Neratinib (HKI-272)

製品コードS2150

Neratinib (HKI-272)化学構造

分子量(MW):557.04

Neratinib (HKI-272) is a highly selective HER2 and EGFR inhibitor with IC50 of 59 nM and 92 nM in cell-free assays; weakly inhibits KDR and Src, no significant inhibition to Akt, CDK1/2/4, IKK-2, MK-2, PDK1, c-Raf and c-Met. Phase 3.

サイズ 価格(税別)  
JPY 24900.00
JPY 78020.00
JPY 161020.00

カスタマーフィードバック(5)

  •  

    Differential sensitivity of EGFR-mutant glioma and lung cancer cell lines to the irreversible EGFR inhibitors HKI-272 and CI-1033. C, HKI-272 is more potent than CI-1033 in blocking EGFR phosphorylation in SKMG3 cells with EGFR EC mutation. SKMG3 cells were treated with the indicated doses of CI-1033 or HKI-272, and whole lysates were analyzed by immunoblot with the indicated antibodies.

    Cancer Discov 2012 2, 458-471. Neratinib (HKI-272) purchased from Selleck.

     

    Differential sensitivity of EGFR-mutant glioma and lung cancer cell lines to the irreversible EGFR inhibitors HKI-272 and CI-1033. A, HKI-272 induces cell death in GBM cells with EGFR EC mutation (SKMG3, SF268) but not EGFR wild-type (WT EGFR) cancer cell lines or astrocytes (NHA). Cell death was assessed by trypan blue exclusion after 5 days of inhibitor treatment. Cells lines in black express wild-type EGFR, whereas those in red contain EGFR EC mutations.

    Cancer Discov 2012 2, 458-471. Neratinib (HKI-272) purchased from Selleck.

  • HER2 mutations V777L, D769H, V842I, G309A induce gain-of-function over HER2 WT in MCF10A mammary epithelial cells. B, HER2 WT, L755S, and del.755–759 cells were grown in Matrigel in the presence of DMSO vehicle (0.5%), neratinib (0.5  μmol/L) or gefitinib (0.5  μmol/L). Phase contrast images were obtained as in A. C,  MCF10A-HER2 WT or mutants were seeded in soft agar. After 7 days of growth, they were treated with DMSO vehicle (0.5%), lapatinib (0.5 μmol/L) or neratinib (0.5 μmol/L) for an additional week. Error bars represent 95% highest posterior density intervals. *, Significant difference between the HER2 mutant and HER2 WT; #, the effect of inhibitor treatment was significant (95% highest posterior density interval did not contain 0 for both).  D, photomicrographs of the colonies in soft agar on day 12, magnification ×40. 

    Cancer Discov 2013 3, 224-37. Neratinib (HKI-272) purchased from Selleck.

    (C, D) Cells were treated as mentioned above for the indicated times and processed for immunofluorescence experiments with anti-ErbB2 antibody (green). Nuclei were stained with DAPI (blue). Examples of intracellular ErbB2 punctae are indicated with yellow triangles. Scale bar = 10 μm.

    Cancer Lett, 2016, 382(2):176-185. Neratinib (HKI-272) purchased from Selleck.

  • Mean IC50 value of Neratinib. *IC50 is the mean concentration of drug that reduced cell survival by 50% in at least two experiments. Data are shown as mean ± SD (n=6) of one representative experiment. Similar results were obtained in three experiments. *p < 0.05; **p < 0.01;*** p < 0.001

    Oncotarget, 2016, 7(36):58038-58050. Neratinib (HKI-272) purchased from Selleck.

製品安全説明書

HER2阻害剤の選択性比較

生物活性

製品説明 Neratinib (HKI-272) is a highly selective HER2 and EGFR inhibitor with IC50 of 59 nM and 92 nM in cell-free assays; weakly inhibits KDR and Src, no significant inhibition to Akt, CDK1/2/4, IKK-2, MK-2, PDK1, c-Raf and c-Met. Phase 3.
ターゲット
HER2 [1]
(Cell-free assay)
EGFR [1]
(Cell-free assay)
KDR [1]
(Cell-free assay)
Src [1]
(Cell-free assay)
59 nM 92 nM 800 nM 1.4 μM
体外試験

Neratinib weakly inhibits tyrosine kinases KDR and Src with IC50 of 0.8 μM and 1.4 μM, respectively, being 14- and 24-fold less active compared with HER2. Neratinib displays no activity against other serine-threonine kinases such as Akt, cyclin D1/cdk4, cyclin E/cdk2, cyclin B1/cdk1, IKK-2, MK-2, PDK1, c-Raf, and Tpl-2, as well as the tyrosine kinase c-Met. Neratinib selectively inhibits the proliferation of 3T3 cells transfected with the HER2 (3T3/neu), as well as two other HER-2-overexpressing SK-Br-3 and BT474 cells with IC50 values of 2-3 nM, displaying >230-fold potency compared with non-transfected 3T3 cells as well as MDA-MB-435 and SW620 which are EGFR- and HER2-negative. Neratinib also inhibits the proliferation of EGFR-dependent A431 cells with an IC50 of 81 nM. Neratinib reduces HER2 receptor autophosphorylation in BT474 cells with an IC50 of 5 nM, and EGF-dependent phosphorylation of EGFR in A431 cells with IC50 of 3 nM. Blocking of HER-2 by Neratinib results in inhibition of downstream MAPK and Akt pathways with IC50 of 2 nM, more potently than Trastuzumab. Neratinib inhibits the cyclin D1 expression and the phosphorylation of the Rb-susceptibility gene production in BT474 cells with IC50 of 9 nM, leading to G1-S arrest and ultimately decreased cell proliferation. [1]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 NYLiT5h1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NI[0dmFKSzVyPECuNFA2KM7:TR?= MWmyOFAxQTB4NB?=
EFM-192A MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHTLR|JKSzVyPECuNFA2KM7:TR?= NWPVcJgzOjRyMEmwOlQ>
HCC1569 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{LjV2lEPTB:MD6wNFUh|ryP M4nvclI1ODB7ME[0
HCC1954 M3nFRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NU\6d4Z1UUN3MEywMlAxPSEQvF2= NUjQb4NjOjRyMEmwOlQ>
MDA-MB-175 MmH1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWPJZ3pkUUN3MEywMlAxPSEQvF2= MnnaNlQxODlyNkS=
MDA-MB-361 NXyzZol1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWXJR|UxRDBwMEC1JO69VQ>? NUfCPIE5OjRyMEmwOlQ>
SK-BR-3 NGT3UoFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml7yTWM2ODxyLkCwOUDPxE1? MXKyOFAxQTB4NB?=
UACC-812 M13HVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2nUe2lEPTB:MD6wNFUh|ryP MXOyOFAxQTB4NB?=
UACC-893 MlqwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF3LdVNKSzVyPECuNFA2KM7:TR?= NIH3VXIzPDByOUC2OC=>
SUM-225 M2jSR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHDTWM2OD1yLkCxJO69VQ>? M33xNFI1ODB7ME[0
SUM-190 M1O5WWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\kZ2pKSzVyPUCuNFEh|ryP MmHJNlQxODlyNkS=
ZR-75-1 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWfJR|UxRTBwMEOg{txO MoTCNlQxODlyNkS=
HCC70 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1;VT2lEPTB;MD6wN{DPxE1? MVOyOFAxQTB4NB?=
BT-20 MoPNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHK1[I1KSzVyPUCuNFch|ryP MmTUNlQxODlyNkS=
MDA-MB-453 NUmwcXR2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MU\JR|UxRTBwMEmg{txO MlG5NlQxODlyNkS=
HCC1187 NUfwSmRmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYDJR|UxRTBwMUCg{txO NUT6XJBsOjRyMEmwOlQ>
EFM-19 NIDz[|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoryTWM2OD1yLkGxJO69VQ>? MUmyOFAxQTB4NB?=
T-47D NVjXPWRyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1f2RmlEPTB;MD6xOkDPxE1? NVG3Xo5[OjRyMEmwOlQ>
MDA-MB-134 NUWwNpdIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV\JR|UxRTBwMUeg{txO NYLLc2JCOjRyMEmwOlQ>
HCC38 M1XYcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVTqfWxYUUN3ME2wMlI2KM7:TR?= NUnJR|l7OjRyMEmwOlQ>
MDA-MB-435 NEfTeYFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4L5UWlEPTB;MD6zN{DPxE1? NI\vTHozPDByOUC2OC=>
MDA-MB-468 M4[ydmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{LSNWlEPTB;MD6zN{DPxE1? NHLKO5QzPDByOUC2OC=>
CAMA-1 NGe1dnVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlL6TWM2OD1yLkO3JO69VQ>? M{HYcFI1ODB7ME[0
MDA-MB-436 NWDsdG5xT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1TZOWlEPTB;MD60NUDPxE1? MYqyOFAxQTB4NB?=
MCF-7 NHLHTHpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWDJR|UxRTBwNEGg{txO MYWyOFAxQTB4NB?=
MDA-MB-415 MkPQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NInqVIlKSzVyPUCuOFIh|ryP NVvEZYZEOjRyMEmwOlQ>
HCC1806 NFX5N3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4LPWGlEPTB;MD60OEDPxE1? NWKwU4pFOjRyMEmwOlQ>
HCC1395 Ml7JS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3PaV2lEPTB;MD60PUDPxE1? NWq3[VFDOjRyMEmwOlQ>
HCC1937 M{XkOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MonOTWM2OD1yLkWwJO69VQ>? M37n[lI1ODB7ME[0
HCC1143 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2HEWWlEPTB;MD61OEDPxE1? NHHwNlczPDByOUC2OC=>
UACC-732 M4faPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1PvSmlEPTB;MD62OUDPxE1? NYX0XWt{OjRyMEmwOlQ>
MDA-MB-231 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkTWTWM2OD1zLkCwJO69VQ>? MVGyOFAxQTB4NB?=
MDA-MB-157 NIrK[FNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MorLTWM2OD1zLkGyJO69VQ>? M2G3SlI1ODB7ME[0
BT-549 NIKy[GZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXLJR|UxRTFwMUSg{txO NH36bmIzPDByOUC2OC=>
KPL-1 NELRNGVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVrJR|UxRTFwOEmg{txO MmnYNlQxODlyNkS=
CAL-51 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLtV2VkUUN3ME2xMlg6KM7:TR?= MmrDNlQxODlyNkS=
BT474 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYD3XpZHUUN3ME2wMlAxOzJ|INMxJFAvODByN{Wg{txO MmfMNlM5OTZ{NUS=
SKBR3 NILOUYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkLKTWM2OD1yLkCwO|UhyrFiMD6wNFUh|ryP M4D2WFI{QDF4MkW0
MDAMB453 MlTZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIjyV41KSzVyPUGuOVkhyrFiMD6xO|kh|ryP NYjoPIJbOjN6MU[yOVQ>
KB M{TOdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVzJR|UxRTRwMUOgxtEhOC52NzFOwG0> MXKyNlQ6OTl|NR?=
KBv200 M1nK[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVvJR|UxRTZwMEOgxtEhOC54NDFOwG0> MVKyNlQ6OTl|NR?=
MCF-7 NEPKcXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVHXVJBGUUN3ME2zMlMxKMLzIECuOFEh|ryP NYr3V2ZCOjJ2OUG5N|U>
MCF-7/Adr NFvNS4ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUPJR|UxRSB{Lki4JOKyKDBwM{Cg{txO M{nKTVIzPDlzOUO1
MCF-7 NYjYe5pmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mmn3TWM2OD1|LkCyJOKyKDBwM{Sg{txO M1e2bVIzPDlzOUO1
MCF-7/FLV1000 Mn;sS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVTUTYwyUUN3ME23MlA6KMLzIECuO|Eh|ryP M2DSWlIzPDlzOUO1
HL60 M{PMWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXrQPGRnUUN3ME2yMlI3KMLzIECuNlMh|ryP Mm\wNlI1QTF7M{W=
HL60/Adr MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEXZ[2NKSzVyPUGuOFIhyrFiMD6xOUDPxE1? M{\u[FIzPDlzOUO1
HEK293/pcDNA3.1 NIG5Wm1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkfyTWM2OD13LkK5JOKyKDBwNUOg{txO MkHYNlI1QTF7M{W=
HEK293/ABCB1 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWrJR|UxRTZwOUGgxtEhOC55MDCg{txO M4TOU|IzPDlzOUO1
SKBR M4XCZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml\zNE4xOS1zMECgcm0> M2Hp[lMuPyCm MnTJbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MVOyNVQ5PzZyNR?=
L858R(EGFR) NEHyRnpE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M1rzO4Rm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NHjC[XQyPzNzMUCwNi=>
L858R/T790M(EGFR) MoK4R4VtdCCYaXHibYxqfHliQYPzZZk> Ml70[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NEG5[5AyPzNzMUCwNi=>
G776insV_G/C MmnpR4VtdCCYaXHibYxqfHliQYPzZZk> NVLuc3Vp\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NUT0cYx[OTd|MUGwNFI>
wild-type NInNPJhE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NIrweWll\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MUmxO|MyOTByMh?=
A775insYVMA MWHD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NIPhRmpl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MXSxO|MyOTByMh?=
G776insV_G/L NFv4VlNE\WyuIG\pZYJqdGm2eTDBd5NigQ>? Mkm5[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? Mn;jNVc{OTFyMEK=
P780insGSP MkjkR4VtdCCYaXHibYxqfHliQYPzZZk> NW\NOVN5\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NWX6Z5RZOTd|MUGwNFI>
NCI-H1781 NGfXTXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4fheIlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> M13PVVE3QDF6NkG4
HCC827 NUCzdllIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXrhOmREcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz M2XnRlE3QDF6NkG4
H3255 NULzV5l6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXXpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NYPicpFyOTZ6MUi2NVg>
NCI-H1975 NF\h[JVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUHpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= Mk\qNVY5OTh4MUi=
A549 M2ftOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYrpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NWPiZ3VjOTZ6MUi2NVg>
3T3 MmLrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2HPPGlEPTB;N{CwJOKyKDd6IH7N MUGxOVE4OzByOB?=
3T3/neu M1zDW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXHTcmdDUUN3ME2zJOKyKDBwMUSgcm0> M1zyRlE2OTd|MEC4
SK-Br-3 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXjhWlhiUUN3ME2yJOKyKDBwMUigcm0> NEPodo0yPTF5M{CwPC=>
BT 474 NVH5RYp5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3;pemlEPTB;MjFCtUAxNjB4IH7N NFK4dFUyPTF5M{CwPC=>
A431 NWf0PXI2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXHXXGhGUUN3ME24NUDDuSB7IH7N NHX1[ZoyPTF5M{CwPC=>
MDA-MB-435 M1y0bmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYjJR|UxRTl4MDFCtUAyPjVibl2= NHq0d3oyPTF5M{CwPC=>
SW620 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHuw[FZKSzVyPU[5NEDDuSB6NDDuUS=> MnXpNVUyPzNyMEi=

多くの細胞株試験データを見る場合、クリックしてください

体内試験 Oral administration of Neratinib significantly inhibits the growth of 3T3/neu xenografts, with inhibition of 34%, 53%, 98%, and 98% at dose of 10, 20, 40, and 80 mg/kg/day, respectively. Consistent with the inhibition of HER-2 phosphorylation by 84% within 1 hour of administration at 40 mg/kg/day, Neratinib inhibits the growth of BT474 xenografts by 70-82%, 67%, and 93% at dose of 5, 10, and 40 mg/kg/day, respectively. Neratinib is also effective against SK-OV-3 xenografts with inhibition of 31% and 85% at 5 and 60 mg/kg/day, respectively. Neratinib is less potent against EGFR-dependent A431 xenografts than HER-2-dependent tumors, with 32% and 44% inhibition at 5 and 20 mg/kg/day, respectively. Neratinib displays little activity against MCF-7 and MX-1 xenografts expressing low levels of HER-2 and EGFR, with only 28% inhibition at 80 mg/kg/day, suggesting that Neratinib has selective activity for cells expressing HER-2 or EGFR. [1]

お薦めの試験操作(参考用のみ)

キナーゼ試験:[1]
+ 展開

Cell-free autophosphorylation assay using time-resolved fluorometry:

Neratinib is prepared as 10 mg/mL stocks in DMSO and diluted in 25 mM HEPES (pH 7.5; 0.002 ng/mL-20 μg/mL). Purified recombinant COOH-terminal fragments of HER2 (amino acids 676-1255) or epidermal growth factor receptor (EGFR) (amino acids 645-1186) [diluted in 100 mM HEPES (pH 7.5) and 50% glycerol] is incubated with increasing concentrations of Neratinib in 4 mM HEPES (pH 7.5), 0.4 mM MnCl2, 20 μM sodium vanadate, and 0.2 mM DTT for 15 minutes at room temperature in 96-well ELISA plates. The kinase reaction is initiated by the addition of 40 μM ATP and 20 mM MgCl2 and allowed to proceed for 1 hour at room temperature. Plates are washed, and phosphorylation is detected using Europium-labeled anti-phospho-tyrosine antibodies (15 ng/well). After washing and enhancement steps, signal is detected using a Victor2 fluorescence reader (excitation wavelength 340 nm, emission wavelength 615 nm). The concentration of Neratinib that inhibits receptor phosphorylation by 50% (IC50) is calculated from inhibition curves.
細胞試験: [1]
+ 展開
  • 細胞株: 3T3, 3T3/neu, A431, BT474, SK-Br-3, MDA-MB-435, and SW480
  • 濃度: Dissolved in DMSO, final concentrations 0.5 ng/mL-5 μg/mL
  • 反応時間: 2 or 6 days
  • 実験の流れ: Cells are exposed to various concentrations of Neratinib for 2, or 6 days. Cell proliferation is determined using sulforhodamine B, a protein binding dye. Briefly, cells are fixed with 10% trichloroacetic acid and washed extensively with water. Cells are then stained with 0.1% sulforhodamine B and washed in 5% acetic acid. Protein-associated dye is solubilized in 10 mM Tris, and absorbance is measured at 450 nM. The concentration of Neratinib that inhibits cell proliferation by 50% (IC50) is determined from inhibition curves.
    (参考用のみ)
動物試験:[1]
+ 展開
  • 動物モデル: Female athymic (nude) mice implanted s.c. with 3T3/neu, BT474, MCF-7, or SK-OV-3 cells
  • 製剤: Formulated in 0.5% methocellulose-0.4% polysorbate-80 (Tween 80)
  • 投薬量: ~80 mg/kg/day
  • 投与方法: Gavage
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 5 mg/mL (8.97 mM) warming
Water Insoluble
Ethanol Insoluble
体内 左から右までの手順で、溶剤を製品に加えることです:
30% PEG400+0.5% Tween80+5% propylene glycol
5 mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。

化学情報

分子量 557.04
化学式

C30H29ClN6O3

CAS No. 698387-09-6
保管
別名 N/A

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モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

マス 濃度 ボリューム 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02977780 Recruiting Glioblastoma Dana-Farber Cancer Institute|Eli Lilly and Company|Celgene|Puma Biotechnology, Inc.|Accelerate Brain Cancer Cure February 9, 2017 Phase 2
NCT02673398 Recruiting HER2 Positive Breast Carcinoma|Recurrent Breast Carcinoma|Stage IV Breast Cancer City of Hope Medical Center|National Cancer Institute (NCI)|Puma Biotechnology, Inc. October 2016 Phase 2
NCT02932280 Recruiting Solid Tumor|Central Nervous System Tumor|Lymphoma|Leukemia Memorial Sloan Kettering Cancer Center|Milton S. Hershey Medical Center|M.D. Anderson Cancer Center|Stanford University|Arkansas Childrens Hospital Research Institute|Alberta Childrens Hospital|Phoenix Childrens Hospital|University of Texas October 2016 Phase 1|Phase 2
NCT02593708 Recruiting Solid Tumor Michelle Melisko|University of California, San Francisco October 2015 Phase 1
NCT02400476 Recruiting Early Stage HER2+ Breast Cancer Puma Biotechnology, Inc. February 2015 Phase 2
NCT02236000 Recruiting Breast Cancer NSABP Foundation Inc|Puma Biotechnology, Inc. August 2014 Phase 1|Phase 2

技術サポート

ストックの作り方、阻害剤の保管する方法、細胞実験や動物実験に注意すべきな点を全部含めており、製品を取扱う時よくあった質問に対して取扱説明書でお答えいたします。

Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

  • * 必須

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