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 M3S3fGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVHJR|UxRDBwMEC1JO69VQ>? NYTubGlZOjRyMEmwOlQ>
EFM-192A Mor5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mk\DTWM2ODxyLkCwOUDPxE1? M3H6SFI1ODB7ME[0
HCC1569 M1HEdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnzpTWM2ODxyLkCwOUDPxE1? M3nGZlI1ODB7ME[0
HCC1954 MnfyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWHJR|UxRDBwMEC1JO69VQ>? M1n4NlI1ODB7ME[0
MDA-MB-175 M2nWVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIWxPJpKSzVyPECuNFA2KM7:TR?= NEfVT5MzPDByOUC2OC=>
MDA-MB-361 MkfoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NG\YVZNKSzVyPECuNFA2KM7:TR?= M1rjdlI1ODB7ME[0
SK-BR-3 M2PNRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2\sV2lEPTB:MD6wNFUh|ryP NGPlO2ozPDByOUC2OC=>
UACC-812 MnO1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2LKZ2lEPTB:MD6wNFUh|ryP NXnjXlRSOjRyMEmwOlQ>
SUM-225 NX:1OG14T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnLQTWM2OD1yLkCxJO69VQ>? MYiyOFAxQTB4NB?=
SUM-190 M2nkUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mly1TWM2OD1yLkCxJO69VQ>? NFLMdIczPDByOUC2OC=>
ZR-75-1 NXvlToRpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXPyNVV[UUN3ME2wMlA{KM7:TR?= NH\sPWozPDByOUC2OC=>
HCC70 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{DaNmlEPTB;MD6wN{DPxE1? M4XvU|I1ODB7ME[0
BT-20 M1fMVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmnqTWM2OD1yLkC3JO69VQ>? NUTIdodMOjRyMEmwOlQ>
EFM-19 Mo\MS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYfHXmRDUUN3ME2wMlEyKM7:TR?= NYTaPZFrOjRyMEmwOlQ>
T-47D MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXHJR|UxRTBwMU[g{txO NXPm[ZFxOjRyMEmwOlQ>
MDA-MB-134 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGSzRm9KSzVyPUCuNVch|ryP NVHKSIpGOjRyMEmwOlQ>
MDA-MB-435 Ml7iS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mk\qTWM2OD1yLkOzJO69VQ>? NUTrZ3ZDOjRyMEmwOlQ>
MDA-MB-468 Ml;2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVm1RmNKUUN3ME2wMlM{KM7:TR?= NYP3OZU1OjRyMEmwOlQ>
MDA-MB-436 MnjDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWSycZRkUUN3ME2wMlQyKM7:TR?= MXGyOFAxQTB4NB?=
MCF-7 NF\hXnNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYLJR|UxRTBwNEGg{txO MmPxNlQxODlyNkS=
MDA-MB-415 NXLmdIhPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2XqW2lEPTB;MD60NkDPxE1? Ml7UNlQxODlyNkS=
HCC1806 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2OwPGlEPTB;MD60OEDPxE1? MkLVNlQxODlyNkS=
HCC1395 NHT2TIRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVPJR|UxRTBwNEmg{txO MmD5NlQxODlyNkS=
HCC1937 M1fJZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWm3PIo2UUN3ME2wMlUxKM7:TR?= MYSyOFAxQTB4NB?=
HCC1143 M2TCcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWDiT4F4UUN3ME2wMlU1KM7:TR?= NYHi[FJGOjRyMEmwOlQ>
MDA-MB-231 NH7tUlVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTFwMECg{txO MoTjNlQxODlyNkS=
BT-549 MnTxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4fvO2lEPTB;MT6xOEDPxE1? NInJ[XMzPDByOUC2OC=>
KPL-1 NGew[41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnLyTWM2OD1zLki5JO69VQ>? NEPXUJIzPDByOUC2OC=>
CAL-51 NF;4NI1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGrMW|ZKSzVyPUGuPFkh|ryP M1HhTVI1ODB7ME[0
BT474 NIHwZmRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnfWTWM2OD1yLkCwN|I{KMLzIECuNFAxPzVizszN M4jGR|I{QDF4MkW0
SKBR3 NGjRPYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnvyTWM2OD1yLkCwO|UhyrFiMD6wNFUh|ryP MUKyN|gyPjJ3NB?=
MDAMB453 MoXrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF;BfZJKSzVyPUGuOVkhyrFiMD6xO|kh|ryP M1PaRVI{QDF4MkW0
KBv200 NVLJc|V7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1rHdWlEPTB;Nj6wN{DDuSByLk[0JO69VQ>? MUOyNlQ6OTl|NR?=
MCF-7 M3XqU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M37tO2lEPTB;Mz6zNEDDuSByLkSxJO69VQ>? NXn2N4I6OjJ2OUG5N|U>
MCF-7/Adr M{CwbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M37VV2lEPTB;IEKuPFghyrFiMD6zNEDPxE1? M3XUWVIzPDlzOUO1
MCF-7 MoWwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVzJR|UxRTNwMEKgxtEhOC5|NDFOwG0> NHOxO2szOjR7MUmzOS=>
MCF-7/FLV1000 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHj4XFFKSzVyPUeuNFkhyrFiMD63NUDPxE1? MX6yNlQ6OTl|NR?=
HL60 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn[2TWM2OD1{LkK2JOKyKDBwMkOg{txO MVmyNlQ6OTl|NR?=
HL60/Adr NVy5NYpST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml3HTWM2OD1zLkSyJOKyKDBwMUWg{txO M4S1WlIzPDlzOUO1
HEK293/pcDNA3.1 NEThdYFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX3JR|UxRTVwMkmgxtEhOC53MzFOwG0> M4PteVIzPDlzOUO1
HEK293/ABCB1 NUPuT3ZbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mk\ETWM2OD14LkmxJOKyKDBwN{CgJO69VQ>? Mof4NlI1QTF7M{W=
SKBR MofGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF\1[|IxNjBzLUGwNEBvVQ>? MVKzMVch\A>? NHLnZW9qdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M3r6e|IyPDh5NkC1
L858R(EGFR) MYrD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MoPn[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NGCxVWwyPzNzMUCwNi=>
L858R/T790M(EGFR) M2PoUGNmdGxiVnnhZoltcXS7IFHzd4F6 MUDk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz MWCxO|MyOTByMh?=
G776insV_G/C NEjIZ4lE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M3vUZYRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckB1cW2nIHHu[EBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MlXoNVc{OTFyMEK=
wild-type MXnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NU[4bJBs\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NFnHNJgyPzNzMUCwNi=>
A775insYVMA MY\D[YxtKF[rYXLpcIl1gSCDc4PhfS=> NXjhV45M\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NUnqSmNLOTd|MUGwNFI>
G776insV_G/L MYfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MnTB[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MXOxO|MyOTByMh?=
P780insGSP MYXD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NX3a[mFv\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M1PqNlE4OzFzMECy
NCI-H1781 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NELHToJqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MVuxOlgyQDZzOB?=
HCC827 NF3DNXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3uyZ4lvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MUmxOlgyQDZzOB?=
H3255 NHz3OnhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHe5b2dqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MmXsNVY5OTh4MUi=
NCI-H1975 M2rYWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYPpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MmTsNVY5OTh4MUi=
A549 NIDjUVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWe5[HNJcW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz M3nQU|E3QDF6NkG4
3T3 NX3OeWUzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NW\vW4NZUUN3ME23NFAhyrFiN{igcm0> MojNNVUyPzNyMEi=
3T3/neu NGT1O49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEXVSHNKSzVyPUOgxtEhOC5zNDDuUS=> NYC4XZZZOTVzN{OwNFg>
BT 474 NH62XolIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHXSRmdKSzVyPUKgxtEhOC5yNjDuUS=> MYOxOVE4OzByOB?=
A431 NXfscoZjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MonJTWM2OD16MTFCtUA6KG6P NWG4WWhwOTVzN{OwNFg>
MDA-MB-435 M4C5dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYr1dIQ{UUN3ME25OlAhyrFiMU[1JI5O MUWxOVE4OzByOB?=
SW620 NH\JcYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3zudmlEPTB;NkmwJOKyKDh2IH7N MXOxOVE4OzByOB?=

... 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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID