Belinostat (PXD101)

目录号:S1085 别名: NSC726630, PX-105684

Belinostat (PXD101) Chemical Structure

Molecular Weight(MW): 318.35

Belinostat (PXD101)是一种新型HDAC抑制剂,无细胞试验中IC50为27 nM,对耐Cisplatin的肿瘤具有活性。

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RMB 1317.13 现货
RMB 981.69 现货
RMB 3030.32 现货
RMB 4653.78 现货
RMB 7950.07 现货
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客户使用该产品的8个实验数据:

  • 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.

产品安全说明书

HDAC抑制剂选择性比较

生物活性

产品描述 Belinostat (PXD101)是一种新型HDAC抑制剂,无细胞试验中IC50为27 nM,对耐Cisplatin的肿瘤具有活性。
特性 Belinostat是Topotarget的领先药物,已经进行过多次临床试验。
靶点
HDAC [1]
(Cell-free assay)
27 nM
体外研究

Belinostat抑制肿瘤细胞生长(包括A2780, HCT116, HT29, WIL, CALU-3, MCF7, PC3,及HS852),IC50为0.2到0.66 μM。Belinostat 作用于A2780/cp70 和2780AD细胞时活性很低, 这两个细胞是抗cisplatin和doxorubicin的A2780细胞衍生的。Belinostat通过PARP分裂和组蛋白H3/H4的乙酰化而诱导细胞凋亡。[1] Belinostat抑制膀胱癌细胞生长,尤其是5637细胞,细胞在G0-G1期积累, 在S期下降,在 G2-M期上升。[2] Belinostat抑制细胞生长的活性不受多重耐药表现型的影响, 但是docetaxel的活性明显受影响。Belinostat 可以增强docetaxel或carboplatin 抑制OVCAR-3和A2780细胞的活性。Belinostat作用于卵巢癌细胞系也增强微管乙酰化作用。[3] 最新研究显示 Belinostat在TGF-β信号依赖机制中激活蛋白激酶A 和降低survivin mRNA。[4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NB4 MXzD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M32yV|AvOi9{wrFOwG0> NX\rcGh3OjRxNEivO|IhcA>? M2rn[oRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBjd3SqIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MnTGNlU5PjR5M{K=
HL-60  NXjkeol{S2WubDDWbYFjcWyrdImgRZN{[Xl? MXWwMlIwOsLizszN NVv2NYVJOjRxNEivO|IhcA>? MUnk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZo91cCC2aX3lJIFv\CCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NIqyS5QzPTh4NEezNi=>
NB4 NWmxUZVQTnWwY4Tpc44hSXO|YYm= MYOyxsDPxE1? NIfoVI4zPC92ODDo M3La[IJtd2OtczDj[YxtKGO7Y3zlJIlvKFNicHjhd4U> NYGyeJYxOjV6NkS3N|I>
HL-60  NYfPOGM{TnWwY4Tpc44hSXO|YYm= NVvIVFMzOsLizszN NWCzW3JKOjRxNEigbC=> NGPIUGpjdG:la4OgZ4VtdCCleXPs[UBqdiCVIIDoZZNm NGOy[m8zPTh4NEezNi=>
NB4 M2HrOmZ2dmO2aX;uJGF{e2G7 MVGwMlLDqM7:TR?= M4LLZ|I1NzR6L{eyJIg> M1TVNoVvcGGwY3XzJHJCNWmwZIXj[YQh\3KjboXsc4N6fGmlIHTp[oZmemWwdHnheIlwdg>? NU\L[4FoOjV6NkS3N|I>
HL-60  NWn1bGwzTnWwY4Tpc44hSXO|YYm= MknZNE4zyqEQvF2= M3H1XVI1NzR6L{eyJIg> M3ywW4VvcGGwY3XzJHJCNWmwZIXj[YQh\3KjboXsc4N6fGmlIHTp[oZmemWwdHnheIlwdg>? NVfnXXdxOjV6NkS3N|I>
PANC-1 NYLablFTTnWwY4Tpc44hSXO|YYm= NH25bFIyOMLizszN NUXBSo8yOi92L{[gbC=> NXzCPWEyTE2VTx?= NG\oVYhqdmS3Y3XzJGFOWEtiYXP0bZZifGmxbh?= MYmyN|c1OzF7OB?=
PANC-1 NX\pdWhxS2WubDDWbYFjcWyrdImgRZN{[Xl? M3OzXVEwOTEEoN88US=> NI\qSZg1QCCq NWf4N4tvTE2VTx?= MVrk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NEfMco8zOzd2M{G5PC=>
PANC-1 NUDob2lVTnWwY4Tpc44hSXO|YYm= NYXpSVAyOTEEoN88US=> MYOyM|QhcA>? MmP2SG1UVw>? NEDUZnlqdmO{ZXHz[ZMhcW62cnHj[YxtfWyjcjDSU3MhdGW4ZXy= NVvGTm4xOjN5NEOxPVg>
H1666 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVLGSXBVPzMEoHi= MXrEUXNQ MniyTWM2OD5zMDFOwG0> MXSyN|UyPTd3Mh?=
H460 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPPO|LDqGh? NV;kVHplTE2VTx?= NF3WZpBKSzVyPUCuPFYh|ryP NX\JfWRKOjN3MUW3OVI>
H1299 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVS3NuKhcA>? NEO5Oo9FVVOR M2HVVmlEPTB;MT6yJO69VQ>? NXnIRWcyOjN3MUW3OVI>
H520 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYfM[GpSPzMEoHi= M33JUWROW09? NH\5d5lKSzVyPUCuO|Uh|ryP M1HzZVI{PTF3N{Wy
H1975 MoP1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVm3NuKhcA>? NXW5WpJXTE2VTx?= M4W1cmlEPTB;MD62PEDPxE1? NVW0dXFEOjN3MUW3OVI>
H1650 M33MS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3PvW|czyqCq NGTxVWJFVVOR NX63[I9UUUN3ME2wMlg5KM7:TR?= MnHVNlM2OTV5NUK=
H820 MlzCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXjlfolTPzMEoHi= NUK5cFU2TE2VTx?= Ml34TWM2OD1yLkSg{txO NGPkU2EzOzVzNUe1Ni=>
PC9 M2L1WWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYm3NuKhcA>? NGi1U2lFVVOR M3XRWWlEPTB;MD6yPUDPxE1? MXGyN|UyPTd3Mh?=
HCC2279 M2DTVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEjMO3o4OsLiaB?= NFX3[IRFVVOR M13YbmlEPTB;MD60JO69VQ>? MkPONlM2OTV5NUK=
HCC827 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX23NuKhcA>? NYXwWZJCTE2VTx?= M1PyN2lEPTB;MD6yPUDPxE1? Ml7oNlM2OTV5NUK=
HCC2935 M{LVXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoLZO|LDqGh? NYHkeHFxTE2VTx?= NIm3PVBKSzVyPUCuPVch|ryP NXWyephnOjN3MUW3OVI>
HCC4006 NFzjPJJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnXLO|LDqGh? NIDwWolFVVOR Mm\3TWM2OD1yLkS2JO69VQ>? NF7iOGkzOzVzNUe1Ni=>
H460 M3O4[GZ2dmO2aX;uJGF{e2G7 M4fkTFUxOMLibl2= M2LNe|I1yqCq M{jTcmROW09? NYXjfVZp\GWlcnXhd4V{KEWJRmKg[ZhxemW|c3nvci=> MnPJNlM2OTV5NUK=
H1650 NHjDenRHfW6ldHnvckBCe3OjeR?= MlvmOVAxyqCwTR?= MoTPNlTDqGh? NH7MeGdFVVOR MkHT[IVkemWjc3XzJGVITlJiZYjwdoV{e2mxbh?= NHvWT4wzOzVzNUe1Ni=>
PC9 NH34W45HfW6ldHnvckBCe3OjeR?= MWK1NFDDqG6P NFroZoczPMLiaB?= MnXXSG1UVw>? MUfk[YNz\WG|ZYOgSWdHWiCneIDy[ZN{cW:w NXvsVmJzOjN3MUW3OVI>
H460 MoPXSpVv[3Srb36gRZN{[Xl? NFHwbGMxNjVxMT:yJO69VQ>? NHPXRWY1KGh? MoCzSG1UVw>? NFnqe2NqdmirYnn0d{B1cGVibHX2[Yx{KG:oIFHreEApeC2Da4SpJIFv\CCHR1\S NIK2eYMzOzVzNUe1Ni=>
H1650 NX7aUWw4TnWwY4Tpc44hSXO|YYm= Mlj3NE42NzFxMjFOwG0> NGOwTGk1KGh? NIH1S2FFVVOR Mk[0bY5pcWKrdIOgeIhmKGyndnXsd{Bw\iCDa4SgLJAuSWu2KTDhcoQhTUeIUh?= MkXMNlM2OTV5NUK=
PC9 NELxT4RHfW6ldHnvckBCe3OjeR?= MYiwMlUwOS9{IN88US=> NGjjUG01KGh? MkO1SG1UVw>? Mke4bY5pcWKrdIOgeIhmKGyndnXsd{Bw\iCDa4SgLJAuSWu2KTDhcoQhTUeIUh?= MlSxNlM2OTV5NUK=
AsPc1 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2H1RlQ5KGh? MV;FR|UxRTBwMzFOwG0> MU[yN|Q4PTZ7NR?=
Panc0327 M4KxVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\tZ2I1QCCq MWLFR|UxRTBwNTFOwG0> MVuyN|Q4PTZ7NR?=
MiaPaCa2 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIrQdHk1QCCq MlzoSWM2OD1yLkeg{txO NFziSXkzOzR5NU[5OS=>
BxPc3 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY[0PEBp MnXpSWM2OD1zLkCg{txO MX6yN|Q4PTZ7NR?=
Panc0403 NWPDRWFmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUe0PEBp NUPKeJE1TUN3ME2xMlEh|ryP NWfUWotDOjN2N{W2PVU>
Panc1005 M{LsbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUS0PEBp MnToSWM2OD1zLkGg{txO MX6yN|Q4PTZ7NR?=
PL45 MoHnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MljQOFghcA>? NV\3SVFwTUN3ME2yNE45KM7:TR?= NXnJTFhQOjN2N{W2PVU>
Panc0203 NUjqcVQ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M361cVQ5KGh? NEP3dJFGSzVyPUKyMlIh|ryP NEPiT5QzOzR5NU[5OS=>
Panc0327 MWrBdI9xfG:|aYOgRZN{[Xl? MWWxJO69VQ>? NHfSfIgzPCCq NWPKN3dZcW6mdXPld{BieG:ydH;zbZM> Mlm4NlM1PzV4OUW=
Panc1005 NGHjfppCeG:ydH;zbZMhSXO|YYm= MXyxJO69VQ>? NFPUNJYzPCCq NE\mOlVqdmS3Y3XzJIFxd3C2b4Ppdy=> MUeyN|Q4PTZ7NR?=
Panc0403 MYjBdI9xfG:|aYOgRZN{[Xl? M3fMVFEh|ryP NH\k[mgzPCCq NIizRnNqdmS3Y3XzJIFxd3C2b4Ppdy=> MUmyN|Q4PTZ7NR?=
AsPc1 Mnq3SpVv[3Srb36gRZN{[Xl? MoHTNU8yOCEQvF2= NIjqZWkzPCCq NYL4WGdTcW6mdXPld{Ah\3Kxd4ToJIFzemW|dHXkJIlvKEd{L12= MoXjNlM1PzV4OUW=
MiaPaCa2 M1PTTWZ2dmO2aX;uJGF{e2G7 MXuxM|ExKM7:TR?= Mn\DNlQhcA>? Mne4bY5lfWOnczCg[5Jwf3SqIHHydoV{fGWmIHnuJGczN01? NEP2OWUzOzR5NU[5OS=>
T3M4 M{i1fWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFvwWXUxNThyMDDuUS=> Mn\rOFghcA>? MXnpcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NV2zXZd{OjJ4OEG2PVg>
AsPC-1 MkPkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX:wMVgxOCCwTR?= MkD4OFghcA>? MnzQbY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;uJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NHLIWZczOjZ6MU[5PC=>
Panc-1  Mk\nS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVywMVgxOCCwTR?= M{LZd|Q5KGh? MlWybY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;uJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MmWwNlI3QDF4OUi=
T3M4 NELzd5JCeG:ydH;zbZMhSXO|YYm= M4fke|ExOC93MECvNVAxOCCwTR?= MlL4OFghcA>? MWLpcoR2[2W|IHTvd4Uh\GWyZX7k[Y51KGGyb4D0c5Nqew>? NGm2TWwzOjZ6MU[5PC=>
AsPC-1 NH\ZZnBCeG:ydH;zbZMhSXO|YYm= M1LUR|ExOC93MECvNVAxOCCwTR?= MlHvOFghcA>? MmGwbY5lfWOnczDkc5NmKGSncHXu[IVvfCCjcH;weI9{cXN? NF3FWZkzOjZ6MU[5PC=>
Panc-1  NVnoTXBISXCxcITvd4l{KEG|c3H5 M1rmblExOC93MECvNVAxOCCwTR?= MWW0PEBp MoH0bY5lfWOnczDkc5NmKGSncHXu[IVvfCCjcH;weI9{cXN? NWnTRohkOjJ4OEG2PVg>
HBL-2 MkOzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2fKbVI1KGh? M2\1bWlEPTB;MD60JO69VQ>? M3\yVVIxODZ6MEiw
Jeko-1 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUjWUoNXOjRiaB?= NVS5Rmo{UUN3ME2wMlIh|ryP MkDZNlAxPjhyOEC=
Granta-519 NILld|RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVuyOEBp MVzJR|UxRTV4LkOg{txO MonnNlAxPjhyOEC=
HCT116 Mof3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MonLOFghcA>? MlfaSWM2OD1yLkK4JO69VQ>? NI\tenMyPzF{NEW5OC=>
HCT116 MVfGeY5kfGmxbjDBd5NigQ>? Moj2NE46yqEQvF5CpC=> MUWyOEBp NWDiTJhV\G:5bj3y[Yd2dGG2czDUV{Bxem:2ZXnuJIxmfmWuczDh[pRmeiB4wrDoJIlv[3WkYYTpc44> NHfSPHEyPzF{NEW5OC=>

... Click to View More Cell Line Experimental Data

体内研究 Belinostat按10mg/kg剂量处理A2780和A2780/cp70 移植瘤,明显延迟肿瘤生长,但是对动物体重没有影响。[1] 在鼠膀胱细胞中,Belinostat也诱导p21WAF1, HDAC 核心和细胞通讯基因。[2] Belinostat按100mg/kg剂量单独处理A2780移植瘤,产生抗癌功效,肿瘤抑制率(TGI)达47% ,这种抑制存在剂量依赖性。100 mg/kg Belinostat和40 mg/kg Carboplatin联用可以延迟肿瘤生长,从18.6 天到22.5 天。 [3] Bortezomib和Belinostat联用,明显抑制肿瘤,此外,作用于携带抗Bortezomib UMSCC-11A移植瘤的鼠显示肠胃毒性 。[5]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:[1]
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组蛋白脱乙酰基酶活性实验:

汇合培养,用冷PBS中冲洗2遍,按200×g 转速离心5分钟。 细胞悬浮在2体积的溶解 buffer 中,60 mm Tris buffer (pH 为7.4)包含30%甘油和450 mm NaCl,用干冰冻结,然后30oC水浴溶解,循环3次。细胞碎片按1.2×104g转速离心5分钟, 然后上清液储存于−80oC中。使用 [3H]乙酰 CoA,通过p300的重组蛋白包括次黄嘌呤-氨基喋呤-胸腺嘧啶域乙酰化组蛋白H4肽段 (序列为SGRGKGGKGLGKGGAKRHRK)。100 μg H4 肽段与次黄嘌呤-氨基喋呤-胸腺嘧啶buffer(buffer包含50 mM Tris HCl pH为8.0, 5% 甘油, 50 mM KCl, 和0.1 mM EDTA),1 mM DTT, 1 mM 4-(2-氨乙基) ,苯磺酰基氟化物, 1×蛋白酶抑制剂, 50 μL纯化的p300, 及1.85 m [3H]乙酰 CoA (4.50Ci/mmol)混合,最终体积为300 μL,在30oC温育45分钟。p300蛋白 和 20 μL 50% Ni-琼脂糖在4oC下温育1小时,然后离心分离。上清液上样到2 mL Sephadex G15 柱中。加入1毫升蒸馏水,收集三滴样片,重复加入蒸馏水直到体积为4-5 mL,收集40滴样片。用2 mL 闪烁液稀释3微升样片,在闪烁计数板上计数,用于鉴定包含标记肽段的样片。合并样片,测定1 μL组合样本,用于测定每个肽段的放射性。在150 μL buffer,2 μL 细胞抽提物,和2 μL Belinostat的混合液中进行反应。加入2 μL [3H] 标记的底物开始反应。样本在 37oC下温育45分钟,加入HCl 和乙酸(终浓度分别为0.72和0.12 M)终止反应。释放的[3H]乙酸盐加到750 μL of 乙酸乙酯中, 按1.2×104g转速 离心5分钟。上层 (600 μL) 转移到3 mL闪烁液,然后计数。
细胞实验:[1]
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  • Cell lines: A2780, A2780/cp70, 2780AD, HCT116, HT29, WIL, CALU-3, MCF7, PC3,和HS852细胞
  • Concentrations: 0.016到10 μM
  • Incubation Time: 24小时
  • Method: 肿瘤细胞系(A2780, A2780/cp70, 2780AD, HCT116, HT29, WIL, CALU-3, MCF7, PC3,和HS852) 按8×104个细胞/25 cm2 瓶接种在5 mL 培养基中,温育48小时。用Belinostat (0.016 到 10 μm)处理细胞24小时。1 mL 胰蛋白酶/EDTA加到培养瓶中。细胞分离后,加入1 mL培养基,细胞再次悬浮。稀释细胞,按0.5-2×103个细胞/皿移到6cm Petri皿中。37oC下温育10到15天。用PBS冲洗细胞,溶于甲醇,用结晶紫染色,计数大于50个细胞的群落。通过IC50值计算敏感度。
    (Only for Reference)
动物实验:[1]
+ 展开
  • Animal Models: 右侧腹皮下注射A2780, A2780/cp70和HCT116细胞的CD1 nu/nu鼠
  • Formulation: Belinostat 溶解在DMSO中,然后用水稀释,最终浓度10%
  • Dosages: ≤40 mg/kg
  • Administration: 腹腔注射
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 64 mg/mL (201.03 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
2% DMSO+30% PEG 300+ddH2O
10mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 318.35
化学式

C15H14N2O4S

CAS号 414864-00-9
稳定性 powder
in solvent
别名 NSC726630, PX-105684

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01100944 Terminated Thymoma|Thymic Carcinoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) March 4 2010 Phase 1|Phase 2
NCT01686165 Completed Anaplastic Large Cell Lymphoma|Recurrent Adult Diffuse Large Cell Lymphoma|Recurrent Mantle Cell Lymphoma University of Arizona|National Cancer Institute (NCI) August 31 2012 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 Recruiting Relapsed/Refractory Solid Tumors/Hematological Malignancies Spectrum Pharmaceuticals Inc March 2016 Phase 1

技术支持

在订购、运输、储存和使用我们的产品的任何阶段,您遇到的任何问题,均可以通过拨打我们的热线电话400-668-6834,或者技术支持邮箱tech@selleck.cn,直接联系到我们。我们会在24小时内尽快联系您。

操作手册

如果有其他问题,请给我们留言。

  • * 必填项

常见问题及建议解决方法

  • 问题 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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID