Neratinib (HKI-272)

Catalog No.S2150

Neratinib (HKI-272) Chemical Structure

Molecular Weight(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.

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  • 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.

     

    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.

    (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.

Purity & Quality Control

Choose Selective HER2 Inhibitors

Biological Activity

Description 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.
Targets
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
In vitro

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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 M3jRTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEe2UFBKSzVyPECuNFA2KM7:TR?= MVOyOFAxQTB4NB?=
EFM-192A MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2DzbGlEPTB:MD6wNFUh|ryP MnTPNlQxODlyNkS=
HCC1569 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnGwTWM2ODxyLkCwOUDPxE1? NYXDb5VoOjRyMEmwOlQ>
HCC1954 Mm\QS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGHGXY9KSzVyPECuNFA2KM7:TR?= NYLXbVhoOjRyMEmwOlQ>
MDA-MB-175 MmHHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXvRR2pvUUN3MEywMlAxPSEQvF2= Mnv1NlQxODlyNkS=
MDA-MB-361 NIf4c4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXPJR|UxRDBwMEC1JO69VQ>? NGXnR4wzPDByOUC2OC=>
SK-BR-3 M1T1eWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2TheGlEPTB:MD6wNFUh|ryP MkK2NlQxODlyNkS=
UACC-812 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnX5TWM2ODxyLkCwOUDPxE1? M1TpTFI1ODB7ME[0
UACC-893 NWexd3F1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYnJR|UxRDBwMEC1JO69VQ>? MnnUNlQxODlyNkS=
SUM-225 NHHqSJNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3HsOWlEPTB;MD6wNUDPxE1? NVXn[nlyOjRyMEmwOlQ>
SUM-190 NYXxUFMzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV:0WWhmUUN3ME2wMlAyKM7:TR?= NHnsTFMzPDByOUC2OC=>
ZR-75-1 Mm[wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHPxco1KSzVyPUCuNFMh|ryP NIDUOHQzPDByOUC2OC=>
HCC70 M4HlUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWXLSXBlUUN3ME2wMlA{KM7:TR?= NWHNe5k1OjRyMEmwOlQ>
BT-20 Mkm4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUnJR|UxRTBwMEeg{txO Mn31NlQxODlyNkS=
MDA-MB-453 NXvvO4p[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIL1[o5KSzVyPUCuNFkh|ryP NXXiUVBkOjRyMEmwOlQ>
HCC1187 M1;Zdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGSwb5pKSzVyPUCuNVAh|ryP M3[3UVI1ODB7ME[0
EFM-19 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYHZXW1RUUN3ME2wMlEyKM7:TR?= NVXiXmd6OjRyMEmwOlQ>
T-47D MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4O2V2lEPTB;MD6xOkDPxE1? MnS2NlQxODlyNkS=
MDA-MB-134 NVezbYZoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVzRfFhDUUN3ME2wMlE4KM7:TR?= MUCyOFAxQTB4NB?=
HCC38 M3v2NGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWfJR|UxRTBwMkWg{txO MnnNNlQxODlyNkS=
MDA-MB-435 MmTnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1iwXmlEPTB;MD6zN{DPxE1? NXLHOpB2OjRyMEmwOlQ>
MDA-MB-468 M2nRVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoDRTWM2OD1yLkOzJO69VQ>? NGG2b4UzPDByOUC2OC=>
CAMA-1 NXzlUFExT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoOzTWM2OD1yLkO3JO69VQ>? MW[yOFAxQTB4NB?=
MDA-MB-436 Mkj5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2HPbGlEPTB;MD60NUDPxE1? NWfqZphkOjRyMEmwOlQ>
MCF-7 M2rNR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWKydIxuUUN3ME2wMlQyKM7:TR?= NIWwN44zPDByOUC2OC=>
MDA-MB-415 MmK3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mk\MTWM2OD1yLkSyJO69VQ>? MUeyOFAxQTB4NB?=
HCC1806 NG\ITFNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV;QRnFTUUN3ME2wMlQ1KM7:TR?= NIPuN5gzPDByOUC2OC=>
HCC1395 NIrEXoNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHLVZWtKSzVyPUCuOFkh|ryP NWTyblg2OjRyMEmwOlQ>
HCC1937 NHvTSFhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEHLdWZKSzVyPUCuOVAh|ryP Mn2xNlQxODlyNkS=
HCC1143 NYjEWGZvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NITEWpVKSzVyPUCuOVQh|ryP MUKyOFAxQTB4NB?=
UACC-732 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHTRR|hKSzVyPUCuOlUh|ryP MX6yOFAxQTB4NB?=
MDA-MB-231 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVjFZ3czUUN3ME2xMlAxKM7:TR?= MVSyOFAxQTB4NB?=
MDA-MB-157 MlPjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFPEVVRKSzVyPUGuNVIh|ryP NXvtVnB2OjRyMEmwOlQ>
BT-549 NUe0UnJ6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHnD[29KSzVyPUGuNVQh|ryP NEOwO4gzPDByOUC2OC=>
KPL-1 NHvJZXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVjJR|UxRTFwOEmg{txO M3rtW|I1ODB7ME[0
CAL-51 NFnHelJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX;oXI1yUUN3ME2xMlg6KM7:TR?= Mn7KNlQxODlyNkS=
BT474 Mm\lS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEm4cHZKSzVyPUCuNFA{OjNiwsGgNE4xODB5NTFOwG0> NYfufmtDOjN6MU[yOVQ>
SKBR3 NXK3RoRpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn\OTWM2OD1yLkCwO|UhyrFiMD6wNFUh|ryP MWmyN|gyPjJ3NB?=
MDAMB453 NFG3b41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHHNfWZKSzVyPUGuOVkhyrFiMD6xO|kh|ryP M3\5XFI{QDF4MkW0
KB Mn;3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mln3TWM2OD12LkGzJOKyKDBwNEeg{txO NFHC[IUzOjR7MUmzOS=>
KBv200 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF7TNoxKSzVyPU[uNFMhyrFiMD62OEDPxE1? NFm5bVUzOjR7MUmzOS=>
MCF-7 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYHCSFZ{UUN3ME2zMlMxKMLzIECuOFEh|ryP NVvIOXdsOjJ2OUG5N|U>
MCF-7/Adr M4jOdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NITa[4ZKSzVyPTCyMlg5KMLzIECuN|Ah|ryP NYXjO4hyOjJ2OUG5N|U>
MCF-7 MoS0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3L4ZWlEPTB;Mz6wNkDDuSByLkO0JO69VQ>? MXKyNlQ6OTl|NR?=
MCF-7/FLV1000 NIC3N3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1vNSGlEPTB;Nz6wPUDDuSByLkexJO69VQ>? NHn5W2IzOjR7MUmzOS=>
HL60 NUTrNHlGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYfJR|UxRTJwMk[gxtEhOC5{MzFOwG0> MkO0NlI1QTF7M{W=
HL60/Adr NITjeYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYHtOoZbUUN3ME2xMlQzKMLzIECuNVUh|ryP NXW1d5cxOjJ2OUG5N|U>
HEK293/pcDNA3.1 NUjJXYhFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkTSTWM2OD13LkK5JOKyKDBwNUOg{txO M{ToOlIzPDlzOUO1
HEK293/ABCB1 MofGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlGyTWM2OD14LkmxJOKyKDBwN{CgJO69VQ>? M4rQXVIzPDlzOUO1
SKBR M4rZXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX\HZ5lnOC5yMT2xNFAhdk1? NUW2SGl4Oy15IHS= Mn[0bY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MW[yNVQ5PzZyNR?=
L858R(EGFR) M{KzVmNmdGxiVnnhZoltcXS7IFHzd4F6 MYfk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz MnLXNVc{OTFyMEK=
L858R/T790M(EGFR) MU\D[YxtKF[rYXLpcIl1gSCDc4PhfS=> M4XKUIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NUT5XGNIOTd|MUGwNFI>
G776insV_G/C NYLhZpV6S2WubDDWbYFjcWyrdImgRZN{[Xl? M32xVoRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? Ml3vNVc{OTFyMEK=
wild-type NHnXU2hE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NYjUNYQ2\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MnewNVc{OTFyMEK=
A775insYVMA NXvnN5NIS2WubDDWbYFjcWyrdImgRZN{[Xl? NEHFW|dl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MoPENVc{OTFyMEK=
G776insV_G/L NH;GdXZE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NFTFcGZl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NYPnWYVPOTd|MUGwNFI>
P780insGSP MX\D[YxtKF[rYXLpcIl1gSCDc4PhfS=> NXi5OWdz\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MnnLNVc{OTFyMEK=
NCI-H1781 M4C3dmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUTpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MV2xOlgyQDZzOB?=
HCC827 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlfrbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy Ml;ZNVY5OTh4MUi=
H3255 M1Ht[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3Lod4lvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MVWxOlgyQDZzOB?=
NCI-H1975 M4HPW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUDBRXl7cW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz M3[3XlE3QDF6NkG4
A549 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGLIRmFqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NXLGTppyOTZ6MUi2NVg>
3T3 NFrvcWNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYD4O|hwUUN3ME23NFAhyrFiN{igcm0> MmL3NVUyPzNyMEi=
3T3/neu M17HXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoqyTWM2OD1|INMxJFAvOTRibl2= NGSwNJoyPTF5M{CwPC=>
SK-Br-3 M1njUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVTJR|UxRTJiwsGgNE4yQCCwTR?= NHHLS|gyPTF5M{CwPC=>
BT 474 NW[wVVJ7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWLLbZhiUUN3ME2yJOKyKDBwME[gcm0> MYmxOVE4OzByOB?=
A431 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlnoTWM2OD16MTFCtUA6KG6P NF3KNFYyPTF5M{CwPC=>
MDA-MB-435 NYXiUFZ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{iwNWlEPTB;OU[wJOKyKDF4NTDuUS=> MXKxOVE4OzByOB?=
SW620 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVrJR|UxRTZ7MDFCtUA5PCCwTR?= MVuxOVE4OzByOB?=

... Click to View More Cell Line Experimental Data

In vivo 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]

Protocol

Kinase Assay:[1]
+ Expand

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.
Cell Research:[1]
+ Expand
  • Cell lines: 3T3, 3T3/neu, A431, BT474, SK-Br-3, MDA-MB-435, and SW480
  • Concentrations: Dissolved in DMSO, final concentrations 0.5 ng/mL-5 μg/mL
  • Incubation Time: 2 or 6 days
  • Method: 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.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Female athymic (nude) mice implanted s.c. with 3T3/neu, BT474, MCF-7, or SK-OV-3 cells
  • Formulation: Formulated in 0.5% methocellulose-0.4% polysorbate-80 (Tween 80)
  • Dosages: ~80 mg/kg/day
  • Administration: Gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 5 mg/mL warmed (8.97 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
5 mg/mL

* 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 557.04
Formula

C30H29ClN6O3

CAS No. 698387-09-6
Storage powder
in solvent
Synonyms N/A

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  • C1
    V1
    C2
    V2

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • 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):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

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

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

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

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HER2 Signaling Pathway Map

HER2 Inhibitors with Unique Features

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID