Belinostat (PXD101)

製品コードS1085 別名:NSC726630, PX-105684

Belinostat (PXD101)化学構造

分子量(MW):318.35

Belinostat (PXD101) is a novel HDAC inhibitor with IC50 of 27 nM in a cell-free assay, with activity demonstrated in cisplatin-resistant tumors.

サイズ 価格(税別)  
JPY 26560.00
JPY 19920.00
JPY 61420.00
JPY 94620.00
JPY 161020.00

カスタマーフィードバック(8)

  • A375DR and parental cells were seeded 50,000 cells per well in 6-well plates and treated with 1 mMvorinostat (Vor), 0.5 mMbelinostat (Bel), 5 nMpanobinostat (Pan), and/or combination of 5 nM trametinib and 0.125 mM dabrafenib.

    Cell, 2018, 173(6):1413-1425. Belinostat (PXD101) purchased from Selleck.

    (C) Cell lysates were harvested from lung SCC cells after treatment with increasing doses of belinostat (0.1, 0.2, 0.3, 1, 3 lM). Immunoblotting was performed to evaluate the changes in phosphorylated protein levels of the targets identified in 1D (ERK1/2, p38, B-Raf, MEK1/2) as well as PARP. b-Actin shown as loading control.

    Mol Oncol, 2017, 11(8):965-980. Belinostat (PXD101) purchased from Selleck.

  • (B) Western blotting for cyclin D1. Cells were treated for 48 h with 5 μM belinostat and/or 25 or 50 μM ritonavir. Actin was used for the loading control. Representative blots are shown.

    Oncol Res, 2016, 24(5):327-335. Belinostat (PXD101) purchased from Selleck.

    Inhibition of LSD1 activity by HDAC inhibitors. a MDA-MB-231 and MDA-MB-468 cells were exposed to indicated HDAC inhibitors for 24 h.

    Breast Cancer Res Treat 2012 131, 777-789. Belinostat (PXD101) purchased from Selleck.

  • LSD1 and HDAC inhibitors exhibit synergistic growth inhibition. Cells were simultaneously treated with pargyline or HDAC inhibitors for 48 h.

     

     

    Breast Cancer Res Treat 2010 131(3), 777-789. Belinostat (PXD101) purchased from Selleck.

    HDACIs That Simultaneously Inhibit HDACs 1 and 6 Showed Greater Antileukemic Activities than HDACIs that Don,t at Cmax Concentrations. THP-1 cells were treated with LBH-589, PXD101, SAHA, VPA, MS-275 and MGCD0103 at Cmax concentrations for 3 h and 24 h, respectively. The cells post 3 h treatments were washed three times with complete medium and divided into two halves. One half of the cells was resuspended in complete media and cultured for up to 24 h to determine the effects of the 3 h treatments on cell proliferation and apoptosis. The other half of the cells was used to prepare whole cell lysates. Whole cell lysates from the 3 h and 24 h treatments were extracted and subjected to Western blots probed by anti-ac-tubulin or-β-actin antibody (panels A&B), or subjected to HDAC1 enzymatic assays post IP as described in the Materials and Methods (Panels C&D). The effects of the 3 h and 24 h HDACI treatments on cell proliferation, as reflected by percent decrease of live cells relative to untreated cells (panel E), and apoptosis (panel F) were determined by flow cytometry analysis as described in the Materials and Methods.

     

     

    PLoS One 2011 6, e17138. Belinostat (PXD101) purchased from Selleck.

  • Induction of DNA Damage and Bim Is Critical for HDACI-Induced Apoptosis in Pediatric AML Cells. THP-1 cells were treated with the HDACIs at Cmax concentrations for 3 (panel A) and 24 h (panel B), respectively. Whole cell lysates were extracted and subjected to Western blots probed by anti-p21, -c-Myc, -cH2AX, -Bim, or -β-actin antibody.

     

     

    PLoS One 2011 6, e17138. Belinostat (PXD101) purchased from Selleck.

    MDA-MB-231 Breast cancer cells were pretreated with Acetyl-H3 and H3, and then treated with the indicated concentrations of  PXD101.

    Dr. Zhang of Tianjin Medical University. Belinostat (PXD101) purchased from Selleck.

製品安全説明書

HDAC阻害剤の選択性比較

生物活性

製品説明 Belinostat (PXD101) is a novel HDAC inhibitor with IC50 of 27 nM in a cell-free assay, with activity demonstrated in cisplatin-resistant tumors.
特性 Lead compound of Topotarget.
ターゲット
HDAC [1]
(Cell-free assay)
27 nM
体外試験

Belinostat inhibits the growth of tumor cells (A2780, HCT116, HT29, WIL, CALU-3, MCF7, PC3 and HS852) with IC50 from 0.2-0.66 μM. PD101 shows low activity in A2780/cp70 and 2780AD cells, which are cisplatin and doxorubicin-resistant derivatives of A2780 cells. Belinostat could induce apoptosis through PARP cleavage and acetylation of histones H3/H4. [1] Belinostat inhibits bladder cancer cell growth, especially in 5637 cells, which shows accumulation of G0-G1 phase, decrease in S phase and increase in G2-M phase. [2] The growth inhibitory activity of belinostat on cell lines is not strongly influenced by the multidrug-resistant phenotype, whereas the activity of docetaxel is clearly affected. Belinostat could enhance the growth inhibitory activity of docetaxel or carboplatin in OVCAR-3 and A2780 cells. Belinostat also shows enhanced tubulin acetylation in ovarian cancer cell lines. [3] A recent study shows that Belinostat activates protein kinase A in a TGF-β signaling-dependent mechanism and decreases survivin mRNA. [4]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NB4 NI\5V45E\WyuIG\pZYJqdGm2eTDBd5NigQ>? NXToe5BjOC5{L{NCpO69VQ>? M3PrUVI1NzR6L{eyJIg> MUXk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZo91cCC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= M{TUTFI2QDZ2N{Oy
HL-60  MkfIR4VtdCCYaXHibYxqfHliQYPzZZk> NYj2RWJxOC5{L{NCpO69VQ>? NXHiUoRXOjRxNEivO|IhcA>? NFXtbJBl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[m:2aDD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NEPVNYwzPTh4NEezNi=>
NB4 Mn7zSpVv[3Srb36gRZN{[Xl? M3njWVLDqM7:TR?= MWeyOE81QCCq NX7BdWxI[myxY3vzJINmdGxiY4njcIUhcW5iUzDwbIF{\Q>? M{nDd|I2QDZ2N{Oy
HL-60  NWDRfIVzTnWwY4Tpc44hSXO|YYm= NHjvc3EzyqEQvF2= NEH2OJUzPC92ODDo M2PnZ4Jtd2OtczDj[YxtKGO7Y3zlJIlvKFNicHjhd4U> NV\1R2R[OjV6NkS3N|I>
NB4 MWLGeY5kfGmxbjDBd5NigQ>? NFi2V2sxNjMEoN88US=> M121dVI1NzR6L{eyJIg> NX7aS2Nn\W6qYX7j[ZMhWkFvaX7keYNm\CCpcnHueYxw[3m2aXOg[Iln\mW{ZX70bYF1cW:w MmSwNlU5PjR5M{K=
HL-60  NVyzZ4huTnWwY4Tpc44hSXO|YYm= NWDORlFmOC5{wrFOwG0> MkfVNlQwPDhxN{KgbC=> MWLlcohidmOnczDSRU1qdmS3Y3XkJIdz[W63bH;jfZRq[yCmaX\m[ZJmdnSrYYTpc44> NU\SdnF[OjV6NkS3N|I>
PANC-1 MkHZSpVv[3Srb36gRZN{[Xl? M1PTOFExyqEQvF2= NVvQdWwyOi92L{[gbC=> MonISG1UVw>? MoK5bY5lfWOnczDBUXBMKGGldHn2ZZRqd25? NXrRfm1[OjN5NEOxPVg>
PANC-1 NVGzSHAyS2WubDDWbYFjcWyrdImgRZN{[Xl? NFz5fVkyNzFywrFOwG0> NYrM[mM6PDhiaB?= M2TqcmROW09? MUjk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MmTKNlM4PDNzOUi=
PANC-1 Mn7MSpVv[3Srb36gRZN{[Xl? NYDJNlBOOTEEoN88US=> MU[yM|QhcA>? M3XORmROW09? NGey[GVqdmO{ZXHz[ZMhcW62cnHj[YxtfWyjcjDSU3MhdGW4ZXy= MYqyN|c1OzF7OB?=
H1666 Ml65S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mom5O|LDqGh? NUeyW|EyTE2VTx?= MXvJR|UxRjFyIN88US=> MXuyN|UyPTd3Mh?=
H460 NVvGUpVET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVy3NuKhcA>? NEHFeG9FVVOR M{LuOGlEPTB;MD64OkDPxE1? M3S4XlI{PTF3N{Wy
H1299 NYrT[pNuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIXNc2w4OsLiaB?= NHW5N|lFVVOR MX;JR|UxRTFwMjFOwG0> M1vaWVI{PTF3N{Wy
H520 M2rsVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1PHdlczyqCq NYrLNlZVTE2VTx?= NV:0XY13UUN3ME2wMlc2KM7:TR?= MmLyNlM2OTV5NUK=
H1975 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWTXNGFnPzMEoHi= NE\jN5lFVVOR NFjtPIRKSzVyPUCuOlgh|ryP M{DDcFI{PTF3N{Wy
H1650 NV7UN5dIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoPEO|LDqGh? NWP3UYl7TE2VTx?= NWfpZWY4UUN3ME2wMlg5KM7:TR?= MYeyN|UyPTd3Mh?=
H820 NIfVZlNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlvpO|LDqGh? NX\kN2RNTE2VTx?= MojkTWM2OD1yLkSg{txO MUWyN|UyPTd3Mh?=
PC9 NVzQO4FvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn\FO|LDqGh? MWjEUXNQ NFL5OGFKSzVyPUCuNlkh|ryP NUn3[WRXOjN3MUW3OVI>
HCC2279 Mn7CS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1H1[lczyqCq M2\aNWROW09? NFLtTGFKSzVyPUCuOEDPxE1? MkLWNlM2OTV5NUK=
HCC827 M4C3Smdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1j1dlczyqCq MkWwSG1UVw>? NYXFXGRzUUN3ME2wMlI6KM7:TR?= Mom1NlM2OTV5NUK=
HCC2935 NU[1eIxoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWm3NuKhcA>? NGjhXpJFVVOR NVHXfmNSUUN3ME2wMlk4KM7:TR?= MXeyN|UyPTd3Mh?=
HCC4006 NY\OVXg6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWK3NuKhcA>? NVnkb3E5TE2VTx?= NYnFT4s{UUN3ME2wMlQ3KM7:TR?= NXLPemxjOjN3MUW3OVI>
H460 M2XKO2Z2dmO2aX;uJGF{e2G7 M{K1XlUxOMLibl2= Mmj0NlTDqGh? NUO1O4RRTE2VTx?= MoTH[IVkemWjc3XzJGVITlJiZYjwdoV{e2mxbh?= MXeyN|UyPTd3Mh?=
H1650 MonGSpVv[3Srb36gRZN{[Xl? MlXjOVAxyqCwTR?= NHfrN3IzPMLiaB?= Mn3BSG1UVw>? NFfDemtl\WO{ZXHz[ZMhTUeIUjDlfJBz\XO|aX;u MkPJNlM2OTV5NUK=
PC9 M4m5SmZ2dmO2aX;uJGF{e2G7 M4nmPFUxOMLibl2= MXSyOOKhcA>? NHXnWHFFVVOR MYnk[YNz\WG|ZYOgSWdHWiCneIDy[ZN{cW:w MYCyN|UyPTd3Mh?=
H460 MnLoSpVv[3Srb36gRZN{[Xl? M17YSVAvPS9zL{Kg{txO NUOwe2dHPCCq MUHEUXNQ M1;UNolvcGmkaYTzJJRp\SCuZY\lcJMhd2ZiQXv0JEhxNUGtdDmgZY5lKEWJRmK= MVKyN|UyPTd3Mh?=
H1650 MnHISpVv[3Srb36gRZN{[Xl? NYT6b41lOC53L{GvNkDPxE1? MnPlOEBp NYnnXXhuTE2VTx?= MXrpcohq[mm2czD0bIUhdGW4ZXzzJI9nKEGtdDCodE1Cc3RrIHHu[EBGT0[U M1:y[|I{PTF3N{Wy
PC9 NWnsd5Y{TnWwY4Tpc44hSXO|YYm= MkHUNE42NzFxMjFOwG0> NYnDUWZ{PCCq MVfEUXNQ NV;VRnlncW6qaXLpeJMhfGinIHzleoVteyCxZjDBb5QhMHBvQXv0LUBidmRiRVfGVi=> MlfINlM2OTV5NUK=
AsPc1 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX[0PEBp MYnFR|UxRTBwMzFOwG0> M4q0NVI{PDd3Nkm1
Panc0327 M1TGNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWW0PEBp M{\OSWVEPTB;MD61JO69VQ>? NXzCT2VzOjN2N{W2PVU>
MiaPaCa2 NHPMOI5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX6xOlJwPDhiaB?= MnTISWM2OD1yLkeg{txO NHToc3gzOzR5NU[5OS=>
BxPc3 NHO5OlBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVnPNXpJPDhiaB?= MV7FR|UxRTFwMDFOwG0> MWeyN|Q4PTZ7NR?=
Panc0403 NXHyRol{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkPnOFghcA>? MnrwSWM2OD1zLkGg{txO MnLpNlM1PzV4OUW=
Panc1005 Ml\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX7qWIt7PDhiaB?= NWLrUllmTUN3ME2xMlEh|ryP NELIS5EzOzR5NU[5OS=>
PL45 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4mwb|Q5KGh? NHrXcplGSzVyPUKwMlgh|ryP NGLSS4YzOzR5NU[5OS=>
Panc0203 MnPQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlzQOFghcA>? NYrkTo41TUN3ME2yNk4zKM7:TR?= M1nKdFI{PDd3Nkm1
Panc0327 M3OzbmFxd3C2b4Ppd{BCe3OjeR?= MVixJO69VQ>? NGP4TIYzPCCq NX2zc2RpcW6mdXPld{BieG:ydH;zbZM> MX6yN|Q4PTZ7NR?=
Panc1005 MYrBdI9xfG:|aYOgRZN{[Xl? NF3pc2gyKM7:TR?= NHjHPYozPCCq NXrBOWlYcW6mdXPld{BieG:ydH;zbZM> MWqyN|Q4PTZ7NR?=
Panc0403 MXrBdI9xfG:|aYOgRZN{[Xl? NVyyXFNMOSEQvF2= NEHYRYczPCCq M{fBfYlv\HWlZYOgZZBweHSxc3nz MkjSNlM1PzV4OUW=
AsPc1 NYP2[3g2TnWwY4Tpc44hSXO|YYm= NWq1VItqOS9zMDFOwG0> NIjydoQzPCCq MXnpcoR2[2W|IDDndo94fGhiYYLy[ZN1\WRiaX6gS|IwVQ>? MXyyN|Q4PTZ7NR?=
MiaPaCa2 NYDReWZuTnWwY4Tpc44hSXO|YYm= NEjqdXcyNzFyIN88US=> MnrtNlQhcA>? MonlbY5lfWOnczCg[5Jwf3SqIHHydoV{fGWmIHnuJGczN01? MmTUNlM1PzV4OUW=
T3M4 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1\oO|AuQDByIH7N MYO0PEBp NF2zSmFqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> Mn7KNlI3QDF4OUi=
AsPC-1 M3HnUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVSwMVgxOCCwTR?= MW[0PEBp MXvpcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NHfMe3UzOjZ6MU[5PC=>
Panc-1  NVrrNolvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1rQPVAuQDByIH7N MljNOFghcA>? MUnpcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MlvCNlI3QDF4OUi=
T3M4 NWSyPJFbSXCxcITvd4l{KEG|c3H5 NXjrWlRLOTByL{WwNE8yODByIH7N M{LDVVQ5KGh? MX\pcoR2[2W|IHTvd4Uh\GWyZX7k[Y51KGGyb4D0c5Nqew>? MUKyNlY5OTZ7OB?=
AsPC-1 Mk\DRZBweHSxc3nzJGF{e2G7 M2jDXFExOC93MECvNVAxOCCwTR?= M1v6fFQ5KGh? NGDkWo5qdmS3Y3XzJIRwe2ViZHXw[Y5l\W62IHHwc5B1d3Orcx?= M1\xO|IzPjhzNkm4
Panc-1  NHzlRodCeG:ydH;zbZMhSXO|YYm= MV2xNFAwPTByL{GwNFAhdk1? MXe0PEBp NVq3S|VVcW6mdXPld{Bld3OnIHTldIVv\GWwdDDhdI9xfG:|aYO= Mm\XNlI3QDF4OUi=
HBL-2 NVT0fIJtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NULTdZhuOjRiaB?= NIm0V|lKSzVyPUCuOEDPxE1? NYDtcVJkOjByNkiwPFA>
Jeko-1 M1vjXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVnTV5o2OjRiaB?= M3HCRWlEPTB;MD6yJO69VQ>? NXnEWmluOjByNkiwPFA>
Granta-519 NYDIbGljT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXGyOEBp Mmf1TWM2OD13Nj6zJO69VQ>? NFzkbXEzODB4OEC4NC=>
HCT116 NW[5Noc2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MU[0PEBp NVzaUHJpTUN3ME2wMlI5KM7:TR?= MXyxO|EzPDV7NB?=
HCT116 NEjteXdHfW6ldHnvckBCe3OjeR?= MYCwMlnDqM7:TdMg MkTENlQhcA>? MYnkc5dvNXKnZ4XsZZR{KFSVIIDyc5RmcW5ibHX2[Yx{KGGodHXyJFbDqGhiaX7jeYJifGmxbh?= MmHUNVcyOjR3OUS=

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

体内試験 Belinostat indicates significant tumor growth delay in A2780 and A2780/cp70 xenograft at a dose of 10mg/kg with no effects on the body weight. [1] Belinostat also induces p21WAF1, HDAC core and cell communication genes in mouse bladder tumors. [2] Belinostat monotherapy induces dose-proportional antitumor effects with TGI of 47% at a dose of 100mg/kg in A2780 xenograft. The combination of Belinostat (100 mg/kg) with carboplatin (40 mg/kg) could delay tumor growth from 18.6 days to 22.5 days. [3] Combining with bortezomib, Belinostat results in great tumor inhibition and gastrointestinal toxicity in mice with bortezomib-resistant UMSCC-11A xenograft. [5]

お薦めの試験操作(参考用のみ)

キナーゼ試験:[1]
+ 展開

Histone Deacetylase Activity:

Subconfluent cultures are harvested and washed twice in ice cold PBS and pelleted by centrifugation at 200 × g for 5 min. The cell pellet is resuspended in two volumes of lysis buffer [60 mM Tris buffer (pH 7.4) containing 30% glycerol and 450 mM NaCl] and lysed by three freeze (dry ice) thaw (30 °C water bath) cycles. Cell debris is removed by centrifugation at 1.2 × 104 g for 5 min, and the supernatant is stored at −80 °C. Histone H4 peptide (sequence SGRGKGGKGLGKGGAKRHRK corresponding to the 20 NH2-terminal residues) is acetylated by a recombinant protein containing the hypoxanthine-aminopterin-thymidine domain of p300, using [3H]acetyl CoA as a source of acetate. H4 peptide (100 μg) is mixed with hypoxanthine-aminopterin-thymidine buffer (50 mM Tris HCl pH 8.0, 5% glycerol, 50 mM KCl, and 0.1 mM EDTA), 1 mM DTT, 1 mM 4-(2-aminoethyl) benzenesulfonylfluoride, 1 × complete protease inhibitors, 50 μL of purified p300, and 1.85 m [3H]acetyl CoA (4.50Ci/mmol) in a final volume of 300 μL and incubated at 30 °C for 45 min. The p300 protein is removed by incubation with 20 μL of 50% Ni-agaroase beads for 1 hour at 4 °C and centrifugation. The supernatant is applied to a 2 mL Sephadex G15 column, and the flow through is collected. One milliliter of distilled H2O is gently applied, and three drop fractions are collected; this is repeated until 4–5 mL of distilled H2O has been added, and ∼40 fractions are collected. Three microliters of each fraction are diluted in 2 mL of scintillation fluid and counted in a scintillation counter to identify the fractions containing the labeled peptide. These fractions are pooled, and 1 μL of the combined sample is measured to assess the radioactivity in every peptide batch (3-7×103 cpm/μL). For activity assays, the reaction is carried out in a total volume of 150 μL of buffer [60 mM Tris (pH 7.4) containing 30% glycerol] containing 2 μL of cell extract and, where used, 2 μL of belinostat. The reaction is started by the addition of 2 μL of [3H] labeled substrate (acetylated histone H4 peptide corresponding to the 20 NH2-terminal residues). Samples are incubated at 37 °C for 45 min, and the reaction stopped by the addition of HCl and acetic acid (0.72 and 0.12 M final concentrations, respectively). Released [3H]acetate is extracted into 750 μL of ethyl acetate, and samples are centrifuged at 1.2× 104 g for 5 min. The upper phase (600 μL) is transferred to 3 mL of scintillation fluid and counted.
細胞試験: [1]
+ 展開
  • 細胞株: A2780, A2780/cp70, 2780AD, HCT116, HT29, WIL, CALU-3, MCF7, PC3 and HS852
  • 濃度: 0.016 - 10 μM
  • 反応時間: 24 hours
  • 実験の流れ: Tumor cell lines are seeded in 5 mL of medium at a density of 8 × 104 cells/25 cm2 flask and incubated for 48 hours. Cells are exposed to Belinostat (0.016 to 10 μM) for 24 hours. The medium is removed, and 1 mL of trypsin/EDTA is added to each flask. Once the cells have detached, 1 mL of medium is added, the cells are resuspended, and those from the control untreated flask are counted. Cells are diluted and plated into 6-cm Petri dishes (three per flask) at a density of 0.5-2× 103 cells/dish depending on the cell line. Cells from the drug-treated flasks are diluted and plated as for the control flasks. Dishes are incubated for 10–15 days at 37 °C. Cells are washed with PBS, fixed in methanol, and stained with crystal violet, and colonies that contained ≥50 cells counted. Sensitivity is expressed as the IC50 defined as the concentration of belinostat required to reduce the number of colonies to 50% of that of the control untreated cells.
    (参考用のみ)
動物試験:[1]
+ 展開
  • 動物モデル: A2780, A2780/cp70 and HCT116 cells are injected s.c. into the right flank of CD1 nu/nu mice.
  • 製剤: Dissolved in DMSO and then diluted in water to give a final concentration of DMSO of 10%
  • 投薬量: ≤40 mg/kg
  • 投与方法: Administered via i.p.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 64 mg/mL (201.03 mM)
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(文献ではなく、Selleckの実験によるデータ):
2% DMSO+30% PEG 300+ddH2O
混合させたのち直ちに使用することを推奨します。
10mg/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。

化学情報

分子量 318.35
化学式

C15H14N2O4S

CAS No. 414864-00-9
保管
in solvent
別名 NSC726630, PX-105684

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モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備するために必要な希釈率を計算してください。Selleck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

希釈の計算式

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

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 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):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

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

モル濃度計算器

質量 濃度 体積 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03432741 Recruiting Breast Adenocarcinoma|Recurrent Breast Carcinoma|Recurrent Hodgkin Lymphoma|Recurrent Mycosis Fungoides|Recurrent Non-Hodgkin Lymphoma|Recurrent Primary Cutaneous T-Cell Non-Hodgkin Lymphoma|Refractory Hodgkin Lymphoma|Refractory Mycosis Fungoides|Refractory Nodal Marginal Zone Lymphoma|Refractory Non-Hodgkin Lymphoma|Refractory Primary Cutaneous T-Cell Non-Hodgkin Lymphoma|Stage IV Breast Cancer AJCC v6 and v7 Mayo Clinic|National Cancer Institute (NCI) March 27 2018 Phase 1
NCT02737046 Recruiting Adult T-cell Leukemia-Lymphoma|ATLL University of Miami December 12 2016 Phase 2
NCT02875002 Withdrawn Relapsed and Refractory Aggressive B- and T-cell Lymphomas|Lymphoma Yale University|Massey Cancer Center|Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins October 2016 Phase 1
NCT02701673 Withdrawn Lymphoma M.D. Anderson Cancer Center June 2016 Phase 1|Phase 2
NCT02680795 Recruiting Solid Tumors|Hematological Malignancies Spectrum Pharmaceuticals Inc March 2016 Phase 1
NCT02679131 Terminated Relapsed/Refractory Solid Tumors/Hematological Malignancies Spectrum Pharmaceuticals Inc March 2016 Phase 1

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

よくある質問(FAQ)

  • 質問1:

    Could you please give some suggestions for the use of Belinostat in vivo (i.p. injection)?

  • 回答:

    For I.P. injection, S1085 Belinostat (PXD101) can be dissolved in 2% DMSO+30% PEG 300+ddH2O at 10 mg/ml clearly. When preparing the solution, please dissolve the compound in DMSO clearly first. Then add PEG, after they mixed well, then dilute with water. Hope this information is useful to you.

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Tags: Belinostat (PXD101)を買う | Belinostat (PXD101) ic50 | Belinostat (PXD101)供給者 | Belinostat (PXD101)を購入する | Belinostat (PXD101)費用 | Belinostat (PXD101)生産者 | オーダーBelinostat (PXD101) | Belinostat (PXD101)化学構造 | Belinostat (PXD101)分子量 | Belinostat (PXD101)代理店
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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID