Neratinib (HKI-272)


Neratinib (HKI-272)化学構造


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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    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.

  • 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.

    (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.




製品説明 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

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 Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 MmHqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4\jNGlEPTB:MD6wNFUh|ryP MknlNlQxODlyNkS=
EFM-192A M4q0Tmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnG2TWM2ODxyLkCwOUDPxE1? MWKyOFAxQTB4NB?=
HCC1569 MmTwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn3PTWM2ODxyLkCwOUDPxE1? MkDZNlQxODlyNkS=
HCC1954 NG\4[IZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFXyRXlKSzVyPECuNFA2KM7:TR?= MVOyOFAxQTB4NB?=
MDA-MB-361 M{TzXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF;0WXZKSzVyPECuNFA2KM7:TR?= NIjQ[m8zPDByOUC2OC=>
SK-BR-3 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{fpeWlEPTB:MD6wNFUh|ryP M4\kb|I1ODB7ME[0
UACC-812 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmK4TWM2ODxyLkCwOUDPxE1? MmPlNlQxODlyNkS=
UACC-893 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoDETWM2ODxyLkCwOUDPxE1? M2DKXlI1ODB7ME[0
SUM-225 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2DZeWlEPTB;MD6wNUDPxE1? NHLUdGczPDByOUC2OC=>
SUM-190 MlvsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGfreJZKSzVyPUCuNFEh|ryP NXjnNII6OjRyMEmwOlQ>
ZR-75-1 NUL0SoNtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\uTWM2OD1yLkCzJO69VQ>? NGDGfmszPDByOUC2OC=>
BT-20 M1;WR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmrPTWM2OD1yLkC3JO69VQ>? MYiyOFAxQTB4NB?=
MDA-MB-453 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVrJR|UxRTBwMEmg{txO NFXRfY0zPDByOUC2OC=>
HCC1187 M2q4bmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4HYOWlEPTB;MD6xNEDPxE1? MV[yOFAxQTB4NB?=
EFM-19 M2m1TWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIHCTGFKSzVyPUCuNVEh|ryP NVfmbnVkOjRyMEmwOlQ>
T-47D NUmyWVZtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWrJR|UxRTBwMU[g{txO MYGyOFAxQTB4NB?=
MDA-MB-134 NHjreJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFW2[WZKSzVyPUCuNVch|ryP M{ftflI1ODB7ME[0
HCC38 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVrJR|UxRTBwMkWg{txO MVWyOFAxQTB4NB?=
MDA-MB-435 Mne5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHXqenlKSzVyPUCuN|Mh|ryP MlPzNlQxODlyNkS=
MDA-MB-468 M{f1[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MULJR|UxRTBwM{Og{txO NVXFSG9yOjRyMEmwOlQ>
MDA-MB-436 M4TSWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYjuRm5rUUN3ME2wMlQyKM7:TR?= MVuyOFAxQTB4NB?=
MCF-7 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHmwNFdKSzVyPUCuOFEh|ryP M4HxcFI1ODB7ME[0
MDA-MB-415 NHjtfFJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXvCZZNPUUN3ME2wMlQzKM7:TR?= MlzGNlQxODlyNkS=
HCC1806 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mk\CTWM2OD1yLkS0JO69VQ>? MlLYNlQxODlyNkS=
HCC1395 NFu4eGFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{D3dGlEPTB;MD60PUDPxE1? NH[xW|kzPDByOUC2OC=>
HCC1937 M3XmUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX\JR|UxRTBwNUCg{txO NHOyVHMzPDByOUC2OC=>
HCC1143 NWW5dmlHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mlm5TWM2OD1yLkW0JO69VQ>? NXrJSJNEOjRyMEmwOlQ>
UACC-732 M1jzN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF3OS49KSzVyPUCuOlUh|ryP M1GxPVI1ODB7ME[0
MDA-MB-157 M13nPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUDn[5kxUUN3ME2xMlEzKM7:TR?= MUKyOFAxQTB4NB?=
BT-549 NVGx[45ZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2HRfmlEPTB;MT6xOEDPxE1? MX2yOFAxQTB4NB?=
KPL-1 Mo\sS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlTtTWM2OD1zLki5JO69VQ>? NH;Pc5UzPDByOUC2OC=>
CAL-51 M3fzSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUPTOXcyUUN3ME2xMlg6KM7:TR?= M{TiclI1ODB7ME[0
BT474 MlrJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3LkcGlEPTB;MD6wNFMzOyEEsTCwMlAxODd3IN88US=> NYPWOohHOjN6MU[yOVQ>
MDAMB453 M2fn[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2PIbWlEPTB;MT61PUDDuSByLkG3PUDPxE1? NXLEUmhTOjN6MU[yOVQ>
KBv200 NUDwTZh5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGfwR2pKSzVyPU[uNFMhyrFiMD62OEDPxE1? MmH5NlI1QTF7M{W=
MCF-7 Ml[3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmHXTWM2OD1|LkOwJOKyKDBwNEGg{txO MUCyNlQ6OTl|NR?=
MCF-7/Adr MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUjjbodiUUN3ME2gNk45QCEEsTCwMlMxKM7:TR?= MmTENlI1QTF7M{W=
MCF-7 M1fFU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1TRNWlEPTB;Mz6wNkDDuSByLkO0JO69VQ>? NXLqTWxMOjJ2OUG5N|U>
MCF-7/FLV1000 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHrSfmhKSzVyPUeuNFkhyrFiMD63NUDPxE1? NGP1NWMzOjR7MUmzOS=>
HL60 NHXtZ2tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVzyUZI2UUN3ME2yMlI3KMLzIECuNlMh|ryP NVrINYRrOjJ2OUG5N|U>
HL60/Adr M1ja[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mkj2TWM2OD1zLkSyJOKyKDBwMUWg{txO NGrDTIczOjR7MUmzOS=>
HEK293/pcDNA3.1 NVK3[HVzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYjJR|UxRTVwMkmgxtEhOC53MzFOwG0> NFvOV4gzOjR7MUmzOS=>
HEK293/ABCB1 Mo\VS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHfUd2tKSzVyPU[uPVEhyrFiMD63NEAh|ryP MXKyNlQ6OTl|NR?=
SKBR M1mxW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXfHUVJmOC5yMT2xNFAhdk1? MVezMVch\A>? M3zXRolvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NX\zNGNGOjF2OEe2NFU>
L858R(EGFR) NYXOVmdsS2WubDDWbYFjcWyrdImgRZN{[Xl? NVXzTWVq\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M3nNPFE4OzFzMECy
L858R/T790M(EGFR) MYDD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NEf2bmhl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NEmzPWwyPzNzMUCwNi=>
G776insV_G/C M2TyRmNmdGxiVnnhZoltcXS7IFHzd4F6 MUfk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NUfHV3hQOTd|MUGwNFI>
wild-type M1ezfmNmdGxiVnnhZoltcXS7IFHzd4F6 NFTySHFl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NYL5RmIxOTd|MUGwNFI>
A775insYVMA M1Tm[GNmdGxiVnnhZoltcXS7IFHzd4F6 NXv1PGlT\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MXSxO|MyOTByMh?=
G776insV_G/L NFz3[lVE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NELJTVdl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NFvqWGYyPzNzMUCwNi=>
P780insGSP NVjWUXhSS2WubDDWbYFjcWyrdImgRZN{[Xl? MmHJ[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NWLxPFEyOTd|MUGwNFI>
NCI-H1781 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWPpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MVmxOlgyQDZzOB?=
HCC827 MorZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MonLbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NYn4Z3NIOTZ6MUi2NVg>
H3255 Mmj0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYftWIlucW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz Mm[2NVY5OTh4MUi=
NCI-H1975 NIHiWmpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWLpcohq[mm2czDj[YxtKGe{b4f0bEBqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MWSxOlgyQDZzOB?=
A549 NVXlcYdbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlHNbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NIWzWI4yPjhzOE[xPC=>
3T3/neu NV\GUG1lT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF3oXHFKSzVyPUOgxtEhOC5zNDDuUS=> NIX5d4syPTF5M{CwPC=>
SK-Br-3 NV7YZXM3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGnkZ4tKSzVyPUKgxtEhOC5zODDuUS=> M33IXVE2OTd|MEC4
BT 474 M{PETmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2m2U2lEPTB;MjFCtUAxNjB4IH7N Mlr5NVUyPzNyMEi=
A431 MkHNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYrJR|UxRThzINMxJFkhdk1? M4nmO|E2OTd|MEC4


体内試験 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]


+ 展開

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.
細胞試験: [1]
+ 展開
  • 細胞株: 3T3, 3T3/neu, A431, BT474, SK-Br-3, MDA-MB-435, and SW480
  • 濃度: Dissolved in DMSO, final concentrations 0.5 ng/mL-5 μg/mL
  • 反応時間: 2 or 6 days
  • 実験の流れ: 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.
+ 展開
  • 動物モデル: Female athymic (nude) mice implanted s.c. with 3T3/neu, BT474, MCF-7, or SK-OV-3 cells
  • 製剤: Formulated in 0.5% methocellulose-0.4% polysorbate-80 (Tween 80)
  • 投薬量: ~80 mg/kg/day
  • 投与方法: Gavage

溶解度 (25°C)

体外 DMSO 5 mg/mL (8.97 mM) warming
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます:
30% PEG400+0.5% Tween80+5% propylene glycol
5 mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。


分子量 557.04


CAS No. 698387-09-6
別名 N/A





マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)


  • マス




貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1



  • 連続希釈剤

  • 計算結果

  • 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):




チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2


マス 濃度 ボリューム 分子量


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



Handling Instructions


  • * 必須


HER2 Inhibitors with Unique Features


Tags: Neratinib (HKI-272)を買う | Neratinib (HKI-272) ic50 | Neratinib (HKI-272)供給者 | Neratinib (HKI-272)を購入する | Neratinib (HKI-272)費用 | Neratinib (HKI-272)生産者 | オーダーNeratinib (HKI-272) | Neratinib (HKI-272)化学構造 | Neratinib (HKI-272)分子量 | Neratinib (HKI-272)代理店
細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID