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)は一種の高度選択性的なHER2とEGFR阻害剤で、無細胞試験でIC50値が59 nMと92 nMに分かれることです。Neratinib (HKI-272)はKDRとSrcを微弱に抑制して、Akt、CDK1/2/4、IKK-2、MK-2、PDK1、c-Rafとc-Metに対して、著しい抑制作用がありません。臨床3期。

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)は一種の高度選択性的なHER2とEGFR阻害剤で、無細胞試験でIC50値が59 nMと92 nMに分かれることです。Neratinib (HKI-272)はKDRとSrcを微弱に抑制して、Akt、CDK1/2/4、IKK-2、MK-2、PDK1、c-Rafとc-Metに対して、著しい抑制作用がありません。臨床3期。
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 M{P3dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGjuPZZKSzVyPECuNFA2KM7:TR?= M{SzTFI1ODB7ME[0
EFM-192A NF61VoNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnzKTWM2ODxyLkCwOUDPxE1? M2X0cFI1ODB7ME[0
HCC1569 NUDZc5hwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWDyU4t{UUN3MEywMlAxPSEQvF2= NH2y[oszPDByOUC2OC=>
HCC1954 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV7uWVdxUUN3MEywMlAxPSEQvF2= M{DJcFI1ODB7ME[0
MDA-MB-175 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlXrTWM2ODxyLkCwOUDPxE1? M3fZTVI1ODB7ME[0
MDA-MB-361 MnLYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3e0TmlEPTB:MD6wNFUh|ryP NHj3UFQzPDByOUC2OC=>
SK-BR-3 MkPqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M37GVmlEPTB:MD6wNFUh|ryP M4TydlI1ODB7ME[0
UACC-812 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn7yTWM2ODxyLkCwOUDPxE1? NWn3OVFJOjRyMEmwOlQ>
UACC-893 NGrUV|hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Moi3TWM2ODxyLkCwOUDPxE1? MWiyOFAxQTB4NB?=
SUM-225 NHXPTYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1\kcmlEPTB;MD6wNUDPxE1? Ml\SNlQxODlyNkS=
SUM-190 NWKw[nExT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYrJR|UxRTBwMEGg{txO NHzTZYozPDByOUC2OC=>
ZR-75-1 NVztPWFpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnjxTWM2OD1yLkCzJO69VQ>? M3ruR|I1ODB7ME[0
HCC70 M161bGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWjJR|UxRTBwMEOg{txO Mn\QNlQxODlyNkS=
BT-20 NXXYZ|dOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRTBwMEeg{txO M4G3VVI1ODB7ME[0
MDA-MB-453 NVG5ZYxiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYrJR|UxRTBwMEmg{txO NV;EfGpzOjRyMEmwOlQ>
HCC1187 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M37Ic2lEPTB;MD6xNEDPxE1? NG\pN|EzPDByOUC2OC=>
EFM-19 NWi0V|E3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXLrW4F3UUN3ME2wMlEyKM7:TR?= M4nnUVI1ODB7ME[0
T-47D MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnzQTWM2OD1yLkG2JO69VQ>? NEXlOWQzPDByOUC2OC=>
MDA-MB-134 MmPZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1HZfWlEPTB;MD6xO{DPxE1? NUfFc4NtOjRyMEmwOlQ>
HCC38 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3zibGlEPTB;MD6yOUDPxE1? M37BbVI1ODB7ME[0
MDA-MB-435 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlO4TWM2OD1yLkOzJO69VQ>? NUjyO3RGOjRyMEmwOlQ>
MDA-MB-468 M3PCcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIXYOItKSzVyPUCuN|Mh|ryP NHjxbGQzPDByOUC2OC=>
CAMA-1 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkLHTWM2OD1yLkO3JO69VQ>? M{DscFI1ODB7ME[0
MDA-MB-436 NWT2c3NPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWfJR|UxRTBwNEGg{txO Mn;INlQxODlyNkS=
MCF-7 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlLSTWM2OD1yLkSxJO69VQ>? NEn1bGYzPDByOUC2OC=>
MDA-MB-415 M2jTO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHrrSG9KSzVyPUCuOFIh|ryP Mn7rNlQxODlyNkS=
HCC1806 NY\STo5wT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NETSS29KSzVyPUCuOFQh|ryP M4f6NFI1ODB7ME[0
HCC1395 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{DvZWlEPTB;MD60PUDPxE1? NEXpSYUzPDByOUC2OC=>
HCC1937 NITFN|FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUfJR|UxRTBwNUCg{txO NHG2T3UzPDByOUC2OC=>
HCC1143 NFzTblFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWPJR|UxRTBwNUSg{txO NXHqdoRwOjRyMEmwOlQ>
UACC-732 MljpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml[5TWM2OD1yLk[1JO69VQ>? M1nOblI1ODB7ME[0
MDA-MB-231 NVm2RpN{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWrJR|UxRTFwMECg{txO NVX3OIxjOjRyMEmwOlQ>
MDA-MB-157 M1rlTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn\CTWM2OD1zLkGyJO69VQ>? MUGyOFAxQTB4NB?=
BT-549 NEe4NYtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2TFUmlEPTB;MT6xOEDPxE1? NVWy[G41OjRyMEmwOlQ>
KPL-1 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFXhUHdKSzVyPUGuPFkh|ryP MXGyOFAxQTB4NB?=
CAL-51 Mlz2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPsZoRHUUN3ME2xMlg6KM7:TR?= MUSyOFAxQTB4NB?=
BT474 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX;JR|UxRTBwMECzNlMhyrFiMD6wNFA4PSEQvF2= NWrWeI5[OjN6MU[yOVQ>
SKBR3 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIToW3lKSzVyPUCuNFA4PSEEsTCwMlAxPSEQvF2= NWHBXXlkOjN6MU[yOVQ>
MDAMB453 M2HVNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVzJR|UxRTFwNUmgxtEhOC5zN{mg{txO M{X2SFI{QDF4MkW0
KB MkfWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV;JR|UxRTRwMUOgxtEhOC52NzFOwG0> MYqyNlQ6OTl|NR?=
KBv200 NIT2VGZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV3JR|UxRTZwMEOgxtEhOC54NDFOwG0> NXzVN2Q{OjJ2OUG5N|U>
MCF-7 MlrkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUfpS|FRUUN3ME2zMlMxKMLzIECuOFEh|ryP MVmyNlQ6OTl|NR?=
MCF-7/Adr Mm[xS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX7sTXU4UUN3ME2gNk45QCEEsTCwMlMxKM7:TR?= NXrtVnNvOjJ2OUG5N|U>
MCF-7 NVzyRXNvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlyyTWM2OD1|LkCyJOKyKDBwM{Sg{txO NULMNoVYOjJ2OUG5N|U>
MCF-7/FLV1000 M1nrWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXXRdoNnUUN3ME23MlA6KMLzIECuO|Eh|ryP NGnYdnozOjR7MUmzOS=>
HL60 NUe4dWZpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUHBOW9LUUN3ME2yMlI3KMLzIECuNlMh|ryP MmnRNlI1QTF7M{W=
HL60/Adr MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHX3XVJKSzVyPUGuOFIhyrFiMD6xOUDPxE1? MlHINlI1QTF7M{W=
HEK293/pcDNA3.1 MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVXHd3FvUUN3ME21MlI6KMLzIECuOVMh|ryP M3r3SlIzPDlzOUO1
HEK293/ABCB1 Mm\6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2r5TWlEPTB;Nj65NUDDuSByLkewJEDPxE1? NWL5XYFYOjJ2OUG5N|U>
SKBR Mon3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWWwMlAyNTFyMDDuUS=> Mk\iN{04KGR? MnHVbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MVuyNVQ5PzZyNR?=
L858R(EGFR) NWHiXWxbS2WubDDWbYFjcWyrdImgRZN{[Xl? Ml73[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NUTLbIJ7OTd|MUGwNFI>
L858R/T790M(EGFR) NX22WnZCS2WubDDWbYFjcWyrdImgRZN{[Xl? NF\q[lFl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MUexO|MyOTByMh?=
G776insV_G/C NUjEVIRKS2WubDDWbYFjcWyrdImgRZN{[Xl? M3HzcYRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NXzPdZp7OTd|MUGwNFI>
wild-type M1vBd2NmdGxiVnnhZoltcXS7IFHzd4F6 M1:wfIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? M2j4blE4OzFzMECy
A775insYVMA MmGyR4VtdCCYaXHibYxqfHliQYPzZZk> Mkfl[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? M{PLb|E4OzFzMECy
G776insV_G/L MUPD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MVTk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz MUixO|MyOTByMh?=
P780insGSP M3vqfGNmdGxiVnnhZoltcXS7IFHzd4F6 M3HQToRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MljFNVc{OTFyMEK=
NCI-H1781 MkD2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zHT4lvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NYLVb4h[OTZ6MUi2NVg>
HCC827 M3nySWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MW\pcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MoezNVY5OTh4MUi=
H3255 NHnVNXhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml3IbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MoP3NVY5OTh4MUi=
NCI-H1975 NFPCSlZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoPYbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M3jVeVE3QDF6NkG4
A549 NXy5PYJVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIn0UYVqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MonONVY5OTh4MUi=
3T3 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2rlfGlEPTB;N{CwJOKyKDd6IH7N MYCxOVE4OzByOB?=
3T3/neu MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWLrVJdZUUN3ME2zJOKyKDBwMUSgcm0> NVX2dlFvOTVzN{OwNFg>
SK-Br-3 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkjJTWM2OD1{INMxJFAvOThibl2= Ml\rNVUyPzNyMEi=
BT 474 NG\4cWtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mk\ETWM2OD1{INMxJFAvODZibl2= NXr0[JBvOTVzN{OwNFg>
A431 NYSxe3gxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWnJR|UxRThzINMxJFkhdk1? MWixOVE4OzByOB?=
MDA-MB-435 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPLTWM2OD17NkCgxtEhOTZ3IH7N M1noRlE2OTd|MEC4
SW620 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWHyRZVbUUN3ME22PVAhyrFiOESgcm0> M3vUeVE2OTd|MEC4

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 順序で溶剤を入れること:
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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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID