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.

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.
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 MkTzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2XsUmlEPTB:MD6wNFUh|ryP MlLDNlQxODlyNkS=
EFM-192A M1u3cmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIXxSo5KSzVyPECuNFA2KM7:TR?= MUCyOFAxQTB4NB?=
HCC1569 Mn;qS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlfMTWM2ODxyLkCwOUDPxE1? NXjnVGNWOjRyMEmwOlQ>
HCC1954 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoXJTWM2ODxyLkCwOUDPxE1? Mne1NlQxODlyNkS=
MDA-MB-175 M4rkd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUPJR|UxRDBwMEC1JO69VQ>? NHPlb2kzPDByOUC2OC=>
MDA-MB-361 MlfIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2q3OWlEPTB:MD6wNFUh|ryP MXWyOFAxQTB4NB?=
SK-BR-3 M{L3Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXnRV2t5UUN3MEywMlAxPSEQvF2= NVn4U4xjOjRyMEmwOlQ>
UACC-893 M3\BT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXLJR|UxRDBwMEC1JO69VQ>? NILtdHkzPDByOUC2OC=>
SUM-225 Ml34S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXLLeFNqUUN3ME2wMlAyKM7:TR?= NWf1Z4V3OjRyMEmwOlQ>
SUM-190 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUnJR|UxRTBwMEGg{txO NXLNOZVrOjRyMEmwOlQ>
ZR-75-1 NYX0Z49pT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUW0Z4hbUUN3ME2wMlA{KM7:TR?= NXzXc|RTOjRyMEmwOlQ>
HCC70 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWDJR|UxRTBwMEOg{txO MoHINlQxODlyNkS=
BT-20 MkK0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFLVZplKSzVyPUCuNFch|ryP M3nQVVI1ODB7ME[0
MDA-MB-453 NXnxfHk2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH7OeWxKSzVyPUCuNFkh|ryP M2\KRlI1ODB7ME[0
HCC1187 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkDMTWM2OD1yLkGwJO69VQ>? NULycmkyOjRyMEmwOlQ>
T-47D M2XmXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2XpT2lEPTB;MD6xOkDPxE1? M{DCUlI1ODB7ME[0
MDA-MB-134 NU\yTllsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnzYTWM2OD1yLkG3JO69VQ>? MW[yOFAxQTB4NB?=
HCC38 MoHaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTBwMkWg{txO NG\kNWszPDByOUC2OC=>
MDA-MB-435 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHfoNoJKSzVyPUCuN|Mh|ryP NF:4XVEzPDByOUC2OC=>
MDA-MB-468 M2TIc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1LP[GlEPTB;MD6zN{DPxE1? NYrRZWpyOjRyMEmwOlQ>
CAMA-1 M13JZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4fidmlEPTB;MD6zO{DPxE1? MlLkNlQxODlyNkS=
MDA-MB-436 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEHzbG5KSzVyPUCuOFEh|ryP MoP3NlQxODlyNkS=
MCF-7 M1HmZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTUU5VKSzVyPUCuOFEh|ryP MlfaNlQxODlyNkS=
HCC1806 MmXWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlL1TWM2OD1yLkS0JO69VQ>? MlLWNlQxODlyNkS=
HCC1395 M{DncWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWm0c5lzUUN3ME2wMlQ6KM7:TR?= MX2yOFAxQTB4NB?=
HCC1937 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1jFcmlEPTB;MD61NEDPxE1? MXqyOFAxQTB4NB?=
HCC1143 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXPsTZVuUUN3ME2wMlU1KM7:TR?= NXj6R3g3OjRyMEmwOlQ>
UACC-732 NEK1T|ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWnJR|UxRTBwNkWg{txO MUCyOFAxQTB4NB?=
MDA-MB-231 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3TjZWlEPTB;MT6wNEDPxE1? NUHVXJpUOjRyMEmwOlQ>
MDA-MB-157 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEPBZlNKSzVyPUGuNVIh|ryP MUiyOFAxQTB4NB?=
BT-549 MoD3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUmxTXJOUUN3ME2xMlE1KM7:TR?= NGj5c|czPDByOUC2OC=>
KPL-1 M2rOcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHPPSWdKSzVyPUGuPFkh|ryP MXiyOFAxQTB4NB?=
CAL-51 NEP1[GxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXvoW3pGUUN3ME2xMlg6KM7:TR?= NGXGXmczPDByOUC2OC=>
BT474 NFLhc3BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUfJR|UxRTBwMECzNlMhyrFiMD6wNFA4PSEQvF2= M3rqeFI{QDF4MkW0
MDAMB453 NIC1d3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkS2TWM2OD1zLkW5JOKyKDBwMUe5JO69VQ>? NH63XpczOzhzNkK1OC=>
KB MoPaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3e0R2lEPTB;ND6xN{DDuSByLkS3JO69VQ>? NUXRbIFbOjJ2OUG5N|U>
KBv200 Mnq3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MofkTWM2OD14LkCzJOKyKDBwNkSg{txO MVWyNlQ6OTl|NR?=
MCF-7 NVe4Smh{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHjyZXlKSzVyPUOuN|AhyrFiMD60NUDPxE1? M4K5NFIzPDlzOUO1
MCF-7/Adr NGPTRo9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXnGT2pzUUN3ME2gNk45QCEEsTCwMlMxKM7:TR?= MW[yNlQ6OTl|NR?=
MCF-7 M{exXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3X3c2lEPTB;Mz6wNkDDuSByLkO0JO69VQ>? M{\teFIzPDlzOUO1
MCF-7/FLV1000 NFyyUYtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUfJR|UxRTdwMEmgxtEhOC55MTFOwG0> M{jzTVIzPDlzOUO1
HL60 NGrOd|dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoC4TWM2OD1{LkK2JOKyKDBwMkOg{txO NVL2bopKOjJ2OUG5N|U>
HL60/Adr M321VWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MknHTWM2OD1zLkSyJOKyKDBwMUWg{txO NUn1SmJuOjJ2OUG5N|U>
HEK293/pcDNA3.1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVPJR|UxRTVwMkmgxtEhOC53MzFOwG0> M{LEWFIzPDlzOUO1
HEK293/ABCB1 MkPxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MljVTWM2OD14LkmxJOKyKDBwN{CgJO69VQ>? MVyyNlQ6OTl|NR?=
SKBR NFXEN4FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4fTXFAvODFvMUCwJI5O M4rPeFMuPyCm NYTNWmFlcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz MoTMNlE1QDd4MEW=
L858R(EGFR) MkPMR4VtdCCYaXHibYxqfHliQYPzZZk> M{XtfYRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MnfRNVc{OTFyMEK=
L858R/T790M(EGFR) Ml;1R4VtdCCYaXHibYxqfHliQYPzZZk> M2K3RoRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? M2PyfVE4OzFzMECy
G776insV_G/C MknrR4VtdCCYaXHibYxqfHliQYPzZZk> NVXZXZZr\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NXrrSpFlOTd|MUGwNFI>
wild-type M3raZWNmdGxiVnnhZoltcXS7IFHzd4F6 NUD4SY9Q\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= Mn7XNVc{OTFyMEK=
A775insYVMA NV;jR2lsS2WubDDWbYFjcWyrdImgRZN{[Xl? Mkfh[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NELZ[JMyPzNzMUCwNi=>
G776insV_G/L NVrNfoRvS2WubDDWbYFjcWyrdImgRZN{[Xl? Mn[2[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MUexO|MyOTByMh?=
P780insGSP M1rrcmNmdGxiVnnhZoltcXS7IFHzd4F6 NYDUV4sz\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NHPXUFYyPzNzMUCwNi=>
NCI-H1781 NEfjOWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF3yfmFqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> Mnz0NVY5OTh4MUi=
HCC827 NEfaWIFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2jvc4lvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NV7VWGNPOTZ6MUi2NVg>
H3255 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnfSbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M1;LPVE3QDF6NkG4
NCI-H1975 M3G2R2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX3KS5dzcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz M1fvdVE3QDF6NkG4
A549 NXziOJE5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn35bY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NFTQfGgyPjhzOE[xPC=>
3T3 NHvWbG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYTJR|UxRTdyMDFCtUA4QCCwTR?= M3\nc|E2OTd|MEC4
3T3/neu NIm3bY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWLuVYM1UUN3ME2zJOKyKDBwMUSgcm0> NEjYWoQyPTF5M{CwPC=>
BT 474 NGjIfJJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkTlTWM2OD1{INMxJFAvODZibl2= M2HQUlE2OTd|MEC4
A431 MmnuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUjJR|UxRThzINMxJFkhdk1? MWSxOVE4OzByOB?=
MDA-MB-435 M1zI[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2qwWGlEPTB;OU[wJOKyKDF4NTDuUS=> NEXhWHkyPTF5M{CwPC=>
SW620 M3vncWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVfJR|UxRTZ7MDFCtUA5PCCwTR?= MYGxOVE4OzByOB?=

... 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]


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 individually and in order:
30% PEG400+0.5% Tween80+5% propylene glycol
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


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

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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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID