownStream

Related Compounds

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