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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Cited by 15 Publications

6 Customer Reviews

  • 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 M1Tac2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml72TWM2ODxyLkCwOUDPxE1? MUCyOFAxQTB4NB?=
EFM-192A NHmxe5RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{DSS2lEPTB:MD6wNFUh|ryP M3jH[|I1ODB7ME[0
HCC1569 NV[wW3RKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NILCNWNKSzVyPECuNFA2KM7:TR?= NETTXIMzPDByOUC2OC=>
HCC1954 NEjjZYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHvPU4tKSzVyPECuNFA2KM7:TR?= M1rtVlI1ODB7ME[0
MDA-MB-175 NVvwPHIzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NELWXWVKSzVyPECuNFA2KM7:TR?= M1LUSFI1ODB7ME[0
MDA-MB-361 M2HlfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV:2V2dtUUN3MEywMlAxPSEQvF2= MXqyOFAxQTB4NB?=
SK-BR-3 NHLIfYRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1LGO2lEPTB:MD6wNFUh|ryP MUOyOFAxQTB4NB?=
UACC-812 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV:2XGplUUN3MEywMlAxPSEQvF2= M3XaXVI1ODB7ME[0
UACC-893 NGfa[4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVXJR|UxRDBwMEC1JO69VQ>? MUSyOFAxQTB4NB?=
SUM-225 NY\oc4RLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2f0fWlEPTB;MD6wNUDPxE1? MkjoNlQxODlyNkS=
SUM-190 NXiyV5M5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3;a[GlEPTB;MD6wNUDPxE1? NXrrRY94OjRyMEmwOlQ>
ZR-75-1 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFHVZXJKSzVyPUCuNFMh|ryP NXi5W4o3OjRyMEmwOlQ>
HCC70 MmTGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXxVGxEUUN3ME2wMlA{KM7:TR?= NF7nWpUzPDByOUC2OC=>
BT-20 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2HjS2lEPTB;MD6wO{DPxE1? NG[xXZczPDByOUC2OC=>
MDA-MB-453 MmHNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTBwMEmg{txO MmXNNlQxODlyNkS=
HCC1187 NXTTRWpbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGWwTlJKSzVyPUCuNVAh|ryP MXOyOFAxQTB4NB?=
EFM-19 M3TiSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYPJR|UxRTBwMUGg{txO MX[yOFAxQTB4NB?=
T-47D NXLsfXlvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEXnW|NKSzVyPUCuNVYh|ryP MUSyOFAxQTB4NB?=
MDA-MB-134 MoPxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVL6dFRoUUN3ME2wMlE4KM7:TR?= M1XJZVI1ODB7ME[0
HCC38 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFfjbo5KSzVyPUCuNlUh|ryP NE\GTFMzPDByOUC2OC=>
MDA-MB-435 NV7MNlVzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVnlUYFSUUN3ME2wMlM{KM7:TR?= M2SyelI1ODB7ME[0
MDA-MB-468 M2\lVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3LkVmlEPTB;MD6zN{DPxE1? NGTuRoszPDByOUC2OC=>
CAMA-1 NWfLOI94T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUHR[GRnUUN3ME2wMlM4KM7:TR?= MVeyOFAxQTB4NB?=
MDA-MB-436 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGjPZ21KSzVyPUCuOFEh|ryP M4HUcFI1ODB7ME[0
MCF-7 M1Gybmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rpdmlEPTB;MD60NUDPxE1? NFvJdHQzPDByOUC2OC=>
MDA-MB-415 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MU\JR|UxRTBwNEKg{txO NX30No9TOjRyMEmwOlQ>
HCC1806 NUjvV|luT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mnz1TWM2OD1yLkS0JO69VQ>? NVK5VopzOjRyMEmwOlQ>
HCC1395 M4W4Wmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFK4cZZKSzVyPUCuOFkh|ryP NWjNWXRZOjRyMEmwOlQ>
HCC1937 NFHacnlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3zqSGlEPTB;MD61NEDPxE1? NYXvb5p5OjRyMEmwOlQ>
HCC1143 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUTSVlFpUUN3ME2wMlU1KM7:TR?= MUmyOFAxQTB4NB?=
UACC-732 NETUUHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnjuTWM2OD1yLk[1JO69VQ>? NX7GdGNXOjRyMEmwOlQ>
MDA-MB-231 M3rLWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVPJR|UxRTFwMECg{txO Mn:zNlQxODlyNkS=
MDA-MB-157 MlfVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRTFwMUKg{txO MWCyOFAxQTB4NB?=
BT-549 MkO0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3;sXmlEPTB;MT6xOEDPxE1? MVOyOFAxQTB4NB?=
KPL-1 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn7HTWM2OD1zLki5JO69VQ>? NYnrZWtIOjRyMEmwOlQ>
CAL-51 NV3KbWhIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mne0TWM2OD1zLki5JO69VQ>? M4DQfFI1ODB7ME[0
BT474 M1q5cGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3ewW2lEPTB;MD6wNFMzOyEEsTCwMlAxODd3IN88US=> MoHiNlM5OTZ{NUS=
SKBR3 NVL4Vpp[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NI\rco5KSzVyPUCuNFA4PSEEsTCwMlAxPSEQvF2= NHOwOWkzOzhzNkK1OC=>
MDAMB453 MmHNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkTSTWM2OD1zLkW5JOKyKDBwMUe5JO69VQ>? M1jEWlI{QDF4MkW0
KB MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{W0ZmlEPTB;ND6xN{DDuSByLkS3JO69VQ>? MorQNlI1QTF7M{W=
KBv200 Mn3US5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFnrUnJKSzVyPU[uNFMhyrFiMD62OEDPxE1? M37ZTFIzPDlzOUO1
MCF-7 M3LJPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYjqcoI6UUN3ME2zMlMxKMLzIECuOFEh|ryP MWOyNlQ6OTl|NR?=
MCF-7/Adr M132N2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmD5TWM2OD1iMj64PEDDuSByLkOwJO69VQ>? MWGyNlQ6OTl|NR?=
MCF-7 NIDFdXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHrPfnVKSzVyPUOuNFIhyrFiMD6zOEDPxE1? Ml7LNlI1QTF7M{W=
MCF-7/FLV1000 M4D4dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWHJR|UxRTdwMEmgxtEhOC55MTFOwG0> M{HP[lIzPDlzOUO1
HL60 MlnaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIjofoZKSzVyPUKuNlYhyrFiMD6yN{DPxE1? MWSyNlQ6OTl|NR?=
HL60/Adr MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWr0b2FGUUN3ME2xMlQzKMLzIECuNVUh|ryP NYfGNXlrOjJ2OUG5N|U>
HEK293/pcDNA3.1 NULFXXVuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYnJR|UxRTVwMkmgxtEhOC53MzFOwG0> NGjBfo4zOjR7MUmzOS=>
HEK293/ABCB1 NFzpbnJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYnw[XM1UUN3ME22MlkyKMLzIECuO|AhKM7:TR?= MnuzNlI1QTF7M{W=
SKBR NEWwTVdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlLkNE4xOS1zMECgcm0> MXWzMVch\A>? MoHRbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NI\wR3AzOTR6N{[wOS=>
L858R(EGFR) NIr4OGdE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MorJ[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NV23UY52OTd|MUGwNFI>
L858R/T790M(EGFR) MXfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MnzM[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? M3i0UlE4OzFzMECy
G776insV_G/C NIXYN5NE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NI[0bVll\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NWX0VXQyOTd|MUGwNFI>
wild-type MlXBR4VtdCCYaXHibYxqfHliQYPzZZk> NUPxcphE\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NILwfoEyPzNzMUCwNi=>
A775insYVMA M{\6WGNmdGxiVnnhZoltcXS7IFHzd4F6 NXW1WVZO\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MmDtNVc{OTFyMEK=
G776insV_G/L NEH4PZNE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MVvk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz Mo[wNVc{OTFyMEK=
P780insGSP Mmf6R4VtdCCYaXHibYxqfHliQYPzZZk> MX3k[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NWXwdYFrOTd|MUGwNFI>
NCI-H1781 NHrYbYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEHESFZqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M13qWFE3QDF6NkG4
HCC827 NXzYflBnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFOxT|BqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M4HOVFE3QDF6NkG4
H3255 NEHjbWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7oU2pNcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NWjrNFBNOTZ6MUi2NVg>
NCI-H1975 M2PO[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoPobY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MkfUNVY5OTh4MUi=
A549 M2PYemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1\PfYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> Mk[5NVY5OTh4MUi=
3T3 NIPDXI5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1zMUGlEPTB;N{CwJOKyKDd6IH7N MYexOVE4OzByOB?=
3T3/neu M1;WW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWDJR|UxRTNiwsGgNE4yPCCwTR?= NHXhRWQyPTF5M{CwPC=>
SK-Br-3 M3jEfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEDBZYhKSzVyPUKgxtEhOC5zODDuUS=> NIXGeIsyPTF5M{CwPC=>
BT 474 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX36dZo1UUN3ME2yJOKyKDBwME[gcm0> M{DhV|E2OTd|MEC4
A431 NH;HNI1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVi4OHdCUUN3ME24NUDDuSB7IH7N M2e3U|E2OTd|MEC4
MDA-MB-435 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFXTd21KSzVyPUm2NEDDuSBzNkWgcm0> NVnzPVZuOTVzN{OwNFg>
SW620 NVywZZJ6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHLVS|NKSzVyPU[5NEDDuSB6NDDuUS=> NXvMV292OTVzN{OwNFg>

... 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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    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
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

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