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.

Size Price Stock Quantity  
USD 150 In stock
USD 470 In stock
USD 970 In stock

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

3 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.

Purity & Quality Control

Choose Selective HER2 Inhibitors

Click to view more

Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

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)
PDK-1 [1]
(Cell-free assay)
59 nM 92 nM 800 nM 1.4 μM >5 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 NHnL[GRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHfkS|VKSzVyPECuNFA2KM7:TR?= NGT1b4czPDByOUC2OC=>
EFM-192A M3XoVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoPFTWM2ODxyLkCwOUDPxE1? M3LMe|I1ODB7ME[0
HCC1569 M1;yRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnjpTWM2ODxyLkCwOUDPxE1? NFfENXYzPDByOUC2OC=>
HCC1954 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M13kO2lEPTB:MD6wNFUh|ryP M1TkVVI1ODB7ME[0
MDA-MB-175 Mmn1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGjFSopKSzVyPECuNFA2KM7:TR?= MWmyOFAxQTB4NB?=
MDA-MB-361 MmXwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYLJR|UxRDBwMEC1JO69VQ>? MYSyOFAxQTB4NB?=
SK-BR-3 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnX4TWM2ODxyLkCwOUDPxE1? NWfpVVBoOjRyMEmwOlQ>
UACC-812 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGfRdmlKSzVyPECuNFA2KM7:TR?= MnfpNlQxODlyNkS=
UACC-893 M4LlTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mli1TWM2ODxyLkCwOUDPxE1? MUGyOFAxQTB4NB?=
SUM-225 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVPJR|UxRTBwMEGg{txO NIjY[2czPDByOUC2OC=>
SUM-190 M4HMN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mk\MTWM2OD1yLkCxJO69VQ>? NXqxRYR7OjRyMEmwOlQ>
ZR-75-1 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYfJR|UxRTBwMEOg{txO MkGxNlQxODlyNkS=
HCC70 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoHlTWM2OD1yLkCzJO69VQ>? NFjiZYYzPDByOUC2OC=>
BT-20 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4nwfGlEPTB;MD6wO{DPxE1? MlTLNlQxODlyNkS=
MDA-MB-453 NY\WWHNoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M123eGlEPTB;MD6wPUDPxE1? NUHKS3ZbOjRyMEmwOlQ>
HCC1187 MmTiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXnJR|UxRTBwMUCg{txO NFn5XFkzPDByOUC2OC=>
EFM-19 NUTHUmFLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn3aTWM2OD1yLkGxJO69VQ>? M4HRZlI1ODB7ME[0
T-47D NUT3R5ZzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFuwWIVKSzVyPUCuNVYh|ryP M1i5[FI1ODB7ME[0
MDA-MB-134 M2HZdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoXWTWM2OD1yLkG3JO69VQ>? MYqyOFAxQTB4NB?=
HCC38 Mm\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF7QOnVKSzVyPUCuNlUh|ryP MnXtNlQxODlyNkS=
MDA-MB-435 MkD0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2HFcGlEPTB;MD6zN{DPxE1? MlrENlQxODlyNkS=
MDA-MB-468 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml7VTWM2OD1yLkOzJO69VQ>? NXvN[JVWOjRyMEmwOlQ>
CAMA-1 Mm\uS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEX3PZlKSzVyPUCuN|ch|ryP NH7mb3QzPDByOUC2OC=>
MDA-MB-436 M3fRfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4jONmlEPTB;MD60NUDPxE1? M2XGPFI1ODB7ME[0
MCF-7 M2Py[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFrhWYFKSzVyPUCuOFEh|ryP M2jZbFI1ODB7ME[0
MDA-MB-415 NFrRWJRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGi3SVNKSzVyPUCuOFIh|ryP MWWyOFAxQTB4NB?=
HCC1806 NVXaZ4VDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MW\JR|UxRTBwNESg{txO M36zblI1ODB7ME[0
HCC1395 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4exZWlEPTB;MD60PUDPxE1? M{\0TlI1ODB7ME[0
HCC1937 M4PnV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEXFZnhKSzVyPUCuOVAh|ryP M4jrS|I1ODB7ME[0
HCC1143 NX\0bItRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml[5TWM2OD1yLkW0JO69VQ>? NFznR4szPDByOUC2OC=>
UACC-732 NFG0dYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGn1V3dKSzVyPUCuOlUh|ryP M4r4eVI1ODB7ME[0
MDA-MB-231 NWfY[XFXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkG3TWM2OD1zLkCwJO69VQ>? NUfGclZCOjRyMEmwOlQ>
MDA-MB-157 M4Oy[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV3iRpF6UUN3ME2xMlEzKM7:TR?= NEjD[WozPDByOUC2OC=>
BT-549 NFjZclBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFrXeodKSzVyPUGuNVQh|ryP MlvuNlQxODlyNkS=
KPL-1 Mm\RS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{ThXmlEPTB;MT64PUDPxE1? NEDLeo4zPDByOUC2OC=>
CAL-51 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4CwT2lEPTB;MT64PUDPxE1? MlP5NlQxODlyNkS=
BT474 NV3ZOYdHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV\JR|UxRTBwMECzNlMhyrFiMD6wNFA4PSEQvF2= MVOyN|gyPjJ3NB?=
SKBR3 Mn7NS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWnJR|UxRTBwMEC3OUDDuSByLkCwOUDPxE1? M3roblI{QDF4MkW0
MDAMB453 M2n5OWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml:3TWM2OD1zLkW5JOKyKDBwMUe5JO69VQ>? NEXteGgzOzhzNkK1OC=>
KB Mo\KS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEL2eHhKSzVyPUSuNVMhyrFiMD60O{DPxE1? M2m4dVIzPDlzOUO1
KBv200 MmfrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnTxTWM2OD14LkCzJOKyKDBwNkSg{txO NFrHbpIzOjR7MUmzOS=>
MCF-7 M13aTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjITWM2OD1|LkOwJOKyKDBwNEGg{txO M2\pTVIzPDlzOUO1
MCF-7/Adr M{f2OWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVfHOm41UUN3ME2gNk45QCEEsTCwMlMxKM7:TR?= NWX5Zo04OjJ2OUG5N|U>
MCF-7 NGnle2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoDkTWM2OD1|LkCyJOKyKDBwM{Sg{txO NWjXd5BbOjJ2OUG5N|U>
MCF-7/FLV1000 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXLoTplMUUN3ME23MlA6KMLzIECuO|Eh|ryP M4TCNlIzPDlzOUO1
HL60 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3K0SmlEPTB;Mj6yOkDDuSByLkKzJO69VQ>? MYOyNlQ6OTl|NR?=
HL60/Adr Mm[zS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXXJR|UxRTFwNEKgxtEhOC5zNTFOwG0> NVrpTW1TOjJ2OUG5N|U>
HEK293/pcDNA3.1 M{G4Zmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH7ZbWRKSzVyPUWuNlkhyrFiMD61N{DPxE1? NU\RclVNOjJ2OUG5N|U>
HEK293/ABCB1 M1K1UGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1j0dWlEPTB;Nj65NUDDuSByLkewJEDPxE1? MVyyNlQ6OTl|NR?=
SKBR Ml\oS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVy3Z4VSOC5yMT2xNFAhdk1? NY[2SmtWOy15IHS= MkTrbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NEPLNVUzOTR6N{[wOS=>
L858R(EGFR) NWDTTXQ3S2WubDDWbYFjcWyrdImgRZN{[Xl? M4rOR4Rm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MUSxO|MyOTByMh?=
L858R/T790M(EGFR) M1zRc2NmdGxiVnnhZoltcXS7IFHzd4F6 MYfk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz MorqNVc{OTFyMEK=
G776insV_G/C Ml3OR4VtdCCYaXHibYxqfHliQYPzZZk> NVPLS5Ix\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MXyxO|MyOTByMh?=
wild-type M3zi[GNmdGxiVnnhZoltcXS7IFHzd4F6 M3zRSIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NGWxOW4yPzNzMUCwNi=>
A775insYVMA M1zv[mNmdGxiVnnhZoltcXS7IFHzd4F6 M3S3RYRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MmrTNVc{OTFyMEK=
G776insV_G/L NVSwVJllS2WubDDWbYFjcWyrdImgRZN{[Xl? Mofh[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NGTiTlkyPzNzMUCwNi=>
P780insGSP NGnzWZRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? Mki4[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NW\vOoc2OTd|MUGwNFI>
NCI-H1781 NIXpdGRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{O2[YlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NWTlcI9QOTZ6MUi2NVg>
HCC827 NYDGNnhUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWrvZXBQcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NEHS[5UyPjhzOE[xPC=>
H3255 NV\Rco1TT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3ERXZwcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz M1PqTVE3QDF6NkG4
NCI-H1975 NEDLV3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7xdplTcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NWjocplxOTZ6MUi2NVg>
A549 Mn75S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2LUcolvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> M{HB[lE3QDF6NkG4
3T3 NFL1T2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH3FWJhKSzVyPUewNEDDuSB5ODDuUS=> NIfQWooyPTF5M{CwPC=>
3T3/neu MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEC4UlBKSzVyPUOgxtEhOC5zNDDuUS=> MV[xOVE4OzByOB?=
SK-Br-3 MnLuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mo\oTWM2OD1{INMxJFAvOThibl2= NHy3b2YyPTF5M{CwPC=>
BT 474 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlzXTWM2OD1{INMxJFAvODZibl2= MkPRNVUyPzNyMEi=
A431 M2\GVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFrCb2RKSzVyPUixJOKyKDlibl2= NXfXOnB{OTVzN{OwNFg>
MDA-MB-435 Mk\kS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7WTWM2OD17NkCgxtEhOTZ3IH7N NEHYVVIyPTF5M{CwPC=>
SW620 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGrVVlZKSzVyPU[5NEDDuSB6NDDuUS=> NWmxT2d4OTVzN{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 <1 mg/mL
Ethanol <1 mg/mL
In vivo 30% PEG400+0.5% Tween80+5% propylene glycol 5 mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

  • Mass
    Concentration
    Volume
    Molecular Weight

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

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • 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.

  • * Indicates a Required Field

HER2 Signaling Pathway Map

HER2 Inhibitors with Unique Features

Related HER2 Products

Tags: buy Neratinib (HKI-272) | Neratinib (HKI-272) supplier | purchase Neratinib (HKI-272) | Neratinib (HKI-272) cost | Neratinib (HKI-272) manufacturer | order Neratinib (HKI-272) | Neratinib (HKI-272) distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID