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
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6 Customer Reviews

  • (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 MYnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M{f1T|AvOi9{wrFOwG0> NHr1Rm0zPC92OD:3NkBp NEj0Omxl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[m:2aDD0bY1mKGGwZDDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MXGyOVg3PDd|Mh?=
HL-60  MYnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MmDKNE4zNzMEoN88US=> MXmyOE81QC95MjDo MnTq[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJIJwfGhidHnt[UBidmRiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M3q2RVI2QDZ2N{Oy
NB4 MonsSpVv[3Srb36gRZN{[Xl? MXGyxsDPxE1? MmPlNlQwPDhiaB?= MkHmZoxw[2u|IHPlcIwh[3mlbHWgbY4hWyCyaHHz[S=> M1f0OlI2QDZ2N{Oy
HL-60  MYDGeY5kfGmxbjDBd5NigQ>? MnfnNuKh|ryP NHfKfI0zPC92ODDo M1raRYJtd2OtczDj[YxtKGO7Y3zlJIlvKFNicHjhd4U> MnHONlU5PjR5M{K=
NB4 M1qwbWZ2dmO2aX;uJGF{e2G7 NVjUNYlZOC5{wrFOwG0> MUOyOE81QC95MjDo MWHlcohidmOnczDSRU1qdmS3Y3XkJIdz[W63bH;jfZRq[yCmaX\m[ZJmdnSrYYTpc44> NEnsdJgzPTh4NEezNi=>
HL-60  M2PqcWZ2dmO2aX;uJGF{e2G7 NYrpVoNOOC5{wrFOwG0> NFP3b4QzPC92OD:3NkBp MYflcohidmOnczDSRU1qdmS3Y3XkJIdz[W63bH;jfZRq[yCmaX\m[ZJmdnSrYYTpc44> MX:yOVg3PDd|Mh?=
PANC-1 MXjGeY5kfGmxbjDBd5NigQ>? MmXvNVDDqM7:TR?= MWGyM|QwPiCq M2W0TWROW09? M4i5OYlv\HWlZYOgRW1RUyCjY4TpeoF1cW:w Mkn3NlM4PDNzOUi=
PANC-1 MX7D[YxtKF[rYXLpcIl1gSCDc4PhfS=> Mn[1NU8yOMLizszN NIrDSnY1QCCq MVXEUXNQ M1nqboRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M4T1VVI{PzR|MUm4
PANC-1 NFXNPVZHfW6ldHnvckBCe3OjeR?= MkjWNVDDqM7:TR?= MYKyM|QhcA>? MmDHSG1UVw>? MoD2bY5kemWjc3XzJIlvfHKjY3XscJVt[XJiUl;TJIxmfmWu M1XhflI{PzR|MUm4
H1666 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYm3NuKhcA>? NX\mZWFYTE2VTx?= MXzJR|UxRjFyIN88US=> MlfLNlM2OTV5NUK=
H460 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLHO|LDqGh? MnHESG1UVw>? MVjJR|UxRTBwOE[g{txO NIG1d5YzOzVzNUe1Ni=>
H1299 Mn\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWHHclVjPzMEoHi= M3rDSmROW09? MUHJR|UxRTFwMjFOwG0> NHn6O|UzOzVzNUe1Ni=>
H520 M3vIS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{T6NlczyqCq MVzEUXNQ NVu4[lZmUUN3ME2wMlc2KM7:TR?= NY\MZ5h6OjN3MUW3OVI>
H1975 NYDYflVET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWrMVoRpPzMEoHi= MWrEUXNQ MWTJR|UxRTBwNkig{txO M1TG[lI{PTF3N{Wy
H1650 Mnf6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGP0T4I4OsLiaB?= M4jme2ROW09? MYrJR|UxRTBwOEig{txO Mk\ZNlM2OTV5NUK=
H820 MmTXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGDyUVE4OsLiaB?= NH;iNlVFVVOR NYnKSZdvUUN3ME2wMlQh|ryP M1PKdlI{PTF3N{Wy
PC9 NYnIbZk1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2q5T|czyqCq MlPpSG1UVw>? MU\JR|UxRTBwMkmg{txO NGfYRlkzOzVzNUe1Ni=>
HCC2279 M1zieGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4\sd|czyqCq NF;S[HBFVVOR MV\JR|UxRTBwNDFOwG0> MVqyN|UyPTd3Mh?=
HCC827 M1T3Omdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGPqS204OsLiaB?= NVi4OIRjTE2VTx?= NXm1RoFXUUN3ME2wMlI6KM7:TR?= MUmyN|UyPTd3Mh?=
HCC2935 MmDUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MorIO|LDqGh? NIf6d4VFVVOR MoLKTWM2OD1yLkm3JO69VQ>? NFrTV4szOzVzNUe1Ni=>
HCC4006 NUWyT2JWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmXqO|LDqGh? MUnEUXNQ M{[0PGlEPTB;MD60OkDPxE1? NH\DR5YzOzVzNUe1Ni=>
H460 M2CxVGZ2dmO2aX;uJGF{e2G7 NHvG[pU2ODEEoH7N MX[yOOKhcA>? MVzEUXNQ MXPk[YNz\WG|ZYOgSWdHWiCneIDy[ZN{cW:w NETBZXkzOzVzNUe1Ni=>
H1650 MlntSpVv[3Srb36gRZN{[Xl? M3XWZ|UxOMLibl2= NXPBVolbOjUEoHi= Mnn0SG1UVw>? M13K[YRm[3KnYYPld{BGT0[UIHX4dJJme3Orb36= MlKxNlM2OTV5NUK=
PC9 MVLGeY5kfGmxbjDBd5NigQ>? NGPPTos2ODEEoH7N NH;ZZZEzPMLiaB?= MYnEUXNQ Mlv0[IVkemWjc3XzJGVITlJiZYjwdoV{e2mxbh?= MlvoNlM2OTV5NUK=
H460 MXLGeY5kfGmxbjDBd5NigQ>? NIXye3UxNjVxMT:yJO69VQ>? M{KzUFQhcA>? NWW4SY43TE2VTx?= M{fscYlvcGmkaYTzJJRp\SCuZY\lcJMhd2ZiQXv0JEhxNUGtdDmgZY5lKEWJRmK= NHLSWlUzOzVzNUe1Ni=>
H1650 NYr0Sm9pTnWwY4Tpc44hSXO|YYm= NVj5RWdqOC53L{GvNkDPxE1? M4HyNVQhcA>? NULjepU1TE2VTx?= MWfpcohq[mm2czD0bIUhdGW4ZXzzJI9nKEGtdDCodE1Cc3RrIHHu[EBGT0[U Mkf2NlM2OTV5NUK=
PC9 MnrHSpVv[3Srb36gRZN{[Xl? M4nWR|AvPS9zL{Kg{txO M4jXPVQhcA>? M{DMZWROW09? NXzzfYo5cW6qaXLpeJMhfGinIHzleoVteyCxZjDBb5QhMHBvQXv0LUBidmRiRVfGVi=> MkGzNlM2OTV5NUK=
AsPc1 NHf2eoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX20PEBp MWLFR|UxRTBwMzFOwG0> NHHufZMzOzR5NU[5OS=>
Panc0327 NUX5V|RMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MU[0PEBp M4TaS2VEPTB;MD61JO69VQ>? MYiyN|Q4PTZ7NR?=
MiaPaCa2 MkDSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnHROFghcA>? M3LkZmVEPTB;MD63JO69VQ>? MoXPNlM1PzV4OUW=
BxPc3 NGj4ZnpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MY[0PEBp NGrqc4dGSzVyPUGuNEDPxE1? NUm2dlY6OjN2N{W2PVU>
Panc0403 NEjqU2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF7UV|Y1QCCq M3LLNGVEPTB;MT6xJO69VQ>? NEDWZmYzOzR5NU[5OS=>
Panc1005 Mn\lS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYW0PEBp NXPVbG01TUN3ME2xMlEh|ryP NEK2OWQzOzR5NU[5OS=>
PL45 NVzMVWZWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXu0PEBp NVTHelRbTUN3ME2yNE45KM7:TR?= MXKyN|Q4PTZ7NR?=
Panc0203 NE\TWGdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVfqdox5PDhiaB?= MULFR|UxRTJ{LkKg{txO MnzWNlM1PzV4OUW=
Panc0327 MmXURZBweHSxc3nzJGF{e2G7 M2LaNFEh|ryP NUXEdFdZOjRiaB?= NVLJV4FjcW6mdXPld{BieG:ydH;zbZM> NYXJRY1UOjN2N{W2PVU>
Panc1005 NH65VGtCeG:ydH;zbZMhSXO|YYm= NGjUbIwyKM7:TR?= NHPy[WIzPCCq NFzSepVqdmS3Y3XzJIFxd3C2b4Ppdy=> NUWzO45MOjN2N{W2PVU>
Panc0403 MXTBdI9xfG:|aYOgRZN{[Xl? MmrrNUDPxE1? NIrpc4QzPCCq NHvqc5hqdmS3Y3XzJIFxd3C2b4Ppdy=> MYGyN|Q4PTZ7NR?=
AsPc1 MWTGeY5kfGmxbjDBd5NigQ>? MlvTNU8yOCEQvF2= MljINlQhcA>? Mn3MbY5lfWOnczCg[5Jwf3SqIHHydoV{fGWmIHnuJGczN01? NXH2WlM2OjN2N{W2PVU>
MiaPaCa2 M2HzO2Z2dmO2aX;uJGF{e2G7 NY\MOndROS9zMDFOwG0> NF:4[YYzPCCq M1;ROIlv\HWlZYOgJIdzd3e2aDDhdpJme3SnZDDpckBIOi:P NIjCfo4zOzR5NU[5OS=>
T3M4 M2TE[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX\FPGJ3OC16MECgcm0> MkHLOFghcA>? MUjpcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MYeyNlY5OTZ7OB?=
AsPC-1 M2rUV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYiwMVgxOCCwTR?= MoGyOFghcA>? MkDabY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;uJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NILFW4wzOjZ6MU[5PC=>
Panc-1  MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlTSNE05ODBibl2= MkLPOFghcA>? MYTpcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MYKyNlY5OTZ7OB?=
T3M4 NX\lc5FPSXCxcITvd4l{KEG|c3H5 MmXvNVAxNzVyMD:xNFAxKG6P NVvzbW12PDhiaB?= MVPpcoR2[2W|IHTvd4Uh\GWyZX7k[Y51KGGyb4D0c5Nqew>? MWWyNlY5OTZ7OB?=
AsPC-1 MYXBdI9xfG:|aYOgRZN{[Xl? MVmxNFAwPTByL{GwNFAhdk1? MX60PEBp MmG4bY5lfWOnczDkc5NmKGSncHXu[IVvfCCjcH;weI9{cXN? MX2yNlY5OTZ7OB?=
Panc-1  MUTBdI9xfG:|aYOgRZN{[Xl? Ml\CNVAxNzVyMD:xNFAxKG6P MVi0PEBp MWLpcoR2[2W|IHTvd4Uh\GWyZX7k[Y51KGGyb4D0c5Nqew>? NUHYNYo6OjJ4OEG2PVg>
HBL-2 NYjl[5g{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXGyOEBp M{TxU2lEPTB;MD60JO69VQ>? MWmyNFA3QDB6MB?=
Jeko-1 Mn\tS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUnVUlNVOjRiaB?= NEHreZRKSzVyPUCuNkDPxE1? MWeyNFA3QDB6MB?=
Granta-519 MlrPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWWyOEBp NUe5bppGUUN3ME21Ok4{KM7:TR?= MXiyNFA3QDB6MB?=
HCT116 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{Pa[FQ5KGh? NFK2eWFGSzVyPUCuNlgh|ryP MoHQNVcyOjR3OUS=
HCT116 MnXvSpVv[3Srb36gRZN{[Xl? NEOxfI0xNjoEoN88UeKh MVOyOEBp M3X6RYRwf25vcnXneYxifHNiVGOgdJJwfGWrbjDs[ZZmdHNiYX\0[ZIhPsLiaDDpcoN2[mG2aX;u MVWxO|EzPDV7NB?=

... 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]
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  • 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 slightly soluble or insoluble
Ethanol slightly soluble or insoluble
In vivo Add solvents individually and in order:
2% DMSO+30% PEG 300+ddH2O
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

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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

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HDAC Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID