Nilotinib (AMN-107)

Catalog No.S1033

Nilotinib (AMN-107) Chemical Structure

Molecular Weight(MW): 529.52

Nilotinib (AMN-107) is a selective 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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  • 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 selective 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 NFv1ZYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYjJR|UxRTBwMECwNVQ1KM7:TR?= NUXkfVNTW0GQR1XS
KU812 M2PiZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3nTWmlEPTB;MD6wNFI1QCEQvF2= MWDTRW5ITVJ?
EM-2 Ml3HS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2jQXWlEPTB;MD6wNFQyKM7:TR?= MWHTRW5ITVJ?
LAMA-84 MoXzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIfsWG1KSzVyPUCuNFA1QSEQvF2= NHjRUVRUSU6JRWK=
MEG-01 MkjYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXfJR|UxRTBwMEC4Nlgh|ryP NGjzbpFUSU6JRWK=
BV-173 NXPuPGZ2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{G1dWlEPTB;MD6wNVA5QSEQvF2= NF71cpdUSU6JRWK=
KASUMI-1 M{TNZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWP4SZJEUUN3ME2wMlAzPDF|IN88US=> MlixV2FPT0WU
NB7 MoX0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFPNRWhKSzVyPUCuNVM1OzlizszN Mk\nV2FPT0WU
BHT-101 NXnPVZJET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4jH[GlEPTB;MD62OFI3OyEQvF2= MlW0V2FPT0WU
CGTH-W-1 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4Lqe2lEPTB;MD62OFg4KM7:TR?= NU\Ee5ZSW0GQR1XS
HMV-II M1\WPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4S0NmlEPTB;MD63OFg4PCEQvF2= NYLGXXpIW0GQR1XS
NKM-1 NWHqRnpvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUH3bm0yUUN3ME2wMlkxOTVizszN M2nFT3NCVkeHUh?=
LB2241-RCC MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLZXIxIUUN3ME2xMlAzOjJ6IN88US=> M{TtenNCVkeHUh?=
NCI-H1703 NXW2WYtrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3e3emlEPTB;MT6xPFg4KM7:TR?= NXjqeW9bW0GQR1XS
BE-13 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXTJR|UxRTFwMke0NVYh|ryP M3GxNHNCVkeHUh?=
ACN MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYLJR|UxRTFwNUWwO|ch|ryP NYLkb4VGW0GQR1XS
A204 MmnKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYjJR|UxRTFwNUeyNFUh|ryP NVfMc2E3W0GQR1XS
HOP-62 M1fqOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1W5RmlEPTB;MT64NlA4PyEQvF2= M2rHd3NCVkeHUh?=
H9 NFG2cW5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLCTmNKSzVyPUKuO|M4QTNizszN NYXsdGJKW0GQR1XS
HCC1806 NIHpWo9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV\iXZV4UUN3ME2yMlc1OzJ5IN88US=> NFTGfVhUSU6JRWK=
NOS-1 MoruS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn\ETWM2OD1{Lki3NVAzKM7:TR?= M2nnVXNCVkeHUh?=
RS4-11 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1jxWmlEPTB;Mj65NFYzOyEQvF2= M2XrU3NCVkeHUh?=
JAR MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH\peVFKSzVyPUKuPVIxQDRizszN NV3BZ4R1W0GQR1XS
T98G NI\xTHdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXnJR|UxRTNwMEGzNVMh|ryP NF;MdlNUSU6JRWK=
NCI-SNU-1 NH[3V49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUDJR|UxRTNwNECwPVIh|ryP MX;TRW5ITVJ?
SK-MEL-1 M1nTRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWjJR|UxRTNwNEOwNlkh|ryP MWDTRW5ITVJ?
L-363 NFLRclhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml;4TWM2OD1|Lk[xNVA4KM7:TR?= NYmyb4V7W0GQR1XS
SW982 NYLlR2V5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGPYXI1KSzVyPUOuOlQyPjlizszN NUHySndkW0GQR1XS
HT-1080 NF74fpBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVHJR|UxRTNwOUG3O|Uh|ryP M1nkbHNCVkeHUh?=
G-402 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLjN3B5UUN3ME20MlMyOjB|IN88US=> Ml\kV2FPT0WU
HOS NEPkXplIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoDGTWM2OD12LkiwNlgzKM7:TR?= MlfZV2FPT0WU
SK-NEP-1 NXzxUXBkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmrxTWM2OD12LkizNVkyKM7:TR?= MnzOV2FPT0WU
HAL-01 M1L6dmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYTJR|UxRTRwOEiyOFIh|ryP MmixV2FPT0WU
SBC-1 MlLZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIr4enZKSzVyPUSuPVA6ODdizszN NWrqdXVWW0GQR1XS
CTV-1 MlHjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF30NJdKSzVyPUWuOFg6OzhizszN M{[5eXNCVkeHUh?=
LCLC-103H NVXVT3R1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoPuTWM2OD13Lke3OFcyKM7:TR?= NGPRfopUSU6JRWK=
RVH-421 M176RWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3jvTmlEPTB;NT63O|U{PiEQvF2= NGHBNmNUSU6JRWK=
K-562 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF7BWI5KSzVyPUWuPVA{PiEQvF2= NXyz[2tuW0GQR1XS
CAL-33 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLvbW1IUUN3ME22MlMyOzV7IN88US=> M3KzR3NCVkeHUh?=
MDA-MB-361 NIi4b4ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NILiZXpKSzVyPU[uN|M3QTlizszN MWTTRW5ITVJ?
IGROV-1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWfJR|UxRTZwNEexPVEh|ryP MmXOV2FPT0WU
NY NXj6W|VYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHX0SXdKSzVyPU[uOVM2QTlizszN NFPHNolUSU6JRWK=
Ramos-2G6-4C10 NFj2c2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEDObWtKSzVyPU[uOlY6OzFizszN M1;BUXNCVkeHUh?=
HuO9 MmT4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoXaTWM2OD14LkezPVY1KM7:TR?= MmHyV2FPT0WU
MS-1 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX\nSo9WUUN3ME23MlEyQTV|IN88US=> MoXhV2FPT0WU
RPMI-8226 M{fmOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3nxb2lEPTB;Nz6yPFI5PyEQvF2= Ml\VV2FPT0WU
HDLM-2 NGnteFRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLWUWxKSzVyPUeuOFAyPDlizszN M3vJNHNCVkeHUh?=
D-566MG MlfyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHrSboNKSzVyPUeuOFcyPTVizszN M2myS3NCVkeHUh?=
SK-MEL-24 NUj6[XN4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoTPTWM2OD15Lk[zN|kzKM7:TR?= M1K1[nNCVkeHUh?=
COLO-679 NILQZ4JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLKNHpKSzVyPUeuPVg3PzFizszN M2PEdnNCVkeHUh?=
EW-13 M1PINmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2nFTWlEPTB;OD6zNlA2PCEQvF2= NYD1blZwW0GQR1XS
A388 NF63fYRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGOxTWNKSzVyPUiuN|g1QDFizszN NHi0c4pUSU6JRWK=
UM-UC-3 Ml\VS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NG\1V|ZKSzVyPUiuOFM6PTZizszN MYTTRW5ITVJ?
NUGC-3 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2PQdWlEPTB;OD61N|U5OiEQvF2= MXrTRW5ITVJ?
COLO-668 MmXkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYPJR|UxRThwNUm0PVEh|ryP M1POTXNCVkeHUh?=
MOLT-4 MoD2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUnVWZlTUUN3ME24MlYzOzV|IN88US=> NUW1XnV5W0GQR1XS
D-423MG NF65OJdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHzucoZKSzVyPUiuPFM4PTZizszN NWD2PIFtW0GQR1XS
CTB-1 MkO3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVTGXnlYUUN3ME24Mlg4OTJ6IN88US=> M1;tZnNCVkeHUh?=
BCPAP NE\PfmxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWTES5NlUUN3ME25MlAzPTZ{IN88US=> M1vZfHNCVkeHUh?=
GCT NGO0[G5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEO1RW9KSzVyPUmuNFk5OzFizszN MXvTRW5ITVJ?
ACHN NFu0XFJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml3iTWM2OD17LkKzOlMzKM7:TR?= NEXOeGVUSU6JRWK=
KYSE-520 NX74Snp[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYXCfmFRUUN3ME25MlM{PDh{IN88US=> NEfmNHlUSU6JRWK=
LB771-HNC NEjkfYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEGw[4pKSzVyPUmuO|Y1QTdizszN MXvTRW5ITVJ?
MLMA NFzrV3FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU\t[ZRGUUN3ME2xNE4xOTN{IN88US=> MUXTRW5ITVJ?
HEC-1 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYjXTHFoUUN3ME2xNE4zQDB2IN88US=> MVPTRW5ITVJ?
HL-60 Mo\YS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV3KT3ZPUUN3ME2xNE43QDV|IN88US=> NEXvdHFUSU6JRWK=
A101D MnfFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWnvRlhwUUN3ME2xNE45QTJ|IN88US=> MVvTRW5ITVJ?
A2058 M2rTZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYHTZVlEUUN3ME2xNE46OjR3IN88US=> NUnZR|R4W0GQR1XS
KARPAS-45 Mn;WS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1raOWlEPTB;MUGuNFY{PSEQvF2= M3S3O3NCVkeHUh?=
697 NYPte4hlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYnJR|UxRTFzLkKxNFEh|ryP NYfNUZlpW0GQR1XS
NCI-N87 M3Lm[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVniNoVpUUN3ME2xNU44PzNzIN88US=> NXvidWJ4W0GQR1XS
DSH1 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1nxOmlEPTB;MUGuO|k2OyEQvF2= MXrTRW5ITVJ?
HLE NIeyc4FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYmybo5EUUN3ME2xNU45QDN7IN88US=> NUXLb4ZnW0GQR1XS
NCI-H720 MoHRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1XTdmlEPTB;MUKuOlgxOSEQvF2= MUHTRW5ITVJ?
EW-3 Ml7GS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV3JR|UxRTF{LkmzNFch|ryP Ml3EV2FPT0WU
AGS M1LKdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnjsTWM2OD1zMz6wN|UyKM7:TR?= M2jzc3NCVkeHUh?=
ES5 MoXOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV7DdWlWUUN3ME2xN{4xPTF{IN88US=> M3jXeHNCVkeHUh?=
DB NVHVWlVST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3rmN2lEPTB;MUOuN|I2PiEQvF2= MkHpV2FPT0WU
A4-Fuk MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkD6TWM2OD1zMz60NVAzKM7:TR?= NHmyfXNUSU6JRWK=
A427 M4mwfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXXJR|UxRTF|LkS5O|Ih|ryP NYrRSZFjW0GQR1XS
MN-60 NYjNXVZMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWe0Rox[UUN3ME2xN{42QDR|IN88US=> MmfjV2FPT0WU
HCC2218 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NU\tW5l5UUN3ME2xN{42QDV4IN88US=> M2XvOHNCVkeHUh?=
MV-4-11 Mn3KS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoLtTWM2OD1zMz64NVM4KM7:TR?= NX[wSYhoW0GQR1XS
GI-1 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYj3RoM3UUN3ME2xOE4yOTh2IN88US=> MV7TRW5ITVJ?
JVM-3 Mm\tS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mkj1TWM2OD1zND6yOlU3KM7:TR?= MkKyV2FPT0WU
NCI-H2029 M{iyUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3\pNmlEPTB;MUSuNlczPyEQvF2= NH3WWWlUSU6JRWK=
TE-12 M{jxWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVzJR|UxRTF2Lk[wOFYh|ryP M3X1WnNCVkeHUh?=
WM-115 M4DmPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHvCRmlKSzVyPUG1MlU3QDNizszN MlXaV2FPT0WU
BB65-RCC MnvMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MknuTWM2OD1zNj6wNlQyKM7:TR?= NIHhPGJUSU6JRWK=
NCI-H1693 NG[3SG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXjJR|UxRTF4LkO4NFIh|ryP MXrTRW5ITVJ?
KARPAS-299 MojIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUDJR|UxRTF4Lk[yNFMh|ryP NF;2[FNUSU6JRWK=
UACC-257 NULZZm9RT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3;XcWlEPTB;MUeuNFU5OiEQvF2= M1;SdXNCVkeHUh?=
RKO NHTy[|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGrPdpVKSzVyPUG3MlY1OzNizszN MlHoV2FPT0WU
HT-29 M1;wOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFjUepFKSzVyPUG3Mlc5QDlizszN MmTiV2FPT0WU
ES7 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mo\JTWM2OD1zOD6xNVIzKM7:TR?= MmLJV2FPT0WU
DEL Mk\IS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlLMTWM2OD1zOD6zNVczKM7:TR?= Mn7lV2FPT0WU
BT-549 MmT5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEXLeJpKSzVyPUG4MlQxQTJizszN MXzTRW5ITVJ?
NCI-H1755 M1PLZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYTJR|UxRTF6LkW3NlMh|ryP M3fLPXNCVkeHUh?=
HCE-T M1Oydmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MojiTWM2OD1zOD64N|QyKM7:TR?= MV3TRW5ITVJ?
LU-139 M3Podmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXHJb|J1UUN3ME2xPU4xPDV6IN88US=> MUjTRW5ITVJ?
ECC10 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXrJR|UxRTF7LkK0O|Uh|ryP NFXuSodUSU6JRWK=
769-P NI\HW4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVfCbY4yUUN3ME2xPU43OzN3IN88US=> MlfaV2FPT0WU
BALL-1 Mlz1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUTSbVU1UUN3ME2xPU43Pzd3IN88US=> NVn5SY5SW0GQR1XS
LXF-289 NYHGe5FVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoPrTWM2OD1zOT64PVc6KM7:TR?= NYnj[oc6W0GQR1XS
TYK-nu MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGLxZmVKSzVyPUG5Mlk{OTVizszN NVfKZnVtW0GQR1XS
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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