Neratinib (HKI-272)

目录号:S2150

Neratinib (HKI-272) Chemical Structure

Molecular Weight(MW): 557.04

Neratinib (HKI-272)是一种高度选择性的HER2EGFR抑制剂,在无细胞试验中IC50分别为59 nM 和 92 nM;微弱抑制KDR和Src,对Akt,CDK1/2/4,IKK-2,MK-2,PDK1,c-Raf和c-Met没有显著的抑制作用。Phase 3。

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RMB 7933.43 现货
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客户使用该产品的6个实验数据:

  •  

    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.

    Western blot analysis of EGFR, pEGFR, HER2, pHER2, HER3, pHER3, HER4 and pHER4 in parental and neratinib-resistant cells following treatment with 1M neratinib for 2h. Actin was probed as loading control.

    Biochim Biophys Acta, 2018, 1865(8):1073-1087. Neratinib (HKI-272) purchased from Selleck.

产品安全说明书

HER2抑制剂选择性比较

生物活性

产品描述 Neratinib (HKI-272)是一种高度选择性的HER2EGFR抑制剂,在无细胞试验中IC50分别为59 nM 和 92 nM;微弱抑制KDR和Src,对Akt,CDK1/2/4,IKK-2,MK-2,PDK1,c-Raf和c-Met没有显著的抑制作用。Phase 3。
靶点
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
体外研究

Neratinib微弱抑制酪氨酸激酶KDR 和Src,IC50分别为0.8 μM 和 1.4 μM,与 HER-2相比,活性分别弱14和24倍。Neratinib 作用于其他丝-苏氨酸激酶如Akt, cyclin D1/cdk4, cyclin E/cdk2, cyclin B1/cdk1, IKK-2, MK-2, PDK1, c-Raf, 和Tpl-2,以及酪氨酸激酶c-Met没有活性。Neratinib选择性抑制转染 HER-2 (3T3/neu)的3T3细胞增殖,也抑制两种其他 HER-2-过表达的SK-Br-3和 BT474 cells细胞增殖,IC50为 2-3 nM,与未转染的3T3细胞及 EGFR-和 HER-2阴性的MDA-MB-435 和 SW620细胞相比,效果高230倍以上。Neratinib也抑制EGFR-依赖的A431细胞增殖,IC50为81 nM。Neratinib 作用于BT474 细胞,降低HER-2受体自磷酸化, IC50 为5 nM,作用于A431细胞,降低EGF依赖的 EGFR磷酸化,IC50 为3 nM。Neratinib抑制 HER-2,导致下游MAPK和Akt通路受抑制,IC50为2 nM,比Trastuzumab更有效。Neratinib 作用于BT474细胞,抑制cyclin D1表达和 Rb-敏感性基因产物的磷酸化,IC50为9 nM,导致细胞周期停在G1-S期,最终降低细胞增殖。[1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2naV2lEPTB:MD6wNFUh|ryP NHPRSWIzPDByOUC2OC=>
EFM-192A NUPVNmFXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXnJR|UxRDBwMEC1JO69VQ>? NU\1VnFjOjRyMEmwOlQ>
HCC1569 NFHIOGhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkHWTWM2ODxyLkCwOUDPxE1? MkjSNlQxODlyNkS=
HCC1954 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFHSfJhKSzVyPECuNFA2KM7:TR?= NF\1Z|AzPDByOUC2OC=>
MDA-MB-175 MkDYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX7DTlZRUUN3MEywMlAxPSEQvF2= MYiyOFAxQTB4NB?=
MDA-MB-361 MnPSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYP2UWNSUUN3MEywMlAxPSEQvF2= M1zQRVI1ODB7ME[0
SK-BR-3 M{PqV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVG2SIpDUUN3MEywMlAxPSEQvF2= MV:yOFAxQTB4NB?=
UACC-812 NH62XJJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml\PTWM2ODxyLkCwOUDPxE1? M2HkdFI1ODB7ME[0
UACC-893 NGXZW5hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVvhU5ZiUUN3MEywMlAxPSEQvF2= NYDsPGFKOjRyMEmwOlQ>
SUM-225 M3W4ZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWDzUYFbUUN3ME2wMlAyKM7:TR?= M3XKV|I1ODB7ME[0
SUM-190 M3:wWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX3DcGkxUUN3ME2wMlAyKM7:TR?= M4e5eVI1ODB7ME[0
ZR-75-1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3fPSGlEPTB;MD6wN{DPxE1? NGPaWJkzPDByOUC2OC=>
HCC70 NVLod2JNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH\DVVRKSzVyPUCuNFMh|ryP NWqwbZFPOjRyMEmwOlQ>
BT-20 NXO2PZV7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF74PGRKSzVyPUCuNFch|ryP NInYRpIzPDByOUC2OC=>
MDA-MB-453 M3;3fGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnO0TWM2OD1yLkC5JO69VQ>? NGrWXo4zPDByOUC2OC=>
HCC1187 NFGy[5VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2\4bWlEPTB;MD6xNEDPxE1? NVLWdWZvOjRyMEmwOlQ>
EFM-19 NYLhTIJoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnzmTWM2OD1yLkGxJO69VQ>? NUPnZ5NKOjRyMEmwOlQ>
T-47D NXXjb|N[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3z6SGlEPTB;MD6xOkDPxE1? M{f6SlI1ODB7ME[0
MDA-MB-134 M2qxdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2fs[GlEPTB;MD6xO{DPxE1? MWeyOFAxQTB4NB?=
HCC38 NWTwZlVjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVPDXZlnUUN3ME2wMlI2KM7:TR?= M4PoOlI1ODB7ME[0
MDA-MB-435 NHW4[VFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVzJR|UxRTBwM{Og{txO NXyyT4xVOjRyMEmwOlQ>
MDA-MB-468 M1O1eGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mmm3TWM2OD1yLkOzJO69VQ>? MmfWNlQxODlyNkS=
CAMA-1 MmroS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVv6O4U5UUN3ME2wMlM4KM7:TR?= M4D2VFI1ODB7ME[0
MDA-MB-436 MkntS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIfnelFKSzVyPUCuOFEh|ryP NG\UR3QzPDByOUC2OC=>
MCF-7 Mnm5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmnTTWM2OD1yLkSxJO69VQ>? M3Txc|I1ODB7ME[0
MDA-MB-415 MmjzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF3kR5BKSzVyPUCuOFIh|ryP Ml7uNlQxODlyNkS=
HCC1806 MkG4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1TrNGlEPTB;MD60OEDPxE1? MUSyOFAxQTB4NB?=
HCC1395 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUTJR|UxRTBwNEmg{txO MlzYNlQxODlyNkS=
HCC1937 M1z2Smdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2fYW2lEPTB;MD61NEDPxE1? NE\xV4UzPDByOUC2OC=>
HCC1143 M2[2bmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVzzeHRnUUN3ME2wMlU1KM7:TR?= NX\qSG9bOjRyMEmwOlQ>
UACC-732 NGXZcpRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXzJR|UxRTBwNkWg{txO NIOzOVUzPDByOUC2OC=>
MDA-MB-231 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NW\xfmZQUUN3ME2xMlAxKM7:TR?= NF7pXVkzPDByOUC2OC=>
MDA-MB-157 NGHNRmZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NE\iZm1KSzVyPUGuNVIh|ryP MX[yOFAxQTB4NB?=
BT-549 M4O0WWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGThNXJKSzVyPUGuNVQh|ryP NYLse2s1OjRyMEmwOlQ>
KPL-1 NYnUUXNZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml3ITWM2OD1zLki5JO69VQ>? M3TGXFI1ODB7ME[0
CAL-51 Mn;3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1LaZmlEPTB;MT64PUDPxE1? NIfNRZIzPDByOUC2OC=>
BT474 NVz2SI5tT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXTFfo1RUUN3ME2wMlAxOzJ|INMxJFAvODByN{Wg{txO NYTIPGo3OjN6MU[yOVQ>
SKBR3 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVPN[XpxUUN3ME2wMlAxPzViwsGgNE4xODVizszN NHTye4YzOzhzNkK1OC=>
MDAMB453 M1X6UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX7JR|UxRTFwNUmgxtEhOC5zN{mg{txO MXOyN|gyPjJ3NB?=
KB NWHTPJZtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3yzbGlEPTB;ND6xN{DDuSByLkS3JO69VQ>? MX:yNlQ6OTl|NR?=
KBv200 M2nTdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWHsR3ZyUUN3ME22MlA{KMLzIECuOlQh|ryP MkHsNlI1QTF7M{W=
MCF-7 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXyxblBsUUN3ME2zMlMxKMLzIECuOFEh|ryP NHfBSY8zOjR7MUmzOS=>
MCF-7/Adr MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MojaTWM2OD1iMj64PEDDuSByLkOwJO69VQ>? MmLsNlI1QTF7M{W=
MCF-7 NVfHb4FVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUDJWm5PUUN3ME2zMlAzKMLzIECuN|Qh|ryP MVeyNlQ6OTl|NR?=
MCF-7/FLV1000 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXSzPFA3UUN3ME23MlA6KMLzIECuO|Eh|ryP NIjp[oozOjR7MUmzOS=>
HL60 NXXRNWpPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoqzTWM2OD1{LkK2JOKyKDBwMkOg{txO NGjuVXozOjR7MUmzOS=>
HL60/Adr M4TxZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHjhTXFKSzVyPUGuOFIhyrFiMD6xOUDPxE1? MkP1NlI1QTF7M{W=
HEK293/pcDNA3.1 NH7VU3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2DY[2lEPTB;NT6yPUDDuSByLkWzJO69VQ>? NGP4V5IzOjR7MUmzOS=>
HEK293/ABCB1 NUHwd4x1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmLLTWM2OD14LkmxJOKyKDBwN{CgJO69VQ>? M{fwbVIzPDlzOUO1
SKBR MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUmwMlAyNTFyMDDuUS=> MlWxN{04KGR? NGfT[3JqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NUjlS|JjOjF2OEe2NFU>
L858R(EGFR) NX\KdZdFS2WubDDWbYFjcWyrdImgRZN{[Xl? NGrHbnhl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ M4rOWlE4OzFzMECy
L858R/T790M(EGFR) M1LnTWNmdGxiVnnhZoltcXS7IFHzd4F6 Ml34[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NGPoPIwyPzNzMUCwNi=>
G776insV_G/C M1i0fmNmdGxiVnnhZoltcXS7IFHzd4F6 Mke4[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MYmxO|MyOTByMh?=
wild-type MnnmR4VtdCCYaXHibYxqfHliQYPzZZk> NIXKRlRl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NVPTOZVUOTd|MUGwNFI>
A775insYVMA NXnSbodoS2WubDDWbYFjcWyrdImgRZN{[Xl? MWLk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NYnzblRoOTd|MUGwNFI>
G776insV_G/L NVfiOG5nS2WubDDWbYFjcWyrdImgRZN{[Xl? M4\u[YRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NH;pXVEyPzNzMUCwNi=>
P780insGSP MXPD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NWC3VnVy\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NV;JVFZsOTd|MUGwNFI>
NCI-H1781 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGLUW|lqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NVTuSHM3OTZ6MUi2NVg>
HCC827 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFHSSHJqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M3;ZSlE3QDF6NkG4
H3255 M1r3U2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYjpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NFvGZ5UyPjhzOE[xPC=>
NCI-H1975 NXG4cWNuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF;jdJFqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NIj1PJEyPjhzOE[xPC=>
A549 NY[xUllmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFnPPYhqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NH\zTWMyPjhzOE[xPC=>
3T3 MlLaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmHUTWM2OD15MECgxtEhPzhibl2= M3vQRlE2OTd|MEC4
3T3/neu MlK2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIS0O3BKSzVyPUOgxtEhOC5zNDDuUS=> NWq5VldiOTVzN{OwNFg>
SK-Br-3 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH:0fJBKSzVyPUKgxtEhOC5zODDuUS=> MoHlNVUyPzNyMEi=
BT 474 M4fjSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUfJR|UxRTJiwsGgNE4xPiCwTR?= M3TvdFE2OTd|MEC4
A431 MnPLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MY\JR|UxRThzINMxJFkhdk1? MWqxOVE4OzByOB?=
MDA-MB-435 NWPQVoRiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFLob4NKSzVyPUm2NEDDuSBzNkWgcm0> Mk\XNVUyPzNyMEi=
SW620 MnfxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXfvXm1XUUN3ME22PVAhyrFiOESgcm0> MknHNVUyPzNyMEi=

... Click to View More Cell Line Experimental Data

体内研究 Neratinib每天按10, 20, 40, 和80 mg/kg剂量口服处理给药3T3/neu 移植瘤,显著抑制生长,分别抑制34%, 53%, 98%, 和 98%。Neratinib每天按40 mg/kg剂量处理,1小时内抑制 84% HER-2磷酸化,相应地,Neratinib 每天按5, 10, 和 40 mg/kg剂量处理BT474 移植瘤,抑制分别为70-82%, 67%, 和 93%。Neratinib也有效作用于SK-OV-3移植瘤,每天按 5 和 60 mg/kg剂量处理,抑制分别为 31% 和85% 。Neratinib作用于EGFR依赖性A431移植瘤比作用于HER-2-依赖性肿瘤效果弱, 每天按5 和 20 mg/kg剂量处理,抑制分别为32%和44%。Neratinib作用于表达低水平HER-2和EGFR的MCF-7和 MX-1移植瘤几乎没有活性, 每天按80 mg/kg剂量处理抑制只为28%,说明Neratinib 选择性作用于表达HER-2或EGFR的细胞。[1]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:[1]
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使用时间-分辨荧光分析无细胞自磷酸化:

Neratinib 在DMSO 中制备成10 mg/mL 储液,然后在25 mM HEPES (pH 7.5; 0.002 ng/mL-20 μg/mL)中稀释。纯化重组的HER-2 COOH末端片段(第676-1255位氨基酸) 或EGFR COOH末端片段(第 645-1186位氨基酸)[在100 mM HEPES (pH 7.5) 和50% 甘油中稀释] 与浓度不断增高的Neratinib 在96-孔ELISA板上室温下温育15分钟,孔中含4 mM HEPES (pH 7.5), 0.4 mM MnCl2, 20 μM 钒酸钠,及 0.2 mM DTT 。加入 40 μM ATP 和20 mM MgCl2开始激酶反应,然后在室温下反应1小时。冲洗实验板, 使用铕标记的抗-磷酸化-酪氨酸抗体 (15 ng/每孔)检测磷酸化。冲洗后,使用Victor2 荧光读数仪 (激发波长为340 nm,发射波长为615 nm)测定信号。通过抑制曲线测定抑50%受体磷酸时的Neratinib 浓度 (IC50) 。
细胞实验:[1]
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  • Cell lines: 3T3, 3T3/neu, A431, BT474, SK-Br-3, MDA-MB-435, 和SW480
  • Concentrations: 溶于DMSO, 终浓度为0.5 ng/mL-5 μg/mL
  • Incubation Time: 2, 或6天
  • Method: 使用不同浓度Neratinib处理细胞 2, 或6 天。使用sulforhodamine B, 一种蛋白结合染料,测定细胞增殖。细胞与10% 三氯乙酸混合,然后使用水广泛冲洗。使用 0.1% sulforhodamine B对细胞进行染色,使用在5% 乙酸中清洗。蛋白-结合染10 mM Tris中,然后在450 nM处测定吸光度。通过抑制曲线测定抑制50% 细胞增殖时的Neratinib 浓度(IC50)。
    (Only for Reference)
动物实验:[1]
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  • Animal Models: 皮下移植3T3/neu, BT474, MCF-7, 或 SK-OV-3 细胞的雌性无胸腺裸鼠
  • Formulation: 在0.5% 甲基纤维素-0.4% Tween--80 (Tween-80)中配制
  • Dosages: ~80 mg/kg/day
  • Administration: 口服饲喂
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 5 mg/mL warmed (8.97 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
30% PEG400+0.5% Tween80+5% propylene glycol
5 mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 557.04
化学式

C30H29ClN6O3

CAS号 698387-09-6
稳定性 powder
in solvent
别名 N/A

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00878709 Active not recruiting Breast Cancer Puma Biotechnology Inc. July 9 2009 Phase 3
NCT00741260 Completed Breast Cancer Puma Biotechnology Inc. December 9 2008 Phase 1|Phase 2
NCT03094052 Recruiting HER2-positive Breast Cancer University of California San Francisco|Puma Biotechnology Inc. January 4 2017 Phase 2
NCT00777101 Completed Advanced Breast Cancer|Breast Cancer Puma Biotechnology Inc. February 4 2009 Phase 2
NCT00398567 Completed Advanced Breast Cancer Puma Biotechnology Inc. April 4 2007 Phase 1|Phase 2
NCT00300781 Completed Breast Neoplasms|Neoplasms Puma Biotechnology Inc. August 4 2006 Phase 2

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操作手册

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID