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 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVLwbIx6UUN3ME2wMlAxODF2NDFOwG0> NEG2XWRUSU6JRWK=
KU812 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY\JR|UxRTBwMECyOFgh|ryP NVm1cZc6W0GQR1XS
EM-2 NHXYXHJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn\YTWM2OD1yLkCwOFEh|ryP M4PUZXNCVkeHUh?=
LAMA-84 MoDBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFHQZZVKSzVyPUCuNFA1QSEQvF2= MVLTRW5ITVJ?
MEG-01 NVT5UXhnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFvoZY9KSzVyPUCuNFA5OjhizszN M3[wXnNCVkeHUh?=
BV-173 M3nufWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYq2d4FrUUN3ME2wMlAyODh7IN88US=> MnjHV2FPT0WU
KASUMI-1 M37OeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHKxZoZKSzVyPUCuNFI1OTNizszN NUfK[ZMyW0GQR1XS
NB7 NUDneHM4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1v0cmlEPTB;MD6xN|Q{QSEQvF2= NWr4foFXW0GQR1XS
BHT-101 M{jzUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXW1TZk2UUN3ME2wMlY1OjZ|IN88US=> M3zMZnNCVkeHUh?=
CGTH-W-1 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn25TWM2OD1yLk[0PFch|ryP MYHTRW5ITVJ?
HMV-II NF;1bVBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2fMZmlEPTB;MD63OFg4PCEQvF2= MkDPV2FPT0WU
NKM-1 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV;JR|UxRTBwOUCxOUDPxE1? NHr0N3dUSU6JRWK=
LB2241-RCC Ml7YS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NITWVYNKSzVyPUGuNFIzOjhizszN NVjBUYhMW0GQR1XS
NCI-H1703 Mkf4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmfCTWM2OD1zLkG4PFch|ryP MVfTRW5ITVJ?
BE-13 MlLNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV\DeJlLUUN3ME2xMlI4PDF4IN88US=> Mnu0V2FPT0WU
ACN MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVHJR|UxRTFwNUWwO|ch|ryP MnPQV2FPT0WU
A204 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYDJR|UxRTFwNUeyNFUh|ryP MoHPV2FPT0WU
HOP-62 MnPXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVrJR|UxRTFwOEKwO|ch|ryP MmfZV2FPT0WU
H9 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnPETWM2OD1{LkezO|k{KM7:TR?= NWDxWlJZW0GQR1XS
HCC1806 M37JWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3jFVWlEPTB;Mj63OFMzPyEQvF2= MVvTRW5ITVJ?
NOS-1 M3HHfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NG\Mc3dKSzVyPUKuPFcyODJizszN NWjqNog2W0GQR1XS
RS4-11 NF;Cb25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYjIUHFqUUN3ME2yMlkxPjJ|IN88US=> NFXUb|hUSU6JRWK=
JAR MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1[1bGlEPTB;Mj65NlA5PCEQvF2= M3\JZnNCVkeHUh?=
T98G NFzZOpNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3n3WWlEPTB;Mz6wNVMyOyEQvF2= NWfoc|d[W0GQR1XS
NCI-SNU-1 NXvy[op1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFO1XYVKSzVyPUOuOFAxQTJizszN M33kb3NCVkeHUh?=
SK-MEL-1 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV;JR|UxRTNwNEOwNlkh|ryP NEjwSHlUSU6JRWK=
L-363 NHrYVYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mo[1TWM2OD1|Lk[xNVA4KM7:TR?= M3LBWnNCVkeHUh?=
SW982 MnnYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUTJR|UxRTNwNkSxOlkh|ryP MnHwV2FPT0WU
HT-1080 NYHzdVZWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWTJR|UxRTNwOUG3O|Uh|ryP MX3TRW5ITVJ?
G-402 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXW4VllrUUN3ME20MlMyOjB|IN88US=> MoP5V2FPT0WU
HOS M33MNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYq2WGhTUUN3ME20MlgxOjh{IN88US=> MoXRV2FPT0WU
SK-NEP-1 NHHTUHpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLxUZJKSzVyPUSuPFMyQTFizszN NGPtZWVUSU6JRWK=
HAL-01 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M17WOWlEPTB;ND64PFI1OiEQvF2= NHHkUHhUSU6JRWK=
SBC-1 NHyybJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2PDeGlEPTB;ND65NFkxPyEQvF2= M2PyS3NCVkeHUh?=
CTV-1 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NID5Ro9KSzVyPUWuOFg6OzhizszN M2HYPHNCVkeHUh?=
LCLC-103H NYjFT5d{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFXDcGpKSzVyPUWuO|c1PzFizszN NVrlSFlvW0GQR1XS
RVH-421 M3fnemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVLJR|UxRTVwN{e1N|Yh|ryP NXLBS4IyW0GQR1XS
K-562 M{W1Nmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn75TWM2OD13LkmwN|Yh|ryP M1fVWnNCVkeHUh?=
CAL-33 MofUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn23TWM2OD14LkOxN|U6KM7:TR?= MVrTRW5ITVJ?
MDA-MB-361 NHHwW2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWfTelh6UUN3ME22MlM{Pjl7IN88US=> MVzTRW5ITVJ?
IGROV-1 MkjaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFH1[HNKSzVyPU[uOFcyQTFizszN M1fjfHNCVkeHUh?=
NY MmrzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1:5OWlEPTB;Nj61N|U6QSEQvF2= MUPTRW5ITVJ?
Ramos-2G6-4C10 M1rjSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NG\qSG9KSzVyPU[uOlY6OzFizszN M33ENXNCVkeHUh?=
HuO9 NVvIXVRMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{DoO2lEPTB;Nj63N|k3PCEQvF2= NWC4ZlB1W0GQR1XS
MS-1 Mn7qS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnfxTWM2OD15LkGxPVU{KM7:TR?= MluzV2FPT0WU
RPMI-8226 M1S2cGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mmi5TWM2OD15LkK4Nlg4KM7:TR?= NILmO3FUSU6JRWK=
HDLM-2 M1HFcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml\QTWM2OD15LkSwNVQ6KM7:TR?= MoLuV2FPT0WU
D-566MG NWD1PZNiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2[4c2lEPTB;Nz60O|E2PSEQvF2= MYjTRW5ITVJ?
SK-MEL-24 M2L3OGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGX1XJpKSzVyPUeuOlM{QTJizszN MlvBV2FPT0WU
COLO-679 NX7mfWtYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoHxTWM2OD15Lkm4OlcyKM7:TR?= MWPTRW5ITVJ?
EW-13 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mo\wTWM2OD16LkOyNFU1KM7:TR?= MV3TRW5ITVJ?
A388 Mmf0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWLJR|UxRThwM{i0PFEh|ryP NWDXXZA2W0GQR1XS
UM-UC-3 NVfhfIYxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1TuXGlEPTB;OD60N|k2PiEQvF2= MX7TRW5ITVJ?
NUGC-3 M4S5RWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkLCTWM2OD16LkWzOVgzKM7:TR?= NFfEPHJUSU6JRWK=
COLO-668 NGLiUmxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVXJR|UxRThwNUm0PVEh|ryP NETiTmZUSU6JRWK=
MOLT-4 Mnz1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3;DemlEPTB;OD62NlM2OyEQvF2= Ml7hV2FPT0WU
D-423MG NH7EUJZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NG\1VnJKSzVyPUiuPFM4PTZizszN NEDVUYtUSU6JRWK=
CTB-1 Mm\RS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7jTWM2OD16Lki3NVI5KM7:TR?= MX;TRW5ITVJ?
BCPAP NIrYZYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NI[zOmNKSzVyPUmuNFI2PjJizszN NXrVWYgzW0GQR1XS
GCT MnPwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHfoU3FKSzVyPUmuNFk5OzFizszN M1XlZXNCVkeHUh?=
ACHN MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkPZTWM2OD17LkKzOlMzKM7:TR?= MYHTRW5ITVJ?
KYSE-520 NEizS41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoTUTWM2OD17LkOzOFgzKM7:TR?= Mom1V2FPT0WU
LB771-HNC MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlLFTWM2OD17Lke2OFk4KM7:TR?= NYO3WIV5W0GQR1XS
MLMA M2DPb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlHMTWM2OD1zMD6wNVMzKM7:TR?= MljSV2FPT0WU
HEC-1 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MljiTWM2OD1zMD6yPFA1KM7:TR?= MlLyV2FPT0WU
HL-60 NWCwb2IyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFzQWmFKSzVyPUGwMlY5PTNizszN NXK5NGRsW0GQR1XS
A101D NWPlbWxMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX7qfY56UUN3ME2xNE45QTJ|IN88US=> NID1WGxUSU6JRWK=
A2058 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHHu[FdKSzVyPUGwMlkzPDVizszN MUjTRW5ITVJ?
KARPAS-45 M3jpZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmDNTWM2OD1zMT6wOlM2KM7:TR?= NFzL[W5USU6JRWK=
697 M3TwZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWjsNoVuUUN3ME2xNU4zOTBzIN88US=> M1;hUXNCVkeHUh?=
NCI-N87 NYHwdGNPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mo\3TWM2OD1zMT63O|MyKM7:TR?= NVz5XlhWW0GQR1XS
DSH1 MnHlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHmyNYJKSzVyPUGxMlc6PTNizszN M3;Oe3NCVkeHUh?=
HLE NVG4XGQ1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGHHPVNKSzVyPUGxMlg5OzlizszN NYXhW|VXW0GQR1XS
NCI-H720 MkLpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFnDUo5KSzVyPUGyMlY5ODFizszN MXvTRW5ITVJ?
EW-3 NGq5OWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{faS2lEPTB;MUKuPVMxPyEQvF2= MXPTRW5ITVJ?
AGS NH3LZ5dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mm[0TWM2OD1zMz6wN|UyKM7:TR?= M3XucHNCVkeHUh?=
ES5 NULvc4Q2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoTyTWM2OD1zMz6wOVEzKM7:TR?= NVHqbGx1W0GQR1XS
DB MkPYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnW4TWM2OD1zMz6zNlU3KM7:TR?= M2PldXNCVkeHUh?=
A4-Fuk M3\3XWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rEV2lEPTB;MUOuOFExOiEQvF2= M1rNR3NCVkeHUh?=
A427 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{LyU2lEPTB;MUOuOFk4OiEQvF2= NIL1ZpRUSU6JRWK=
MN-60 NIjH[ZlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3;lOWlEPTB;MUOuOVg1OyEQvF2= NVz4[JZXW0GQR1XS
HCC2218 NX[5WVVST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX3JR|UxRTF|LkW4OVYh|ryP MnzYV2FPT0WU
MV-4-11 M3TDOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MY\JR|UxRTF|LkixN|ch|ryP MoHCV2FPT0WU
GI-1 M{PKWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWXpPWJUUUN3ME2xOE4yOTh2IN88US=> M{DJcHNCVkeHUh?=
JVM-3 NVPpc2RET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmHzTWM2OD1zND6yOlU3KM7:TR?= MYnTRW5ITVJ?
NCI-H2029 M1W2dGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkjTTWM2OD1zND6yO|I4KM7:TR?= MkH5V2FPT0WU
TE-12 M{T4U2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUHJR|UxRTF2Lk[wOFYh|ryP NUjseHp1W0GQR1XS
WM-115 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGfNZlJKSzVyPUG1MlU3QDNizszN NV;NSFVoW0GQR1XS
BB65-RCC MorYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYDJR|UxRTF4LkCyOFEh|ryP NInFU4dUSU6JRWK=
NCI-H1693 M{H0b2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYrJTmtxUUN3ME2xOk4{QDB{IN88US=> NEXCR|dUSU6JRWK=
KARPAS-299 M2n2d2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYjJR|UxRTF4Lk[yNFMh|ryP M1\xenNCVkeHUh?=
UACC-257 NHrUe4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX\JR|UxRTF5LkC1PFIh|ryP NEXKXnlUSU6JRWK=
RKO NVzBd4ZCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3HUV2lEPTB;MUeuOlQ{OyEQvF2= NIfnWmJUSU6JRWK=
HT-29 NFfRVYlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHP4W3BKSzVyPUG3Mlc5QDlizszN MWnTRW5ITVJ?
ES7 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmjmTWM2OD1zOD6xNVIzKM7:TR?= M1\4[nNCVkeHUh?=
DEL MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4X1VGlEPTB;MUiuN|E4OiEQvF2= M1\EdXNCVkeHUh?=
BT-549 MoP6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn[2TWM2OD1zOD60NFkzKM7:TR?= MX7TRW5ITVJ?
NCI-H1755 MkLFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX7JR|UxRTF6LkW3NlMh|ryP NGizfIpUSU6JRWK=
HCE-T MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV7JR|UxRTF6LkizOFEh|ryP M4PGfnNCVkeHUh?=
LU-139 MoDkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoPrTWM2OD1zOT6wOFU5KM7:TR?= NUHZTnVWW0GQR1XS
ECC10 NX3ZWld5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF3sNlJKSzVyPUG5MlI1PzVizszN NXzIVXk{W0GQR1XS
769-P M{nSS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWiz[nZmUUN3ME2xPU43OzN3IN88US=> MVfTRW5ITVJ?
BALL-1 MoS5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1nSUmlEPTB;MUmuOlc4PSEQvF2= NFq4VpFUSU6JRWK=
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TYK-nu NF\4PHdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX30dYk{UUN3ME2xPU46OzF3IN88US=> NEPSXYpUSU6JRWK=
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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