Belinostat (PXD101)

Catalog No.S1085 Synonyms: NSC726630, PX-105684

Belinostat (PXD101) Chemical Structure

Molecular Weight(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.

Size Price Stock Quantity  
In DMSO USD 160 In stock
USD 120 In stock
USD 370 In stock
USD 570 In stock
USD 970 In stock
Bulk Discount

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

8 Customer Reviews

  • 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.

Purity & Quality Control

Choose Selective HDAC Inhibitors

Biological Activity

Description Belinostat (PXD101) is a novel HDAC inhibitor with IC50 of 27 nM in a cell-free assay, with activity demonstrated in cisplatin-resistant tumors.
Features Lead compound of Topotarget.
Targets
HDAC [1]
(Cell-free assay)
27 nM
In vitro

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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NB4 NGeyd|JE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NVH4d2J4OC5{L{NCpO69VQ>? MW[yOE81QC95MjDo M2TZcoRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBjd3SqIITpcYUh[W6mIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MXKyOVg3PDd|Mh?=
HL-60  MV3D[YxtKF[rYXLpcIl1gSCDc4PhfS=> Ml:3NE4zNzMEoN88US=> NVHV[YdpOjRxNEivO|IhcA>? NHPBd4pl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[m:2aDD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NVXmO5hVOjV6NkS3N|I>
NB4 NGPtb2RHfW6ldHnvckBCe3OjeR?= MoPzNuKh|ryP MofRNlQwPDhiaB?= MYjicI9kc3NiY3XscEBkgWOuZTDpckBUKHCqYYPl M3raPVI2QDZ2N{Oy
HL-60  NGnOVXhHfW6ldHnvckBCe3OjeR?= MXOyxsDPxE1? NHrtVmczPC92ODDo MmXjZoxw[2u|IHPlcIwh[3mlbHWgbY4hWyCyaHHz[S=> M4C2dVI2QDZ2N{Oy
NB4 MoPLSpVv[3Srb36gRZN{[Xl? MYqwMlLDqM7:TR?= MkLqNlQwPDhxN{KgbC=> MVTlcohidmOnczDSRU1qdmS3Y3XkJIdz[W63bH;jfZRq[yCmaX\m[ZJmdnSrYYTpc44> NGLGboszPTh4NEezNi=>
HL-60  Ml7aSpVv[3Srb36gRZN{[Xl? M3fCO|AvOsLizszN NWPoco9lOjRxNEivO|IhcA>? MUnlcohidmOnczDSRU1qdmS3Y3XkJIdz[W63bH;jfZRq[yCmaX\m[ZJmdnSrYYTpc44> M17UbFI2QDZ2N{Oy
PANC-1 M1\3SWZ2dmO2aX;uJGF{e2G7 NHP4dI0yOMLizszN NXXZ[4tvOi92L{[gbC=> NIT4SGRFVVOR NWP0N4JJcW6mdXPld{BCVVCNIHHjeIl3[XSrb36= NUThfoRyOjN5NEOxPVg>
PANC-1 M3rsdGNmdGxiVnnhZoltcXS7IFHzd4F6 Ml[wNU8yOMLizszN Ml3POFghcA>? M{iy[GROW09? NFewXXFl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NHnSfVIzOzd2M{G5PC=>
PANC-1 M4DoUWZ2dmO2aX;uJGF{e2G7 MmjWNVDDqM7:TR?= MYKyM|QhcA>? M1rXdGROW09? NIDEdHdqdmO{ZXHz[ZMhcW62cnHj[YxtfWyjcjDSU3MhdGW4ZXy= NV;Hc4pnOjN5NEOxPVg>
H1666 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVS3NuKhcA>? NE\pPZBFVVOR MVTJR|UxRjFyIN88US=> NF;UTFQzOzVzNUe1Ni=>
H460 NXLqU4ZXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2r1OVczyqCq M3f5TmROW09? MVzJR|UxRTBwOE[g{txO MWKyN|UyPTd3Mh?=
H1299 NITKTo1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7WSnplPzMEoHi= MVHEUXNQ M{nhR2lEPTB;MT6yJO69VQ>? MoDPNlM2OTV5NUK=
H520 M1zWe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnnBO|LDqGh? MnHnSG1UVw>? NYf6XXNrUUN3ME2wMlc2KM7:TR?= NYjYU4FLOjN3MUW3OVI>
H1975 MnLrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVmxRWZqPzMEoHi= M1S5XmROW09? MkXXTWM2OD1yLk[4JO69VQ>? NH;0fIozOzVzNUe1Ni=>
H1650 MljJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVy3NuKhcA>? M{jvOmROW09? NWPPdnFwUUN3ME2wMlg5KM7:TR?= NFPpUXQzOzVzNUe1Ni=>
H820 NHXOcYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUO3UFhxPzMEoHi= NF;KVYJFVVOR MkPzTWM2OD1yLkSg{txO NGrVS2ozOzVzNUe1Ni=>
PC9 MlXJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1HxdlczyqCq NH\sWGJFVVOR MVzJR|UxRTBwMkmg{txO MVeyN|UyPTd3Mh?=
HCC2279 M1nnbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVftSYpsPzMEoHi= M4[3fmROW09? NHu2d5dKSzVyPUCuOEDPxE1? NYrscnNLOjN3MUW3OVI>
HCC827 MoLLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVnQR4pmPzMEoHi= M1rvdWROW09? MnS4TWM2OD1yLkK5JO69VQ>? M1vrc|I{PTF3N{Wy
HCC2935 NGfjeINIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXzoOWo5PzMEoHi= MmfhSG1UVw>? NXP4eo5YUUN3ME2wMlk4KM7:TR?= Ml\YNlM2OTV5NUK=
HCC4006 MmXqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkfWO|LDqGh? MYLEUXNQ MXzJR|UxRTBwNE[g{txO NWnX[ZJ6OjN3MUW3OVI>
H460 NHTkfm5HfW6ldHnvckBCe3OjeR?= NWDHdY1VPTBywrDuUS=> MUCyOOKhcA>? NIHXd2ZFVVOR MkTN[IVkemWjc3XzJGVITlJiZYjwdoV{e2mxbh?= MlKyNlM2OTV5NUK=
H1650 NFP2c5FHfW6ldHnvckBCe3OjeR?= NXvNOmtNPTBywrDuUS=> NHq0T40zPMLiaB?= MVHEUXNQ M2rtVIRm[3KnYYPld{BGT0[UIHX4dJJme3Orb36= M3nicFI{PTF3N{Wy
PC9 M4mw[mZ2dmO2aX;uJGF{e2G7 MkXXOVAxyqCwTR?= NFO4bIgzPMLiaB?= MYHEUXNQ MV3k[YNz\WG|ZYOgSWdHWiCneIDy[ZN{cW:w MY[yN|UyPTd3Mh?=
H460 NHjuNFNHfW6ldHnvckBCe3OjeR?= NGnNTXoxNjVxMT:yJO69VQ>? NIOzZVQ1KGh? NUfMVZhLTE2VTx?= NXzM[mg3cW6qaXLpeJMhfGinIHzleoVteyCxZjDBb5QhMHBvQXv0LUBidmRiRVfGVi=> MV:yN|UyPTd3Mh?=
H1650 MknqSpVv[3Srb36gRZN{[Xl? NI\LWXUxNjVxMT:yJO69VQ>? M2XEd|QhcA>? NHPNcW5FVVOR NGPZWW1qdmirYnn0d{B1cGVibHX2[Yx{KG:oIFHreEApeC2Da4SpJIFv\CCHR1\S NV;EXnpHOjN3MUW3OVI>
PC9 MYPGeY5kfGmxbjDBd5NigQ>? NFPYfG0xNjVxMT:yJO69VQ>? NUnaZ2dqPCCq Mn;ZSG1UVw>? NG\ZSpRqdmirYnn0d{B1cGVibHX2[Yx{KG:oIFHreEApeC2Da4SpJIFv\CCHR1\S MmfCNlM2OTV5NUK=
AsPc1 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{DRVFQ5KGh? NHTUNWNGSzVyPUCuN{DPxE1? MYqyN|Q4PTZ7NR?=
Panc0327 NVPzO41kT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NELneo41QCCq M3rkVWVEPTB;MD61JO69VQ>? MmToNlM1PzV4OUW=
MiaPaCa2 NHz6fFVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3rKU|Q5KGh? NFHMO2xGSzVyPUCuO{DPxE1? NIDaPZozOzR5NU[5OS=>
BxPc3 M1LLc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnL5OFghcA>? MVTFR|UxRTFwMDFOwG0> NUL1WmtvOjN2N{W2PVU>
Panc0403 Mn[zS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7LOFghcA>? NGTtRYtGSzVyPUGuNUDPxE1? MnHINlM1PzV4OUW=
Panc1005 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUG0fZVkPDhiaB?= NYnUNW1LTUN3ME2xMlEh|ryP NV;3THV2OjN2N{W2PVU>
PL45 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV60PEBp NUi2b|NyTUN3ME2yNE45KM7:TR?= MoDxNlM1PzV4OUW=
Panc0203 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYS0PEBp NGXXcpBGSzVyPUKyMlIh|ryP M{fObFI{PDd3Nkm1
Panc0327 NXfPOHNjSXCxcITvd4l{KEG|c3H5 NGfwU2syKM7:TR?= NVy1XIprOjRiaB?= MVrpcoR2[2W|IHHwc5B1d3Orcx?= NELQZmIzOzR5NU[5OS=>
Panc1005 M4fzTmFxd3C2b4Ppd{BCe3OjeR?= NETOToUyKM7:TR?= Mm\0NlQhcA>? MnPFbY5lfWOnczDhdI9xfG:|aYO= NUS1eZMzOjN2N{W2PVU>
Panc0403 NW\2N4RwSXCxcITvd4l{KEG|c3H5 NVq1e|JuOSEQvF2= MWGyOEBp NGj2dmdqdmS3Y3XzJIFxd3C2b4Ppdy=> NVnYV|F5OjN2N{W2PVU>
AsPc1 M{fTWWZ2dmO2aX;uJGF{e2G7 M{Drd|EwOTBizszN MV2yOEBp MWDpcoR2[2W|IDDndo94fGhiYYLy[ZN1\WRiaX6gS|IwVQ>? NVTidVJEOjN2N{W2PVU>
MiaPaCa2 M{DiT2Z2dmO2aX;uJGF{e2G7 NGn0NHIyNzFyIN88US=> MlTkNlQhcA>? NXXHS4w6cW6mdXPld{Ah\3Kxd4ToJIFzemW|dHXkJIlvKEd{L12= MXKyN|Q4PTZ7NR?=
T3M4 MnvBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zMflAuQDByIH7N M4foWFQ5KGh? Mny0bY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;uJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NYHG[o5wOjJ4OEG2PVg>
AsPC-1 NF7zdYlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXSwMVgxOCCwTR?= MnrJOFghcA>? NH;MeZhqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NV7TNW1ZOjJ4OEG2PVg>
Panc-1  MkjDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4LyO|AuQDByIH7N NU\1ZYVxPDhiaB?= M2H6colvcGmkaYTzJINmdGxicILvcIln\XKjdHnvckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MmTSNlI3QDF4OUi=
T3M4 Ml7YRZBweHSxc3nzJGF{e2G7 NUTZVnlYOTByL{WwNE8yODByIH7N MnrtOFghcA>? MnrRbY5lfWOnczDkc5NmKGSncHXu[IVvfCCjcH;weI9{cXN? NIn3RXYzOjZ6MU[5PC=>
AsPC-1 NF6zcnBCeG:ydH;zbZMhSXO|YYm= MVuxNFAwPTByL{GwNFAhdk1? NFTzO5U1QCCq M4HWbolv\HWlZYOg[I9{\SCmZYDlcoRmdnRiYYDvdJRwe2m| MV2yNlY5OTZ7OB?=
Panc-1  NXXSWndUSXCxcITvd4l{KEG|c3H5 MUexNFAwPTByL{GwNFAhdk1? NE\Jb4I1QCCq M{XST4lv\HWlZYOg[I9{\SCmZYDlcoRmdnRiYYDvdJRwe2m| MWmyNlY5OTZ7OB?=
HBL-2 M1\NRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmfmNlQhcA>? MXPJR|UxRTBwNDFOwG0> MX[yNFA3QDB6MB?=
Jeko-1 NVrRdY1ET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYmyOEBp M{nU[2lEPTB;MD6yJO69VQ>? NE\Z[lkzODB4OEC4NC=>
Granta-519 NYDmSlYyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWTiVmk1OjRiaB?= NUH4bZhkUUN3ME21Ok4{KM7:TR?= NXjMZplOOjByNkiwPFA>
HCT116 MlfoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml3oOFghcA>? MXHFR|UxRTBwMkig{txO NWTUN4txOTdzMkS1PVQ>
HCT116 NYW5[Ig3TnWwY4Tpc44hSXO|YYm= Ml3oNE46yqEQvF5CpC=> NGHVeVEzPCCq M1jzZoRwf25vcnXneYxifHNiVGOgdJJwfGWrbjDs[ZZmdHNiYX\0[ZIhPsLiaDDpcoN2[mG2aX;u NWLZfpNzOTdzMkS1PVQ>

... Click to View More Cell Line Experimental Data

In vivo 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]

Protocol

Kinase Assay:[1]
+ Expand

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.
Cell Research:[1]
+ Expand
  • Cell lines: A2780, A2780/cp70, 2780AD, HCT116, HT29, WIL, CALU-3, MCF7, PC3 and HS852
  • Concentrations: 0.016 - 10 μM
  • Incubation Time: 24 hours
  • Method: 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.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: A2780, A2780/cp70 and HCT116 cells are injected s.c. into the right flank of CD1 nu/nu mice.
  • Formulation: Dissolved in DMSO and then diluted in water to give a final concentration of DMSO of 10%
  • Dosages: ≤40 mg/kg
  • Administration: Administered via i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 64 mg/mL (201.03 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order:
2% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.
10mg/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 318.35
Formula

C15H14N2O4S

CAS No. 414864-00-9
Storage powder
in solvent
Synonyms NSC726630, PX-105684

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

  • Mass
    Concentration
    Volume
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1
    V1
    C2
    V2

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • 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):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01273155 Recruiting Neoplasms|Lymphomas National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) December 22, 2010 Phase 1
NCT02737046 Recruiting Adult T-cell Leukemia-Lymphoma|ATLL University of Miami November 2016 Phase 2
NCT02875002 Not yet recruiting Relapsed and Refractory Aggressive B- and T-cell Lymphomas|Lymphoma Yale University|Massey Cancer Center|Sidney Kimmel Comprehensive Cancer Center October 2016 Phase 1
NCT02701673 Withdrawn Lymphoma M.D. Anderson Cancer Center June 2016 Phase 1|Phase 2
NCT02679131 Recruiting Relapsed/Refractory Solid Tumors/Hematological Malignancies Spectrum Pharmaceuticals, Inc March 2016 Phase 1
NCT02680795 Recruiting Solid Tumors|Hematological Malignancies Spectrum Pharmaceuticals, Inc March 2016 Phase 1

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.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

Frequently Asked Questions

  • Question 1:

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

  • Answer:

    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.

HDAC Signaling Pathway Map

HDAC Inhibitors with Unique Features

Related HDAC Products

Tags: buy Belinostat (PXD101) | Belinostat (PXD101) supplier | purchase Belinostat (PXD101) | Belinostat (PXD101) cost | Belinostat (PXD101) manufacturer | order Belinostat (PXD101) | Belinostat (PXD101) distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID