Biological Activity

Bioactivity / Mechanism

MS-275 (entinostat) is a benzamide HDAC inhibitor. In a recombinant enzyme panel, its IC50 values were 0.243, 0.453 and 0.248 μM for HDAC1, HDAC2 and HDAC3, respectively, while the other tested HDAC isoforms had IC50 values >10 μM. These values depend on the assay conditions. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target	Activity	Value
HDAC1 (Cell-free assay)		0.51 μM
HDAC3 (Cell-free assay)		1.7 μM

Cellular Effect

Cell Line	Activity	Value	Description	Reference
A2780	CC50	3000 nM	Antiproliferative activity against human A2780 cells after 72 hrs by celltiter-blue cell viability assay	[PMID: 19441846]
A2780	IC50	3000 nM	Antiproliferative activity against human A2780 cells by CellTiter-Blue cell viability assay	[PMID: 18370373]
A2780	IC50	5.89 μM	Antiproliferative activity against human A2780 cells after 48 hrs by MTT assay	[PMID: 28340413]
A-375	IC50	3.67 μM	Antiproliferative activity against human A375 cells assessed as reduction in cell growth incubated for 72 hrs by CCK-8 assay	[PMID: 31003060]
A-375	IC50	3.67 μM	Antiproliferative activity against human A375 cells after 72 hrs by CCK-8 assay	[PMID: 29202397]
A549	IC50	< 0.1 μM	Antiproliferative activity against human A549 cells after 48 hrs by MTT assay	[PMID: 22705022]
A549	IC50	1.48 μM	Cytotoxicity against human A549 cells assessed as reduction in cell viability incubated for 72 hrs by MTS assay	[PMID: 33588178]
A549	IC50	1.48 μM	Antiproliferative activity against human A549 cells measured after 48 hrs by MTT assay	[PMID: 35041998]
A549	IC50	1.71 μM	Antiproliferative activity against human A549 cells assessed as inhibition of cell viability measured for 48 hrs by microplate reader based CCK-8 assay	[PMID: 34097389]
A549	IC50	1200 nM	Growth inhibition of human A549 cells after 48 hrs by SRB assay	[PMID: 30476825]
A549	CC50	1200 nM	Antiproliferative activity against human P53 expressing A549 cells after 72 hrs by celltiter-blue cell viability assay	[PMID: 19441846]
A549	IC50	1200 nM	Antiproliferative activity against human A549 cells by CellTiter-Blue cell viability assay	[PMID: 18370373]
A549	GI50	18.37 μM	Antiproliferative activity against human A549 cells after 48 hrs by MTT assay	[PMID: 28629630]
A549	IC50	3.11 μM	Antiproliferative activity against human A549 cells after 48 hrs by MTT assay	[PMID: 28340413]
A549	IC50	3.134 μM	Cytotoxicity against human A549 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	[PMID: 26140961]
A549	IC50	3.58 μM	Compound was tested for antiproliferative activity against human A549 cancer cell lines using MTT assay	[PMID: 14667227]
A549	IC50	5.41 μM	Antiproliferative activity against human A549 cells incubated for 72 hrs by MTT assay	[PMID: 25953722]
A549	IC50	5.41 μM	Antiproliferative activity against human A549 cells assessed as inhibition of cell growth after 72 hrs by MTT-based assay	[PMID: 25874326]
A549	GI50	5.76 μM	Growth inhibition of human A549 cells after 48 hrs by sulforhodamine B assay	[PMID: 28395150]
A549	IC50	7.15 μM	Antiproliferative activity against human A549 cells assessed as reduction in cell growth incubated for 72 hrs by CCK-8 assay	[PMID: 31003060]

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In Vitro Studies

Entinostat inhibited growth across a human tumor cell panel with substantial model dependence. In a separate SH-SY5Y ATP assay, continuous exposure produced a lower 96 h IC50 than a 6 h pulse followed by washout (1.328 versus 8.086 μM), showing that exposure duration affects the cellular response. [1,2]

Recombinant HDAC isoform inhibition

Biochemical assay · Recombinant HDAC1–10 enzyme panel [1]

MS-275 inhibited HDAC1, HDAC2 and HDAC3 at submicromolar concentrations; all other tested isoforms had IC50 >10 μM under this assay. Values are assay endpoints, not cellular treatment concentrations.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
HDAC1 enzyme inhibition	IC50 0.243 μM	[1]
HDAC2 enzyme inhibition	IC50 0.453 μM	[1]
HDAC3 enzyme inhibition	IC50 0.248 μM	[1]
HDAC8, HDAC4, HDAC5, HDAC7, HDAC9, HDAC6 and HDAC10 enzyme inhibition	IC50 >10 μM for each	[1]

Literature-Reported Treatment Conditions

Treatment concentration: Serial inhibitor dilutions; exact concentration series not specified in the read methods.
Exposure duration: 15 min enzyme–inhibitor preincubation; 3 h reaction
Method: Fluorescent acetylated peptide substrate conversion; Caliper LabChip separation/detection
Vehicle: 1% DMSO in assay buffer
Reported limits: No uncertainty or replicate count attached to Table 2 MS-275 entries.

Methods and source locations

Compound reported in the paper: MS-275 (Entinostat); Compound label in the paper: MS-275

Evidence for the named compound under the reported conditions; no inference of equivalence of supplier lots or formulations.

Table 2; Experimental Procedures: Enzymatic HDAC Activity Assays; Results: Benzamide HDACi Are More Isoform-selective than Hydroxamate HDACi

HDAC1 enzyme inhibition: Caliper LabChip — Table 2; Experimental Procedures: Enzymatic HDAC Activity Assays; Results: Benzamide HDACi Are More Isoform-selective than Hydroxamate HDACi

HDAC2 enzyme inhibition: Caliper LabChip — Table 2; Experimental Procedures: Enzymatic HDAC Activity Assays; Results: Benzamide HDACi Are More Isoform-selective than Hydroxamate HDACi

HDAC3 enzyme inhibition: Caliper LabChip — Table 2; Experimental Procedures: Enzymatic HDAC Activity Assays; Results: Benzamide HDACi Are More Isoform-selective than Hydroxamate HDACi

HDAC8, HDAC4, HDAC5, HDAC7, HDAC9, HDAC6 and HDAC10 enzyme inhibition: Caliper LabChip — Table 2; Experimental Procedures: Enzymatic HDAC Activity Assays; Results: Benzamide HDACi Are More Isoform-selective than Hydroxamate HDACi

Exposure-dependent SH-SY5Y ATP response

Cell-based study · Human SH-SY5Y neuroblastoma cells [1]

At a 96 h ATP endpoint, the MS-275 IC50 was 1.328 μM with constant exposure and 8.086 μM after a 6 h pulse followed by washout. The assay measures ATP-associated viability/metabolism and does not directly enumerate apoptotic cells.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
ATP-associated cell viability after constant exposure	IC50 1.328 μM	[1]
ATP-associated cell viability after 6 h pulse and washout	IC50 8.086 μM	[1]

Literature-Reported Treatment Conditions

Treatment concentration: Serial concentrations; IC50 values reported as endpoints below.
Exposure duration: 96 h total; continuous exposure or 6 h pulse followed by drug-free medium
Method: CellTiter-Glo ATP luminescence
Vehicle: 0.1% DMSO; DMSO control defines 100% cell metabolism
Reported limits: Table 4 gives no MS-275-specific uncertainty or replicate count; Fig. 7 duplicate curves depict compound 1 and SAHA, not MS-275.

Methods and source locations

Compound reported in the paper: MS-275 (Entinostat); Compound label in the paper: MS-275

Evidence for the named compound under the reported conditions; no inference of equivalence of supplier lots or formulations.

Table 4; Experimental Procedures: SH-SY5Y Cell Viability Assay and Data Analysis; Results: Washout of HDACi Reduces Cellular Cytotoxicity

ATP-associated cell viability after constant exposure: CellTiter-Glo at 96 h — Table 4; Experimental Procedures: SH-SY5Y Cell Viability Assay and Data Analysis; Results: Washout of HDACi Reduces Cellular Cytotoxicity

ATP-associated cell viability after 6 h pulse and washout: CellTiter-Glo at 96 h — Table 4; Experimental Procedures: SH-SY5Y Cell Viability Assay and Data Analysis; Results: Washout of HDACi Reduces Cellular Cytotoxicity

Human tumor cell growth sensitivity panel

Cell-based study · Ten human tumor cell lines: A2780, Calu-3, HL-60, K562, St-4, HT-29, KB-3-1, Capan-1, 4-1St, HCT-15 [2]

Three-day neutral-red assay showed heterogeneous sensitivity, with IC50 ranging from 0.0415 μM in A2780 to 4.71 μM in HCT-15. The structurally related 3′-amino analogue was less active in every tested line; 5-fluorouracil showed a different sensitivity pattern.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
A2780 growth inhibition	IC50 0.0415 μM	[2]
Calu-3 growth inhibition	IC50 0.195 μM	[2]
HL-60 growth inhibition	IC50 0.212 μM	[2]
K562 growth inhibition	IC50 0.589 μM	[2]
St-4 growth inhibition	IC50 0.820 μM	[2]
HT-29 growth inhibition	IC50 1.29 μM	[2]
KB-3-1 growth inhibition	IC50 1.46 μM	[2]
Capan-1 growth inhibition	IC50 1.70 μM	[2]
4-1St growth inhibition	IC50 1.92 μM	[2]
HCT-15 growth inhibition	IC50 4.71 μM	[2]

Literature-Reported Treatment Conditions

Treatment concentration: Graded drug concentrations; exact series not provided.
Exposure duration: 3 days
Method: Neutral-red uptake; IC50 estimated from growth inhibition versus log concentration
Reported limits: Cell-assay vehicle, replicate count and IC50 uncertainty not stated in the relevant method/table.

Methods and source locations

Compound reported in the paper: MS-275 (Entinostat); Compound label in the paper: MS-27-275

Evidence for the named compound under the reported conditions; no inference of equivalence of supplier lots or formulations.

Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

A2780 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

Calu-3 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

HL-60 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

K562 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

St-4 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

HT-29 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

KB-3-1 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

Capan-1 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

4-1St growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

HCT-15 growth inhibition: Neutral-red assay — Table 1; Materials and Methods: Chemicals and Evaluation of in Vitro Sensitivity; Results: In Vitro Antiproliferative Activity

In Vivo Studies

Oral MS-27-275 showed model-dependent activity in human tumor xenografts: seven of eight models responded, whereas HCT-15 did not. Higher dosing caused weight loss and poor appearance, and the figure caption reports deaths in a Calu-3 test group without identifying their cause. These findings do not establish a general safety margin. [2]

In separate mouse experiments, MS-275 increased lung vascular leakage and increased lung colonies after intravenous melanoma-cell delivery. The latter model tests experimental extravasation and colonization rather than the full course of spontaneous metastasis; its direction should not be generalized to all tumor models. [3]

Human tumor xenograft response and nonresponse

Animal study · Eight human tumor xenograft models in female BALB/c-nu/nu mice [2]

The paper reports activity in seven of eight tumor models and no response in HCT-15. Selected arms describe the common 24.5 mg/kg dose. The 49 mg/kg dose tested in KB-3-1, 4-1St, St-4 and Capan-1 caused weight loss and poor appearance; it was reduced for subsequent models. No gross weight loss was reported at 24.5 mg/kg. Absence of gross weight loss does not establish safety.

Conditions shared by the study groups

Route: Oral
Frequency: Once daily, 5 days/week
Treatment course: 4 weeks
Vehicle: MS-27-275 dissolved in 0.05 N HCl and 0.1% Tween 80, as reported.

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
KB-3-1 xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	Tumor growth suppressed relative to control.	[2]
4-1St xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	Tumor growth suppressed relative to control.	[2]
St-4 xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	Tumor growth suppressed relative to control.	[2]
Capan-1 xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	Moderate growth inhibition.	[2]
A2780 xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	Marked growth inhibition.	[2]
HT-29 xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	Marked growth inhibition.	[2]
Calu-3 xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	Moderate growth inhibition; caption reports deaths in a test group without identifying cause.	[2]
HCT-15 xenograft at 24.5 mg/kg 24.5 mg/kg	Untreated/control group in Fig. 5A; exact control vehicle administration not specified.	No tumor-growth response at the tested regimen.	[2]

KB-3-1 xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; KB-3-1 xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

4-1St xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; 4-1St xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

St-4 xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; St-4 xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

Capan-1 xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; Capan-1 xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

A2780 xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; A2780 xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

HT-29 xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; HT-29 xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

Calu-3 xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; Calu-3 xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

HCT-15 xenograft at 24.5 mg/kg: Model: Female BALB/c-nu/nu mice, age 7 weeks; HCT-15 xenograft; Reported limits: 4 or 5 mice per experimental group; exact model/group n not assigned in text.

Methods and source locations

Compound reported in the paper: MS-275 (Entinostat); Compound label in the paper: MS-27-275

Evidence for the named compound under the reported conditions; no inference of equivalence of supplier lots or formulations.

Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

KB-3-1 xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

4-1St xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

St-4 xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

Capan-1 xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

A2780 xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

HT-29 xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

Calu-3 xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

HCT-15 xenograft at 24.5 mg/kg · Fig. 5A image and caption; Materials and Methods: In Vivo Antitumor Activity; Results: In Vivo Antitumor Activity

Increased lung vascular permeability

Animal study · Female C57BL/6N mice, 7–8 weeks old [3]

MS-275 increased lung Evans blue extravasation compared with vehicle after four days of treatment. This is a vascular leakage assay, not an antitumor efficacy assay.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Extravasated Evans blue in lungs	Direction and significance Increased; **p < .01; n = 3; mean ± s.e.m.	[3]

Conditions shared by the study groups

Route: Oral gavage
Frequency: Daily
Treatment course: 4 consecutive days
Vehicle: DMSO vehicle comparator identified in Fig. 4 caption; complete Miles formulation not explicit.

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
MS-275 lung vascular leakage 30 mg/kg/day	Vehicle-treated mice	Increased extravasated Evans blue in lung; **p < .01; n = 3, mean ± s.e.m.	[3]

MS-275 lung vascular leakage: Model: Female C57BL/6N mice, 7–8 weeks old; Reported limits: No exact mean extracted from graph. Caption lists unpaired t-test or Bonferroni correction without panel-specific assignment.

Methods and source locations

Compound reported in the paper: MS-275 (Entinostat); Compound label in the paper: MS-275

Evidence for the named compound under the reported conditions; no inference of equivalence of supplier lots or formulations.

Fig. 4a image/caption; Materials and methods: Vascular permeability assay (Miles assay)

Extravasated Evans blue in lungs: Evans blue extraction and absorbance at 620 nm — Fig. 4a image/caption; Materials and methods: Vascular permeability assay (Miles assay)

MS-275 lung vascular leakage · Fig. 4a image/caption; Materials and methods: Vascular permeability assay (Miles assay)

Increased lung colonies in an experimental extravasation model

Animal study · B16-F10 intravenous experimental metastasis model in female C57BL/6N mice [3]

Pretreatment with MS-275 increased lung melanoma colonies relative to vehicle. The authors caution that intravenous tumor-cell delivery does not reproduce the full process of spontaneous metastasis, and prior spontaneous models showed antimetastatic effects.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Lung surface melanoma colonies	Direction and significance Increased; **p < .01; n = 5; mean ± s.e.m.	[3]

Conditions shared by the study groups

Route: Oral gavage
Frequency: Daily
Treatment course: 4 consecutive days ending on cell injection day; lung colony endpoint day 14
Vehicle: 200 μL water containing 1% DMSO and 30% polyethylene glycol 400

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
MS-275 pretreatment and lung colony formation 30 mg/kg/day	Same vehicle without MS-275	Increased lung surface colonies; **p < .01; n = 5; mean ± s.e.m.	[3]

MS-275 pretreatment and lung colony formation: Model: Female C57BL/6N mice, 7–8 weeks; intravenously introduced B16-F10 melanoma cells; Reported limits: No exact mean extracted from graph; randomization/blinding not stated in read methods.

Methods and source locations

Compound reported in the paper: MS-275 (Entinostat); Compound label in the paper: MS-275

Evidence for the named compound under the reported conditions; no inference of equivalence of supplier lots or formulations.

Fig. 5a image/caption; Materials and methods: In vivo metastasis assay; Discussion model limitation

Lung surface melanoma colonies: Lung surface colony count; unpaired t-test — Fig. 5a image/caption; Materials and methods: In vivo metastasis assay; Discussion model limitation

MS-275 pretreatment and lung colony formation · Fig. 5a image/caption; Materials and methods: In vivo metastasis assay; Discussion model limitation

Specifications

Manufacturer	Adooq Bioscience
Actions	Inhibitor
CAS Number	209783-80-2
Applications	HDAC inhibitor
Formula	C₂₁H₂₀N₄O₃
Molecular Weight	376.4
Synonyms	SNDX-275; MS-275
SMILES	C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	71 mg/mL (188.62 mM)
Water	Insoluble
Ethanol	Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration: 9 mg/mL
Vehicle: 2% DMSO+30% PEG 300+ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Lauffer BE, Mintzer R, Fong R, et al. Histone deacetylase (HDAC) inhibitor kinetic rate constants correlate with cellular histone acetylation but not transcription and cell viability The Journal of biological chemistry (2013). PMID: 23897821 DOI: 10.1074/jbc.m113.490706 Source material
[2] Saito A, Yamashita T, Mariko Y, et al. A synthetic inhibitor of histone deacetylase, MS-27-275, with marked in vivo antitumor activity against human tumors Proceedings of the National Academy of Sciences of the United States of America (1999). PMID: 10200307 DOI: 10.1073/pnas.96.8.4592 Source material
[3] Kashio T, Shirakura K, Kinoshita M, et al. HDAC inhibitor, MS-275, increases vascular permeability by suppressing Robo4 expression in endothelial cells Tissue barriers (2021). PMID: 33955828 DOI: 10.1080/21688370.2021.1911195 Source material

Publications

8 publications citing this product

Chaitra Rai, .et al. , Signal Transduct Target Ther, 2026, Jun 5;11(1):218 PMID: 42248845
Siva Singothu, .et al. , ACS Infect Dis, 2025, Jul 11;11(7):1922-1933 PMID: 40509567
Wenguang Liu, .et al. , Biochem Biophys Res Commun, 2024, Dec 20:739:150970 PMID: 39550862
Vivek Bora, .et al. , Can J Physiol Pharmacol, 2021, 6 October PMID: 34614370
Taito Kashio, .et al. , Tissue Barriers, 2021, May 6;1911195 PMID: 33955828
Ting-Yu Chang, .et al. , Biomed Pharmacother, 2021, Jun;138:111485 PMID: 33740521
Arshdeep Singh, .et al. , Eur J Med Chem, 2021, Apr 5;215:113169 PMID: 33588178
Minoru Ueda, .et al. , Plant Physiol, 2017, Dec; 175(4): 1760-1773 PMID: 29018096

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Entinostat (MS-275)

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Biological Activity

Bioactivity / Mechanism

Target & Activity

Cellular Effect

In Vitro Studies

Recombinant HDAC isoform inhibition

Literature-Reported Treatment Conditions

Exposure-dependent SH-SY5Y ATP response

Literature-Reported Treatment Conditions

Human tumor cell growth sensitivity panel

Literature-Reported Treatment Conditions

In Vivo Studies

Human tumor xenograft response and nonresponse

Conditions shared by the study groups

Increased lung vascular permeability

Conditions shared by the study groups

Increased lung colonies in an experimental extravasation model

Conditions shared by the study groups

Specifications

Storage & Solubility

In Vitro Solubility

Reported Solubility

Preparing Stock Solutions

In Vivo Preparation

Storage

Research References

Publications

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