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.

サイズ 価格(税別)  
JPY 24900.00
JPY 78020.00
JPY 161020.00



    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.




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 Mn:3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlroTWM2ODxyLkCwOUDPxE1? MVyyOFAxQTB4NB?=
EFM-192A MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHnOc|dKSzVyPECuNFA2KM7:TR?= NFvRR|MzPDByOUC2OC=>
HCC1569 M{n0VGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml;uTWM2ODxyLkCwOUDPxE1? MUiyOFAxQTB4NB?=
HCC1954 NUDNT2pnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXLxfVF[UUN3MEywMlAxPSEQvF2= MoOxNlQxODlyNkS=
MDA-MB-175 MoHoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH\DVplKSzVyPECuNFA2KM7:TR?= NX;KcFdiOjRyMEmwOlQ>
MDA-MB-361 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWTJR|UxRDBwMEC1JO69VQ>? M13OZVI1ODB7ME[0
SK-BR-3 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkLGTWM2ODxyLkCwOUDPxE1? M1v6c|I1ODB7ME[0
UACC-812 MnHLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M17hW2lEPTB:MD6wNFUh|ryP NY\6W|VUOjRyMEmwOlQ>
SUM-225 NHTqcJVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVLJR|UxRTBwMEGg{txO NXnCfopWOjRyMEmwOlQ>
SUM-190 MlP3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWLJR|UxRTBwMEGg{txO NWWxTJFYOjRyMEmwOlQ>
ZR-75-1 M{LDdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoH6TWM2OD1yLkCzJO69VQ>? MmXjNlQxODlyNkS=
HCC70 MnTFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkTITWM2OD1yLkCzJO69VQ>? M1LidFI1ODB7ME[0
BT-20 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVPJR|UxRTBwMEeg{txO NUTFcml6OjRyMEmwOlQ>
MDA-MB-453 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MojETWM2OD1yLkC5JO69VQ>? M2PUdlI1ODB7ME[0
HCC1187 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{nLXWlEPTB;MD6xNEDPxE1? NYeyfpNbOjRyMEmwOlQ>
EFM-19 MljhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTBwMUGg{txO NHvPNWUzPDByOUC2OC=>
T-47D MkPES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGTyXopKSzVyPUCuNVYh|ryP NIDKOmszPDByOUC2OC=>
MDA-MB-134 NFjNdYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUjjNXV[UUN3ME2wMlE4KM7:TR?= MVSyOFAxQTB4NB?=
HCC38 NHjhd|NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmnhTWM2OD1yLkK1JO69VQ>? NI[4W3QzPDByOUC2OC=>
MDA-MB-435 M3u2dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnztTWM2OD1yLkOzJO69VQ>? MXmyOFAxQTB4NB?=
MDA-MB-468 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYjv[|B2UUN3ME2wMlM{KM7:TR?= NIjPdG4zPDByOUC2OC=>
CAMA-1 M1;UPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NITySWlKSzVyPUCuN|ch|ryP M{\6PFI1ODB7ME[0
MCF-7 NWjtT|U5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYrJR|UxRTBwNEGg{txO NFG2[Y8zPDByOUC2OC=>
HCC1806 M3nsPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXXtcnJqUUN3ME2wMlQ1KM7:TR?= M1vvfVI1ODB7ME[0
HCC1395 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mm[3TWM2OD1yLkS5JO69VQ>? M4f0PFI1ODB7ME[0
HCC1937 M13XTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NULvdmh1UUN3ME2wMlUxKM7:TR?= MWiyOFAxQTB4NB?=
HCC1143 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVfJR|UxRTBwNUSg{txO MonBNlQxODlyNkS=
UACC-732 M1HFUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFzGOGFKSzVyPUCuOlUh|ryP MVyyOFAxQTB4NB?=
MDA-MB-231 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV7JR|UxRTFwMECg{txO M2\SV|I1ODB7ME[0
BT-549 Ml[3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlnpTWM2OD1zLkG0JO69VQ>? MmPLNlQxODlyNkS=
KPL-1 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGnKcmFKSzVyPUGuPFkh|ryP MXWyOFAxQTB4NB?=
CAL-51 NUX6W2VOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlvnTWM2OD1zLki5JO69VQ>? MUKyOFAxQTB4NB?=
BT474 NEOzU|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3LtfWlEPTB;MD6wNFMzOyEEsTCwMlAxODd3IN88US=> NUHUe5BzOjN6MU[yOVQ>
KB MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLPTWM2OD12LkGzJOKyKDBwNEeg{txO NHrqSZkzOjR7MUmzOS=>
KBv200 MmnwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFXrfXpKSzVyPU[uNFMhyrFiMD62OEDPxE1? NXHjVnNnOjJ2OUG5N|U>
MCF-7 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHu2fWpKSzVyPUOuN|AhyrFiMD60NUDPxE1? NVfLc4NJOjJ2OUG5N|U>
MCF-7/Adr M4LTSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUXJVpJHUUN3ME2gNk45QCEEsTCwMlMxKM7:TR?= NYLifGs4OjJ2OUG5N|U>
MCF-7 NIjlPFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYrJR|UxRTNwMEKgxtEhOC5|NDFOwG0> NFj3WYQzOjR7MUmzOS=>
MCF-7/FLV1000 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUT6dnpZUUN3ME23MlA6KMLzIECuO|Eh|ryP NGfjeG0zOjR7MUmzOS=>
HL60 NIjRRXJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1;3[WlEPTB;Mj6yOkDDuSByLkKzJO69VQ>? MUCyNlQ6OTl|NR?=
HL60/Adr Mkn5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUnJR|UxRTFwNEKgxtEhOC5zNTFOwG0> MVGyNlQ6OTl|NR?=
HEK293/pcDNA3.1 NF;U[G9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTVwMkmgxtEhOC53MzFOwG0> Ml7VNlI1QTF7M{W=
HEK293/ABCB1 MmnUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXrJR|UxRTZwOUGgxtEhOC55MDCg{txO MnPBNlI1QTF7M{W=
SKBR M3;CSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXWwMlAyNTFyMDDuUS=> M2LDWlMuPyCm NULESYt1cW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz M1;o[|IyPDh5NkC1
L858R(EGFR) MnTjR4VtdCCYaXHibYxqfHliQYPzZZk> MUDk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz NWTtfWFVOTd|MUGwNFI>
L858R/T790M(EGFR) NYfoV3JzS2WubDDWbYFjcWyrdImgRZN{[Xl? NFjpV5ll\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NVHPfIdpOTd|MUGwNFI>
G776insV_G/C NGD0UIRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NH\QR21l\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MmXPNVc{OTFyMEK=
wild-type NWrUWGh5S2WubDDWbYFjcWyrdImgRZN{[Xl? MV;k[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz MVGxO|MyOTByMh?=
A775insYVMA M3:4VGNmdGxiVnnhZoltcXS7IFHzd4F6 NF\GZXBl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4hfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MmfDNVc{OTFyMEK=
G776insV_G/L NEXHcHhE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MlLT[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NI\rOpUyPzNzMUCwNi=>
P780insGSP MUfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NXn4bFZV\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKHSrbXWgZY5lKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NWrhWZZIOTd|MUGwNFI>
NCI-H1781 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnezbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M4[3flE3QDF6NkG4
HCC827 NGOwNpNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnewbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NIfoZmUyPjhzOE[xPC=>
H3255 MoTzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX;0WHlscW6qaXLpeJMh[2WubDDndo94fGhiaX6geIlu\SCjbnSg[I9{\SCmZYDlcoRmdnRibXHucoVz MW[xOlgyQDZzOB?=
NCI-H1975 NYrFbplKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4nXO4lvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> M2LuWlE3QDF6NkG4
A549 NHjrWplIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn\QbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NI[3bXgyPjhzOE[xPC=>
3T3 M2rVXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH;oVnNKSzVyPUewNEDDuSB5ODDuUS=> NITFWnUyPTF5M{CwPC=>
3T3/neu NE\2XYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVrJR|UxRTNiwsGgNE4yPCCwTR?= M2\FO|E2OTd|MEC4
SK-Br-3 Ml\jS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4T4UGlEPTB;MjFCtUAxNjF6IH7N NVzEeXRnOTVzN{OwNFg>
BT 474 NH;xdldIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXS2ZWxsUUN3ME2yJOKyKDBwME[gcm0> NVy0[JhVOTVzN{OwNFg>
MDA-MB-435 MmnhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRTl4MDFCtUAyPjVibl2= Mo\GNVUyPzNyMEi=
SW620 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4LDUGlEPTB;NkmwJOKyKDh2IH7N NEPFVnkyPTF5M{CwPC=>


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 左から右までの手順で、溶剤を製品に加えることです:
30% PEG400+0.5% Tween80+5% propylene glycol
5 mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)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