Nilotinib (AMN-107)

Catalog No.S1033

Nilotinib (AMN-107) Chemical Structure

Molecular Weight(MW): 529.52

Nilotinib (AMN-107) is a Bcr-Abl inhibitor with IC50 less than 30 nM in Murine myeloid progenitor cells.

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In DMSO USD 91 In stock
USD 70 In stock
USD 210 In stock
USD 470 In stock

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5 Customer Reviews

  • Ba/F3-p210T315I cells were treated with indicated concentrations of nilotinib with or without PDMP for 24 h. Apoptosis was determined as in A. Data are shown as percentage of sub-G1 for apoptosis in triplicate cultures. *P<0.05.

    FASEB J 2011 25, 3661-3673. Nilotinib (AMN-107) purchased from Selleck.

    Effect of nilotinib on Bcr-Abl kinase activity in ABCB1- and ABCG2- overexpressing CD34+CD38- cells. K562 parental cells and CD34+CD38- subpopulation isolated from K562 cells were treated with nilotinib at 0.01, 0.1 and 1.0 umol/L for 12 h. Equal amount of protein was loaded for western blot analysis as described in the Experimental section. The experiments were repeated at least three times independently, and a representative experiment is shown.

    Molecules 2014 19, 3356-75. Nilotinib (AMN-107) purchased from Selleck.

  •  

    Inhibition of thymidine (a and b) and cytarabine (c and d) uptake with nilotinib. The legend is similar to Fig. 1, except that imatinib was replaced by nilotinib.

    Leukemia Res 2012 36, 1311-1314. Nilotinib (AMN-107) purchased from Selleck.

    Nilotinib up-regulates the ERK survival signal in prostate cancer cells. (B and C) Immunoblot analyses of DU-145 cells (B) or DU-145 cells in comparison with LNCaP and PC-3 cells (C) treated with nilotinib for the expression of phospho-ERK1/2 T202/Y204 and total ERK. Immunoblot for GAPDH is shown as a loading control.

    Urol Oncol 2014 0.1016/j.urolonc.2014.06.001. Nilotinib (AMN-107) purchased from Selleck.

  • Immunohistochemical staining of xenografted DU-145 cells after 21 days of treatment with 75 mg/kg/d of nilotinib for phospho-ERK1/2 T202/Y204 expression. It can be noted that tumors explanted from vehicle-treated mice showed mostly positivity at the tumor periphery, whereas tumors explanted from nilotinib-treated mice showed a more evenly distributed phospho-ERK immunostaining (left panels). Quantification of phospho-ERK-positive DU-145 xenografts explanted after 21 days of treatment. Mean and standard errors of positive cells per high-power field (HPF; x40) from at least 3 tumors are given (right panel).

    Urol Oncol 2014 0.1016/j.urolonc.2014.06.001. Nilotinib (AMN-107) purchased from Selleck.

Purity & Quality Control

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Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

Biological Activity

Description Nilotinib (AMN-107) is a Bcr-Abl inhibitor with IC50 less than 30 nM in Murine myeloid progenitor cells.
Features A selective inhibitor of native and mutant Bcr-Abl.
Targets
Bcr-Abl [1]
(Murine myeloid progenitor cells)
<30 nM
In vitro

Nilotinib inhibits proliferation, migration, and actin filament formation, as well as the expression of α-SMA and collagen in activated HSCs. Nilotinib induces apoptosis of HSCs, which is correlated with reduced bcl-2 expression, increases p53 expression, cleavage of PARP, as well as increases expression of PPARγ and TRAIL-R. Nilotinib also induces cell cycle arrest, accompanied by increased expression of p27 and downregulation of cyclin D1. Interestingly, Nilotinib not only inhibits activation of PDGFR, but also TGFRII through Src. Nilotinib significantly inhibits PDGF and TGFβ-simulated phosphorylation of ERK and Akt. Furthermore, PDGF- and TGFβ-activated phosphorylated form(s) of Abl in human HSCs are inhibited by Nilotinib. [2] Nilotinib inhibits most imatinib-resistant Bcr-Abl mutations, except for T315I. [3] Nilotinib inhibits PDGF-DD-mediated ERK1/2 activation, basal and PDGF-DD-mediated activation of PDGFRβ and Akt, and schwannoma proliferation. Nilotinib is more potent than imatinib, exerting its maximal inhibitory effect at concentrations lower than steady-state trough plasma levels. [4] Nilotinib also significantly reduces the expression levels of the genes for TGF-β1 and platelet-derived growth factor (PDGF). Nilotinib treatment also significantly inhibits the PDGF-induced proliferation of lung fibroblasts. [5] Nilotinib inhibits the proliferation of Ba/F3 cells expressing p210- and p190-Bcr-Abl, or K562 and Ku-812F cells with IC50 values ≤12 nM. [6]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
EoL-1-cell M4DGXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYPJR|UxRTBwMECwNVQ1KM7:TR?= NYKzZlExW0GQR1XS
KU812 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{LZUmlEPTB;MD6wNFI1QCEQvF2= MXPTRW5ITVJ?
EM-2 NIG1eppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoHGTWM2OD1yLkCwOFEh|ryP M1zDbHNCVkeHUh?=
LAMA-84 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4jtdWlEPTB;MD6wNFQ6KM7:TR?= NEK4ZXlUSU6JRWK=
MEG-01 NFLyT3lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWnJR|UxRTBwMEC4Nlgh|ryP NFfwW4hUSU6JRWK=
BV-173 MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYL6fZZxUUN3ME2wMlAyODh7IN88US=> NULHSGNmW0GQR1XS
KASUMI-1 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX\JR|UxRTBwMEK0NVMh|ryP MoqyV2FPT0WU
NB7 NXHSfVBiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXHJR|UxRTBwMUO0N|kh|ryP MVHTRW5ITVJ?
BHT-101 NFjIU5FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWe1fm9FUUN3ME2wMlY1OjZ|IN88US=> MlS1V2FPT0WU
CGTH-W-1 NUHMTopRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoP2TWM2OD1yLk[0PFch|ryP NXm3RYx5W0GQR1XS
HMV-II M33Hdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkjRTWM2OD1yLke0PFc1KM7:TR?= M3rzTXNCVkeHUh?=
NKM-1 M4rIOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXHJR|UxRTBwOUCxOUDPxE1? NXm5VJY1W0GQR1XS
LB2241-RCC NFjiWFFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX7JR|UxRTFwMEKyNlgh|ryP NVT0SlVoW0GQR1XS
NCI-H1703 M4XZbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnXBTWM2OD1zLkG4PFch|ryP NEnaToNUSU6JRWK=
BE-13 NES1NIpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1L0O2lEPTB;MT6yO|QyPiEQvF2= MWjTRW5ITVJ?
ACN MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGHXZ2VKSzVyPUGuOVUxPzdizszN MVXTRW5ITVJ?
A204 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4roUWlEPTB;MT61O|IxPSEQvF2= MlH4V2FPT0WU
HOP-62 NY\pPJZwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH;3[|BKSzVyPUGuPFIxPzdizszN NWD6cVF4W0GQR1XS
H9 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3SwPGlEPTB;Mj63N|c6OyEQvF2= NGTwc2tUSU6JRWK=
HCC1806 NW[xWo1PT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUO2WVVUUUN3ME2yMlc1OzJ5IN88US=> MYrTRW5ITVJ?
NOS-1 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1z6[mlEPTB;Mj64O|ExOiEQvF2= MoPWV2FPT0WU
RS4-11 NFH3RZhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVPJR|UxRTJwOUC2NlMh|ryP MXPTRW5ITVJ?
JAR NFnkToxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYK2dY1QUUN3ME2yMlkzODh2IN88US=> NULL[WtWW0GQR1XS
T98G M3PtRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmrqTWM2OD1|LkCxN|E{KM7:TR?= NYHnZXp[W0GQR1XS
NCI-SNU-1 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVrJR|UxRTNwNECwPVIh|ryP NVTjTWpvW0GQR1XS
SK-MEL-1 Mlm2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoLYTWM2OD1|LkSzNFI6KM7:TR?= NWXFT|JsW0GQR1XS
L-363 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLiSVVJUUN3ME2zMlYyOTB5IN88US=> NHfsToZUSU6JRWK=
SW982 NUS0dINnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUHzOJBvUUN3ME2zMlY1OTZ7IN88US=> MUDTRW5ITVJ?
HT-1080 M4CzTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF7OXI5KSzVyPUOuPVE4PzVizszN NX\wcYRoW0GQR1XS
G-402 Mnf5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWPJR|UxRTRwM{GyNFMh|ryP MmLuV2FPT0WU
HOS M1m1c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHy3WFlKSzVyPUSuPFAzQDJizszN M{G1UXNCVkeHUh?=
SK-NEP-1 NHvid5VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWTnV2lbUUN3ME20Mlg{OTlzIN88US=> Mn7EV2FPT0WU
HAL-01 MljCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVXJR|UxRTRwOEiyOFIh|ryP M1H6fHNCVkeHUh?=
SBC-1 Mn31S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYPoT3NyUUN3ME20MlkxQTB5IN88US=> M1LSVnNCVkeHUh?=
CTV-1 M4DiNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\QToVKSzVyPUWuOFg6OzhizszN MVLTRW5ITVJ?
LCLC-103H M4HTc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWfJR|UxRTVwN{e0O|Eh|ryP Mn23V2FPT0WU
RVH-421 M3[y[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIPyZldKSzVyPUWuO|c2OzZizszN NHr6R3pUSU6JRWK=
K-562 NWHjNYh5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWfJR|UxRTVwOUCzOkDPxE1? NGfNbFBUSU6JRWK=
CAL-33 MkCwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGfXWFRKSzVyPU[uN|E{PTlizszN MV7TRW5ITVJ?
MDA-MB-361 NWPFRpIxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4jFN2lEPTB;Nj6zN|Y6QSEQvF2= NXPhV3REW0GQR1XS
IGROV-1 NWDLbWhCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1XWWmlEPTB;Nj60O|E6OSEQvF2= NIfV[5pUSU6JRWK=
NY MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXTJR|UxRTZwNUO1PVkh|ryP NVe1TlVtW0GQR1XS
Ramos-2G6-4C10 NEm3VZJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIG0NI9KSzVyPU[uOlY6OzFizszN MUnTRW5ITVJ?
HuO9 NYLvWZpRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX[yRmV1UUN3ME22Mlc{QTZ2IN88US=> NU\JfVhGW0GQR1XS
MS-1 NVHDTJp4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYP1NGNnUUN3ME23MlEyQTV|IN88US=> MoHIV2FPT0WU
RPMI-8226 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEe1eIVKSzVyPUeuNlgzQDdizszN MmOyV2FPT0WU
HDLM-2 NWm2[Fl{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmfDTWM2OD15LkSwNVQ6KM7:TR?= MlzQV2FPT0WU
D-566MG MnXOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGPXZ|FKSzVyPUeuOFcyPTVizszN MUPTRW5ITVJ?
SK-MEL-24 M{fG[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnrCTWM2OD15Lk[zN|kzKM7:TR?= NVfv[nl1W0GQR1XS
COLO-679 M2PXW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYSyToFNUUN3ME23Mlk5PjdzIN88US=> MXHTRW5ITVJ?
EW-13 NVHhclFZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEXydHhKSzVyPUiuN|IxPTRizszN NFfUcnhUSU6JRWK=
A388 M1SzSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWrue|F3UUN3ME24MlM5PDhzIN88US=> Ml;MV2FPT0WU
UM-UC-3 NGDwS4JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkHSTWM2OD16LkSzPVU3KM7:TR?= NHXle5NUSU6JRWK=
NUGC-3 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4XYe2lEPTB;OD61N|U5OiEQvF2= M4DQe3NCVkeHUh?=
COLO-668 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{n3cmlEPTB;OD61PVQ6OSEQvF2= NH25blZUSU6JRWK=
MOLT-4 Mn;JS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkTZTWM2OD16Lk[yN|U{KM7:TR?= Ml3mV2FPT0WU
D-423MG NIfRXVlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUG2c25wUUN3ME24Mlg{PzV4IN88US=> NH3ESlFUSU6JRWK=
CTB-1 MlHKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWDJR|UxRThwOEexNlgh|ryP NGnOV5VUSU6JRWK=
BCPAP MnLrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2PJOWlEPTB;OT6wNlU3OiEQvF2= MlX5V2FPT0WU
GCT MonIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXXJR|UxRTlwMEm4N|Eh|ryP NHLtZWZUSU6JRWK=
ACHN MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnjYTWM2OD17LkKzOlMzKM7:TR?= NX7wOYRKW0GQR1XS
KYSE-520 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH7XSINKSzVyPUmuN|M1QDJizszN NYTKbpZKW0GQR1XS
LB771-HNC M1fVbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2\N[GlEPTB;OT63OlQ6PyEQvF2= MW\TRW5ITVJ?
MLMA MoXuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{f2NGlEPTB;MUCuNFE{OiEQvF2= MUPTRW5ITVJ?
HEC-1 M3ricWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYnJR|UxRTFyLkK4NFQh|ryP MmTCV2FPT0WU
HL-60 MoOxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF3OW|ZKSzVyPUGwMlY5PTNizszN NF7yfHBUSU6JRWK=
A101D NIPEOIxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlzKTWM2OD1zMD64PVI{KM7:TR?= Mm\GV2FPT0WU
A2058 MmjDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MULJR|UxRTFyLkmyOFUh|ryP MoTEV2FPT0WU
KARPAS-45 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NITze5FKSzVyPUGxMlA3OzVizszN NGHZVXNUSU6JRWK=
697 NYXuUZFRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXvuXIc2UUN3ME2xNU4zOTBzIN88US=> MmTFV2FPT0WU
NCI-N87 M{L3OGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHLlOmZKSzVyPUGxMlc4OzFizszN NFu0ZpVUSU6JRWK=
DSH1 MmjyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXLKdJNFUUN3ME2xNU44QTV|IN88US=> M2TCfHNCVkeHUh?=
HLE MorMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFzjV2xKSzVyPUGxMlg5OzlizszN MmrwV2FPT0WU
NCI-H720 MkXqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFPUfJZKSzVyPUGyMlY5ODFizszN M3rCOnNCVkeHUh?=
EW-3 MlvTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUPJR|UxRTF{LkmzNFch|ryP M2PTWnNCVkeHUh?=
AGS NYfxO4FOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkTtTWM2OD1zMz6wN|UyKM7:TR?= M3[0SHNCVkeHUh?=
ES5 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkLFTWM2OD1zMz6wOVEzKM7:TR?= MUnTRW5ITVJ?
DB MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV\JR|UxRTF|LkOyOVYh|ryP NHOwW|BUSU6JRWK=
A4-Fuk NYH6cGR7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1HhUGlEPTB;MUOuOFExOiEQvF2= M1rWUnNCVkeHUh?=
A427 M1:1eGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnLpTWM2OD1zMz60PVczKM7:TR?= NGXLS3FUSU6JRWK=
MN-60 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{\XeGlEPTB;MUOuOVg1OyEQvF2= NHvvXIlUSU6JRWK=
HCC2218 NGTFV2xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWLJR|UxRTF|LkW4OVYh|ryP NVTnd29RW0GQR1XS
MV-4-11 NFHi[oZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVTp[VRHUUN3ME2xN{45OTN5IN88US=> NUS2R2k{W0GQR1XS
GI-1 M{nCXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3TjeGlEPTB;MUSuNVE5PCEQvF2= NIDVWlVUSU6JRWK=
JVM-3 MonqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHLsXoVKSzVyPUG0MlI3PTZizszN MmnRV2FPT0WU
NCI-H2029 MlrmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlPtTWM2OD1zND6yO|I4KM7:TR?= MmTOV2FPT0WU
TE-12 M2rx[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUDJR|UxRTF2Lk[wOFYh|ryP MnvFV2FPT0WU
WM-115 MmXSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NI\NTmRKSzVyPUG1MlU3QDNizszN MlnGV2FPT0WU
BB65-RCC NYLhS2t3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHfhe5JKSzVyPUG2MlAzPDFizszN M3rYfXNCVkeHUh?=
NCI-H1693 MkfSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYTJR|UxRTF4LkO4NFIh|ryP M{LMfXNCVkeHUh?=
KARPAS-299 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGfieGZKSzVyPUG2MlYzODNizszN Mor6V2FPT0WU
UACC-257 Ml7QS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTF5LkC1PFIh|ryP NHvYNGNUSU6JRWK=
RKO MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFK4b2lKSzVyPUG3MlY1OzNizszN NIjCeJFUSU6JRWK=
HT-29 Ml:wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH3BXo1KSzVyPUG3Mlc5QDlizszN MWHTRW5ITVJ?
ES7 NGDoSVVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX24TVNwUUN3ME2xPE4yOTJ{IN88US=> Mln5V2FPT0WU
DEL MlfES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NETIb5BKSzVyPUG4MlMyPzJizszN NVPCbHp4W0GQR1XS
BT-549 NYrXOmU3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHfwd|dKSzVyPUG4MlQxQTJizszN MVfTRW5ITVJ?
NCI-H1755 M1rQd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUTJR|UxRTF6LkW3NlMh|ryP M3HpenNCVkeHUh?=
HCE-T NFflU2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3fHN2lEPTB;MUiuPFM1OSEQvF2= MV7TRW5ITVJ?
LU-139 MkPYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYKxVYNjUUN3ME2xPU4xPDV6IN88US=> NVHUS4pMW0GQR1XS
ECC10 NHHiPYlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkTqTWM2OD1zOT6yOFc2KM7:TR?= NEnUN|VUSU6JRWK=
769-P NWfIbYNQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{fkOGlEPTB;MUmuOlM{PSEQvF2= NX\hcmljW0GQR1XS
BALL-1 M4nFRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYrnSmpiUUN3ME2xPU43Pzd3IN88US=> NHXje5JUSU6JRWK=
LXF-289 M32xN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVXMTFFxUUN3ME2xPU45QTd7IN88US=> NUPrXYNIW0GQR1XS
TYK-nu NGS3[2JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGjZepdKSzVyPUG5Mlk{OTVizszN NWrQPXVmW0GQR1XS
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... Click to View More Cell Line Experimental Data

In vivo Nilotinib reduces collagen deposition and α-SMA expression in CCl4 and BDL-induced fibrosis. Nilotinib could induce HSC undergoing apoptosis, which is correlated with downregulation of bcl-2. [2] Nilotinib attenuates the extent of lung injury and fibrosis. Nilotinib therapy significantly reduces the levels of hydroxyproline on days 14 and 21, which is accompanied by decreased expression levels of transforming growth factor (TGF)-β1 and PDGFRβ. [5] AMN107 prolongs survival of mice injected with Bcr-Abl-transformed hematopoietic cell lines or primary marrow cells, and prolongs survival in imatinib-resistant CML mouse models. [6]

Protocol

Cell Research:[4]
+ Expand
  • Cell lines: Human primary Schwann and schwannoma cells
  • Concentrations: 1-10 μM
  • Incubation Time: 72 hours
  • Method: Human primary Schwann and schwannoma cells are seeded on precoated 96-well plates. Nilotinib is added 40 minutes before stimulation with 100 ng/mL PDGF-DD, and cells are cultured for 72 hours (3 days). Because the half-life of Nilotinib is 18 hours, one-half of the originally added concentrations are added freshly every day. In addition to DAPI staining and determination of the total cell number, the more sensitive and accurate BrdU incorporation method is used to detect proliferating cells. Total cell amount (DAPI) and number of dividing cells (BrdU-positive) are blindly counted using an inverted fluorescent microscope and 200 × magnification. All cells in every well are counted. The total cell number per well differed between various cell batches and is 100–300 cells/well.
    (Only for Reference)
Animal Research:[6]
+ Expand
  • Animal Models: Systemic 32D Bcr-Abl leukemia model in Female BALB/c mice, Bioluminescent Bcr-Abl model of CML in Female NOD-SCID mice and Bone marrow transplant Bcr-Abl model of CML in syngeneic Balb/c recipient mice
  • Formulation: 10% NMP-90% PEG300, PEG300
  • Dosages: 75 mg/kg, 100 mg/kg
  • Administration: Oral administration
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 27 mg/mL (50.98 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 4% DMSO+30% PEG 300+5% Tween 80+ddH2O 3mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 529.52
Formula

C28H22F3N7O

CAS No. 641571-10-0
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02973711 Not yet recruiting Leukemia, Chronic Myeloid University of Michigan Cancer Center February 2017 Phase 1|Phase 2
NCT02954978 Recruiting Parkinson Disease|Parkinsons Disease With Dementia Georgetown University January 2017 Phase 2
NCT02947893 Recruiting Alzheimers Disease Georgetown University January 2017 Phase 2
NCT02602314 Not yet recruiting Chronyc Myeloid Leukemia Gruppo Italiano Malattie EMatologiche dellAdulto December 2016 Phase 4
NCT02709083 Recruiting Chronic Myelogenous Leukemia|Chronic Myeloid Leukemia|Leukemia Emory University October 2016 Phase 2
NCT02917720 Not yet recruiting Chronic Myeloid Leukemia European LeukemiaNet|Heidelberg University|Ludwig-Maximilians - University of Munich October 2016 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID