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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客户使用Selleck该产品发表文献15篇:

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 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXTRWWR{UUN3MEywMlAxPSEQvF2= M37vfVI1ODB7ME[0
EFM-192A NFLhOm9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVTJR|UxRDBwMEC1JO69VQ>? NYOzPXBxOjRyMEmwOlQ>
HCC1569 Mmm5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4P3XGlEPTB:MD6wNFUh|ryP M1fBU|I1ODB7ME[0
HCC1954 M4LGdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPyTWM2ODxyLkCwOUDPxE1? NFr6U3ozPDByOUC2OC=>
MDA-MB-175 M2nBeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGm4ZZdKSzVyPECuNFA2KM7:TR?= MnzYNlQxODlyNkS=
MDA-MB-361 Ml7FS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn22TWM2ODxyLkCwOUDPxE1? NUX3S3ZHOjRyMEmwOlQ>
SK-BR-3 MljQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NILaTGNKSzVyPECuNFA2KM7:TR?= M1HDW|I1ODB7ME[0
UACC-812 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXTJR|UxRDBwMEC1JO69VQ>? NF7wSpgzPDByOUC2OC=>
UACC-893 NIfzUWFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4\2d2lEPTB:MD6wNFUh|ryP Moi2NlQxODlyNkS=
SUM-225 M4\4bGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkDWTWM2OD1yLkCxJO69VQ>? M2HRVFI1ODB7ME[0
SUM-190 NUjCdZpwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml\jTWM2OD1yLkCxJO69VQ>? M3jZRlI1ODB7ME[0
ZR-75-1 Mo\TS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXfJR|UxRTBwMEOg{txO NEK3PW8zPDByOUC2OC=>
HCC70 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MorOTWM2OD1yLkCzJO69VQ>? Mlj3NlQxODlyNkS=
BT-20 M4DROWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHiwfHpKSzVyPUCuNFch|ryP NY\mboxNOjRyMEmwOlQ>
MDA-MB-453 NFjYSG9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFnQOGRKSzVyPUCuNFkh|ryP M1TI[lI1ODB7ME[0
HCC1187 MlfMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zVRWlEPTB;MD6xNEDPxE1? NUn1NFA3OjRyMEmwOlQ>
EFM-19 MmXjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUTkZpB[UUN3ME2wMlEyKM7:TR?= NU\kTVBoOjRyMEmwOlQ>
T-47D NIPxenBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXXJR|UxRTBwMU[g{txO MnH0NlQxODlyNkS=
MDA-MB-134 NHfFUWxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYHJR|UxRTBwMUeg{txO MXmyOFAxQTB4NB?=
HCC38 M2DiXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MknWTWM2OD1yLkK1JO69VQ>? M3u5eVI1ODB7ME[0
MDA-MB-435 MoXPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEi0RZVKSzVyPUCuN|Mh|ryP MlHjNlQxODlyNkS=
MDA-MB-468 NVK2NmJXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGLRbnFKSzVyPUCuN|Mh|ryP NIXifVEzPDByOUC2OC=>
CAMA-1 M4X1Umdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUKxcHhjUUN3ME2wMlM4KM7:TR?= NX23cWo{OjRyMEmwOlQ>
MDA-MB-436 M1Lp[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlfFTWM2OD1yLkSxJO69VQ>? MUOyOFAxQTB4NB?=
MCF-7 M4HJV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MojVTWM2OD1yLkSxJO69VQ>? M132blI1ODB7ME[0
MDA-MB-415 MoT1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVvJR|UxRTBwNEKg{txO NEPUZXAzPDByOUC2OC=>
HCC1806 NX;Td2dPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYLJR|UxRTBwNESg{txO M{WzdlI1ODB7ME[0
HCC1395 M1TmVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUHXfVlPUUN3ME2wMlQ6KM7:TR?= NF7HOJczPDByOUC2OC=>
HCC1937 NV71[mtIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVLJR|UxRTBwNUCg{txO MoHuNlQxODlyNkS=
HCC1143 M3TxZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn:yTWM2OD1yLkW0JO69VQ>? M{W3bVI1ODB7ME[0
UACC-732 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NY\lR2lHUUN3ME2wMlY2KM7:TR?= M4XnUFI1ODB7ME[0
MDA-MB-231 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1exbmlEPTB;MT6wNEDPxE1? NYPqbotUOjRyMEmwOlQ>
MDA-MB-157 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFfaZVNKSzVyPUGuNVIh|ryP MUCyOFAxQTB4NB?=
BT-549 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkWyTWM2OD1zLkG0JO69VQ>? NYCxW|l6OjRyMEmwOlQ>
KPL-1 MnLRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHPUZmlKSzVyPUGuPFkh|ryP NGr3d3gzPDByOUC2OC=>
CAL-51 M3;Fe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVfJR|UxRTFwOEmg{txO NUXEUWxKOjRyMEmwOlQ>
BT474 NGDTcVZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUDJR|UxRTBwMECzNlMhyrFiMD6wNFA4PSEQvF2= MoKxNlM5OTZ{NUS=
SKBR3 Mn\NS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4fTeGlEPTB;MD6wNFc2KMLzIECuNFA2KM7:TR?= MYWyN|gyPjJ3NB?=
MDAMB453 NGPwTHBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHrOb4RKSzVyPUGuOVkhyrFiMD6xO|kh|ryP NUDPbGlnOjN6MU[yOVQ>
KB M1zuWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnXQTWM2OD12LkGzJOKyKDBwNEeg{txO MUeyNlQ6OTl|NR?=
KBv200 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn3ITWM2OD14LkCzJOKyKDBwNkSg{txO MWeyNlQ6OTl|NR?=
MCF-7 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NInZVWtKSzVyPUOuN|AhyrFiMD60NUDPxE1? M2WwT|IzPDlzOUO1
MCF-7/Adr MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4e3NWlEPTB;IEKuPFghyrFiMD6zNEDPxE1? NIfE[ZAzOjR7MUmzOS=>
MCF-7 MoTxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF:1SVJKSzVyPUOuNFIhyrFiMD6zOEDPxE1? NEXuOYQzOjR7MUmzOS=>
MCF-7/FLV1000 M164c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFq1c|BKSzVyPUeuNFkhyrFiMD63NUDPxE1? NHXsZmkzOjR7MUmzOS=>
HL60 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlrTTWM2OD1{LkK2JOKyKDBwMkOg{txO NGOxRoszOjR7MUmzOS=>
HL60/Adr M1\lbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWfJR|UxRTFwNEKgxtEhOC5zNTFOwG0> NGjTUZIzOjR7MUmzOS=>
HEK293/pcDNA3.1 NHXkVGZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGm2doFKSzVyPUWuNlkhyrFiMD61N{DPxE1? Mn71NlI1QTF7M{W=
HEK293/ABCB1 NWDSU29sT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYLuPJk{UUN3ME22MlkyKMLzIECuO|AhKM7:TR?= NF:wSVYzOjR7MUmzOS=>
SKBR MnfBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4DLW|AvODFvMUCwJI5O M3PGZVMuPyCm MoHFbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MVWyNVQ5PzZyNR?=
L858R(EGFR) NX;BW2Q2S2WubDDWbYFjcWyrdImgRZN{[Xl? NYHJc2lv\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MWKxO|MyOTByMh?=
L858R/T790M(EGFR) MXfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NGLYdG9l\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MmLzNVc{OTFyMEK=
G776insV_G/C NVjJPVFES2WubDDWbYFjcWyrdImgRZN{[Xl? NYTCdVJv\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MUCxO|MyOTByMh?=
wild-type MUDD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MWTk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz M2nkOFE4OzFzMECy
A775insYVMA Mmr0R4VtdCCYaXHibYxqfHliQYPzZZk> NYnWT3Q2\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NXPDUGFWOTd|MUGwNFI>
G776insV_G/L MkHvR4VtdCCYaXHibYxqfHliQYPzZZk> NHn4TFBl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MV6xO|MyOTByMh?=
P780insGSP NWnrW4RjS2WubDDWbYFjcWyrdImgRZN{[Xl? M1u2eoRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MlXFNVc{OTFyMEK=
NCI-H1781 MkHXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGD1N|lqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NXjzS25JOTZ6MUi2NVg>
HCC827 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH64UIRqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MkLBNVY5OTh4MUi=
H3255 MoTRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVi0eIhUcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NVz4[pZ5OTZ6MUi2NVg>
NCI-H1975 M2\aW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVW1ZWZbcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NFHmWXMyPjhzOE[xPC=>
A549 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmK2bY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NYPLcmFpOTZ6MUi2NVg>
3T3 NVe4ZW1xT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYnJR|UxRTdyMDFCtUA4QCCwTR?= NXvHW3VGOTVzN{OwNFg>
3T3/neu NUnzSmJLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXjRSFQxUUN3ME2zJOKyKDBwMUSgcm0> NHrOWmgyPTF5M{CwPC=>
SK-Br-3 NYPw[XB[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXHJR|UxRTJiwsGgNE4yQCCwTR?= Mli4NVUyPzNyMEi=
BT 474 M2\tR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmTwTWM2OD1{INMxJFAvODZibl2= MUexOVE4OzByOB?=
A431 MkfYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXHIOFd6UUN3ME24NUDDuSB7IH7N NF\YVIkyPTF5M{CwPC=>
MDA-MB-435 M124U2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUX0SYdXUUN3ME25OlAhyrFiMU[1JI5O NYDEfVBlOTVzN{OwNFg>
SW620 NVKwZnNHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIDPeG5KSzVyPU[5NEDDuSB6NDDuUS=> NEnYPZIyPTF5M{CwPC=>

... 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
NCT03812393 Not yet recruiting Triple Negative Breast Cancer|Early-stage Breast Cancer|HER2-positive Breast Cancer West Cancer Center|Celcuity|Puma Biotechnology Inc. January 28 2019 Phase 2
NCT03812393 Not yet recruiting Triple Negative Breast Cancer|Early-stage Breast Cancer|HER2-positive Breast Cancer West Cancer Center|Celcuity|Puma Biotechnology Inc. January 28 2019 Phase 2
NCT03457896 Recruiting Metastatic Colorectal Cancer NSABP Foundation Inc|Puma Biotechnology Inc. May 18 2018 Phase 2
NCT03457896 Recruiting Metastatic Colorectal Cancer NSABP Foundation Inc|Puma Biotechnology Inc. May 18 2018 Phase 2
NCT03101748 Recruiting Malignant Neoplasm of Breast M.D. Anderson Cancer Center|Puma Biotechnology Inc. January 29 2018 Phase 1|Phase 2
NCT03101748 Recruiting Malignant Neoplasm of Breast M.D. Anderson Cancer Center|Puma Biotechnology Inc. January 29 2018 Phase 1|Phase 2

技术支持

在订购、运输、储存和使用我们的产品的任何阶段,您遇到的任何问题,均可以通过拨打我们的热线电话400-668-6834,或者技术支持邮箱tech@selleck.cn,直接联系到我们。我们会在24小时内尽快联系您。

操作手册

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID