Entinostat (MS-275)
Catalog No.S1053 Synonyms: SNDX-275
Molecular Weight(MW): 376.41
Entinostat (MS-275) strongly inhibits HDAC1 and HDAC3 with IC50 of 0.51 μM and 1.7 μM in cell-free assays, compared with HDACs 4, 6, 8, and 10. Phase 3.
14 Customer Reviews
-
(A) U87 cells were cultured in the presence of DMSO, 1 uM MS-275 alone, 100 ng/ml IFN-λ1 alone, or both for the course of 4 d. Cell numbers were manually determined by hemacytometer counting at the indicated time points. (B, F) Cell proliferation of U87 cells or U87 spheroids in 3D culture with indicated treatment were performed using the WST-1 assay, which measures active cellular metabolism. (C) U87 spheroid formation in 3D culture was photographed at day 14 in culture (representative images are shown; 200x magnification). (D-E) Quantification of the relative sizes and numbers of U87 spheroids in (C). (G) Cell cycle analysis was performed in U87 cells with indicated treatment using propidium iodide staining. Numbers in the histogram show fractions (percent) of sub-G1, N, 2N, and polyploidy from left to right. (H) U87 cells with indicated treatment were stained with Annexin V-FITC and 7-AAD. Numbers indicate the percentage of FITC-positive cells (upper left quadrant). FITC, fluorescein isothiocyanate; 7-AAD, 7-Aminoactinomycin. In all panels, data represent the mean and SEM of at least three experiments.
PLoS Biol 2014 12, e1001758. Entinostat (MS-275) purchased from Selleck.
Inhibition of HDAC1-mediated DNMT1 deacetylation promotes DNMT1 proteasomal degradation. (A) Knockout of HAUSP potentiates HDAC inhibitor (HDACi)-induced DNMT1 degradation. Parental or HAUSP KO DLD1 cells were treated or not with 5 μM HDACi MS-275 for 72 hours and cell lysates were blotted with the indicated antibodies. (B) HDAC inhibition induces DNMT1 ubiquitination. HAUSP WT or KO cells were treated with or without HDACi for 24 hours and MG132 for 12 hours before being harvested to make cell lysates. DNMT1 immunoprecipitates were blotted with an antibody against ubiquitin. Because the abundance of DNMT1 in the HAUSP KO cells is lower than in WT cells, more KO cells were used than WT cells to obtain equal amounts of precipitated DNMT1 proteins. (C) DNMT1 is acetylated after HDACi treatment. DNMT1 immunoprecipitates from cells treated with HDACi were blotted with an antibody against acetylated lysine (Ac-K). (D) A DNMT1 acetylation site mutant is resistant to HDACi-induced degradation. HEK 293 cells were transfected with WT DNMT1 or a DNMT1 mutant lacking four known acetylation sites (K173R, K1113R, K115R, and K117R) and treated with MS-275 for 48 hours and with CHX for 24 hours. Cell lysates were blotted with the indicated antibodies. (E) Knockdown of HDAC1 decreases the abundance of DNMT1. RKO cells were treated with the indicated concentration of doxycycline (Dox) for 48 hours to induce expression of an shRNA directed against HDAC1. Western blots were performed with the indicated antibodies. (F) Knockdown of HDAC1 leads to increased acetylation of DNMT1. RKO cells expressing an inducible HDAC1 shRNA were treated with or without Dox (4 mg/ml) for 36 hours and then with MG132 for 12 hours. DNMT1 immunoprecipitates were blotted with an antibody against Ac-K. Cell lysates were also blotted with antibodies against HDAC1 and b-actin.
Sci Signal 2010 3, ra80. Entinostat (MS-275) purchased from Selleck.
-
The E3 ligase UHRF1 ubiquitinates DNMT1. (A) HDAC inhibition enhances DNMT1 interaction with UHRF1. HEK 293 cells were transfected with plasmids expressing Myc-DNMT1 and Flag-UHRF1 and treated with or without MS-275 for 24 hours. Myc-DNMT1 immunoprecipitates were blotted with the indicated antibodies. (B and C) HDAC inhibition enhances the interaction of endogenous DNMT1 and UHRF1. Cells were treated with or without MS-275 and UHRF1 (B) or DNMT1 (C) immunoprecipitates were blotted with the indicated antibodies. (D) UHRF1 ubiquitinates DNMT1. HEK 293 cells were transfected with the indicated plasmids. Antibodies against Myc immunoprecipitates were blotted with antibody against HA to detect ubiquitinated DNMT1. Myc-DNMT1D, DNMT1 mutant lacking the HAUSP-interacting domain. UHRF1DRING, UHRF1 with a RING domain deletion. (E) Knockdown of UHRF1 blocks HDACi-induced DNMT1 degradation. HEK 293 cells were transfected with control siRNA or siRNAs against UHRF1 and treated with or without MS-275. Western blotting was performed with the indicated antibodies. (F) Overexpression of UHRF1 leads to degradation of a DNMT1 mutant lacking the HAUSP-interacting domain (DNMT1D). Full-length DNMT1 or DNMT1D was cotransfected into HEK 293 cells with the indicated expression vectors. Cell lysates were blotted with the indicated antibodies. (G) DNMT1, HAUSP, UHRF1, HDAC1, and PCNA associate with Tip60. Flag-tagged Tip60 immunoprecipitates were blotted with the indicated antibodies.
Sci Signal 2010 3, ra80. Entinostat (MS-275) purchased from Selleck.
HAUSP KO cells are more sensitive to HDACi-induced apoptosis.(A) HDAC inhibition induces apoptosis in HAUSP KO cells.HAUSP WT or KO cells were treated with or without MS-275 at the indicated concentration for 72 hours, then fixed and stained with propidium iodide. Flow cytometric analyses were used to profile sub-G1, G1, and G2-M cell populations. Apoptotic cells were quantified after the indicated clones were treated with either 5 or 10 μM MS-275. The means and SDs of three independent experiments were plotted (*P<0.001, t test). (B) HDAC inhibition induces apoptosis in HAUSP KO cells but leads to G2-M arrest in WT cells.Cell cycle profiles of HAUSP WT or KOcells that were treated or not with 5 μM MS-275. (C)HDAC inhibition increases the abundance of apoptotic cell markers. The indicated cells were treated with or without MS-275 for 72 hours.Cell lysates were blotted with antibodies against cleaved caspase 3 and β-actin. (D) Ectopic overexpression of DNMT1 in HAUSP KO cells suppresses apoptosis. HAUSP KO clones or HAUSP KO cells inducibly
overexpressingDNMT1 were treatedwith 10 μM MS-275. Apoptotic cell populations were quantified by fluorescence-activated cell sorting (FACS) analyses (*P < 0.001, t test). Cell lysates from these cells were blotted with the indicated antibodies. (E) HDAC inhibition arrests the growth of HAUSP KO cells. DLD1, HAUSP KO, and KO cells ectopically expressing HAUSP were treated with the indicated concentration of MS-275 for 4 days. Cell numbers were determined and data from eight replicates were plotted (**P <0.001, t test). (FandG) HDACi inhibits tumor xenograft formation ofHAUSP KOcells.Athymic nudemice (five in each group)were injectedsubcutaneously and bilaterallywith cells of the indicated genotypes. Mice were treated with or without MS-275 at 15mg/kg for 4 weeks. Tumors were harvested and photographed (F). Tumor sizes of the indicated groupsweremeasuredweekly and theaveragevolumes at each timepoint were plotted (G).MANOVA analyses were performed to determine whether there was an overall difference of the tumor sizes, as well as whether there was a difference in development over time of tumor sizes between the two groups (P < 0.0001).Sci Signal 2010 3, ra80. Entinostat (MS-275) purchased from Selleck.
-
Numerous APC (+) oligodendrocytes (middle upper panel) with ellipsoid nuclei labeled with Sytox (left upper panel) were observed in 8 week old Thy-1 mitoCFP control MONs. NF-200 (+) neurofilaments extended along the MON as linear individual fibers (right upper panel). A period of OGD (60 min) caused a significant loss of APC (+) oligodendrocytes, a gain in the appearance of pyknotic nuclei (dense, brighter nuclei, white arrows, OGD panel), and loss of NF-200 (+) axon structures, which were, replaced with axonal head and bulb formation (white asterisks). Pretreatment with SAHA (1uM) or MS-275 (1uM) effectively preserved APC (+) oligodendrocytes, together with numerous linear individual NF-200 (+) axons. Note fewer pyknotic nuclei (white arrows, SAHA and MS-275 panels) after OGD in MONs treated with SAHA or MS-275.
J Neurosci 2011 31, 3990-9. Entinostat (MS-275) purchased from Selleck.
Notch1ICD, Notch2ICD, and Notch3ICD were transduced into human aortic SMCs, which were then treated with HDAC inhibitors TSA or MS-275 or with vehicle DMSO (con). The top 2 rows are different exposures of the same blot to detect the epitope tags on the N ICD constructs. Longer (top row) and shorter ( second row) exposures are shown because t he level of N2ICD expression was lower than that of N1ICD and N3ICD. SMC markers were analyzed and were similarly induced by activation of each Notch r eceptor. Both TSA and MS-275 significantly suppressed the induction of SMC proteins by Notch activation.
J Am Heart Assoc 2012 1, e000901. Entinostat (MS-275) 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 2012 131, 777-789. Entinostat (MS-275) purchased from Selleck.
Histone acetylation in the spinal cord after HDACI treatment. Histone acetylation in the lumbar spinal cord of mice receiving i.t. SAHA (25 μg) or MS-275 (0.5 μg) for 30 min was analyzed by immunoblot (A, B) and immunofluorescent histochemistry (C) for antigens indicated. Animals receiving i.t. saline were used as control. Images of the H3K9/18ac signals in the left half of the lumbar spinal cord are shown in the first row in C. Immunosignals of indicated antigens in the superficial dorsal horn are presented in the rest rows in C.
Mol Pain 2010 6, 51. Entinostat (MS-275) purchased from Selleck.
-
B. Confluent quiescent foreskin fibroblasts were treated with HDAC1 inhibitor or vehicle for 24 hours. Type I procollagen protein levels in whole cell lysates were determined by immunoblotting. A representative result of three independent experiments is shown. The band density was evaluated by densitometry. C. Under the same conditions, mRNA levels of the α1(I) collagen (COL1A1) gene were determined using reverse transcription quantitative real-time PCR. The graph represents -fold change in COL1A1 mRNA levels in comparison to unstimulated controls, which were arbitrarily set at 100. The mean and SD from three separate experiments are shown. * p<0.05 versus control cells treated with vehicle.
PLoS One 2013 8, e74930. Entinostat (MS-275) 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.
Exp Dermatol 2010 19, 1096-1102. Entinostat (MS-275) purchased from Selleck.
-
HCT116 p53 null cells were treated with different HDACIs (1 μM TSA, 5 μM M344, 1 μM MS-275, 5 mM But, 10 mM VPA) for 24 h, and their expression of GRP78, PERK-eIF2α axis and ATF4, ATF3, CHOP and DR5 proteins.
Biochem Biophys Res Commun 2014 10.1016/j.bbrc.2014.01.184. Entinostat (MS-275) purchased from Selleck.
HCT116 p53 null cells were treated with different HDACIs (1 μM TSA, 5 μM M344, 1 μM MS-275, 5 mM But, 10 mM VPA) for 24 h. ATF4, ATF3, CHOP and DR5 proteins were measured by Western blot.
Biochem Biophys Res Commun 2014 10.1016/j.bbrc.2014.01.184. Entinostat (MS-275) purchased from Selleck.
-
HDAC inhibition increases SMN-luciferase reporter mRNA levels. qRT-PCR was used to measure increases of SMN-luciferase mRNA following treatment with HDAC inhibitors. Fold increase of mRNA was normalized to GAPDH.
Biochem Bioph Res Co 2010 414, 25-30. Entinostat (MS-275) purchased from Selleck.
Western blot analysis of Acetyl-H3 and H3. 0-20μM MS-275 was added.
2011 Dr. Zhang of Tianjin Medical University. Entinostat (MS-275) purchased from Selleck.
Purity & Quality Control
Choose Selective HDAC Inhibitors
Biological Activity
| Description | Entinostat (MS-275) strongly inhibits HDAC1 and HDAC3 with IC50 of 0.51 μM and 1.7 μM in cell-free assays, compared with HDACs 4, 6, 8, and 10. Phase 3. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Targets |
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| In vitro |
MS-275 shows inhibitory to HDACs by 2'-amino group. MS-275 induces accumulation of p21WAF1/CIP1 and gelsolin in K562 cell. MS-275 could reduce S-phase cells and induce G1-phase cells in A2780 cell. MS-275 inhibits the proliferation of human tumor cell lines including A2780, Calu-3, HL-60, K562, St-4, HT-29, KB-3-1, Capan-1, 4-1St and HCT-15 with IC50 from 41.5 nM to 4.71 μM, which due to HAD-inhibition. [1] MS-275 is not sensitive to other HDACs (4, 6, 8 and 10) with IC50 about/above 100 μM. [2] MS-275 shows great inhibition to human leukemia and lymphoma cells, including U937, HL-60, K562, and Jurkat. MS-275 also decreases expression of cyclin D1 and the antiapoptotic proteins Mcl-1 and XIAP. [3] |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Cell Data |
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| In vivo | MS-275 exhibits great antitumor activity against human tumor xenografts except HCT-15 at 49 mg/kg. [1] MS-275 demonstrates promising therapeutic potential in both solid and hematologic malignancies, as well as regulation of physiologic and aberrant gene expression. [4] MS-275, combination with IL-2, has great antitumor activity to renal cell carcinoma xenograft model, which due to decreased T regulatory cells and increased splenocytes. [5] |
Protocol
| Kinase Assay: |
+ Expand
Standard HDAC Assays: Rat liver enzyme is diluted 1:6 with HDAC buffer. Recombinant human HDACs are diluted 1:4 in HDAC buffer. For standard HDAC assays, 60 μL of HDAC buffer is mixed with 10 μL of diluted enzyme solution at 30 °C. The HDAC reaction is started by adding 30 μL substrate solution in HDAC buffer followed by 30 min of incubation at 30 °C. The reaction is stopped by adding 100 μL trypsin solutions (10 mg/ml trypsin in 50 mM Tris-HCl [pH 8.0], 100 mM NaCl, 2 μM TSA). After a 20 min incubation period at 30 °C, the release of AMC is monitored by measuring the fluorescence at 460 nm (λex = 390 nm). Fluorescence intensity is calibrated using free AMC. For standard time course experiments, 20 pmol of substrate is used in the initial 100 μL HDAC reaction. Km and Vmax values are determined by measuring the fluorescence AMC generated by enzymatic cleavage of 2–50 pmol of substrate. The experimental data are analyzed using a Hanes plot. The AMC signals are recorded against a blank with buffer and substrate but without the enzyme. |
|---|---|
| Cell Research: |
+ Expand
|
| Animal Research: |
+ Expand
|
Solubility (25°C)
| In vitro | DMSO | 75 mg/mL (199.25 mM) |
|---|---|---|
| Water | Insoluble | |
| Ethanol | Insoluble | |
| In vivo | Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 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 | 376.41 |
|---|---|
| Formula | C21H20N4O3 |
| CAS No. | 209783-80-2 |
| Storage | powder |
| in solvent | |
| Synonyms | SNDX-275 |
Bio Calculators
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)
*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
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 )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
Enter the chemical formula of a compound to calculate its molar mass and elemental composition:
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
Clinical Trial Information
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT03838042 | Not yet recruiting | CNS Tumor|Solid Tumor | University Hospital Heidelberg|German Cancer Research Center | March 2019 | Phase 1|Phase 2 |
| NCT03829930 | Not yet recruiting | Prostate Adenocarcinoma | George Washington University | March 1 2019 | Phase 1 |
| NCT03765229 | Recruiting | Melanoma | UNC Lineberger Comprehensive Cancer Center|Syndax Pharmaceuticals Inc. | March 2019 | Phase 2 |
| NCT03838042 | Not yet recruiting | CNS Tumor|Solid Tumor | University Hospital Heidelberg|German Cancer Research Center | March 2019 | Phase 1|Phase 2 |
| NCT03829930 | Not yet recruiting | Prostate Adenocarcinoma | George Washington University | March 1 2019 | Phase 1 |
| NCT03765229 | Recruiting | Melanoma | UNC Lineberger Comprehensive Cancer Center|Syndax Pharmaceuticals Inc. | March 2019 | Phase 2 |
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.
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.
Frequently Asked Questions
-
Question 1:
I would like to use Entinostat（Catalog No.S1053） for animal study. What is your recommendation for the solvent? What is the role of PEG 300 in this case? Can I use DMSO only and dilute it with PBS or HBSS?
-
Answer:
2%DMSO/30%PEG/68%Water is recommended. PEG is an important polymer that helps with the solubility of hydrophobic drugs. If you use DMSO only and dilute it with PBS or HBSS, Entinostat will likely to precipitate out since it has very low solubility in water.
