Trichostatin A (TSA)

Name: Trichostatin A (TSA)
Brand: Selleck Chemicals
SKU: S1045
Rating: 5 (142 reviews)

For research use only.

Catalog No.S1045

142 publications

CAS No. 58880-19-6

Trichostatin A (TSA) is an HDAC inhibitor with IC50 of ~1.8 nM in cell-free assays.

Selleck's Trichostatin A (TSA) has been cited by 142 publications

Cell, 2019, 178(5):1115-1131

PubMed: 31442404 ( click the link to review the publication )

Cell Metab, 2019, 29(4):886-900

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Nature, 2017, 551(7679):247-250

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Cell, 2017, 171(4):824-835.e18

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Nat Biotechnol, 2015, 10.1038/nbt.3130

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Cancer Cell, 2014, 26(4):534-48

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Autophagy, 2020, 10.1080/15548627.2019.1709762

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Autophagy, 2020, 15:1-13

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Theranostics, 2020, 10(21):9644-9662

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Theranostics, 2020, 10(15):6790-6805

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mBio, 2020, 11(5)e02343-20

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Free Radic Biol Med, 2020, 10.1016/j.freeradbiomed.2020.01.016

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Cell Death Dis, 2020, 11(9):765

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Signal Transduct Target Ther, 2020, 13;5(1):53

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Cells, 2020, 21;9(5):E1280

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Front Immunol, 2020, 3;11:36

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Mol Neurobiol, 2020, 10.1007/s12035-019-01812-5

PubMed: 31919777 ( click the link to review the publication )

Am J Cancer Res, 2020, 10(2):523-535

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Oncogenesis, 2020, 13;9(5):48

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Mol Cancer Res, 2020, 10.1158/1541-7786.MCR-19-0669

PubMed: 32238439 ( click the link to review the publication )

Immunol Cell Biol, 2020, 98(4):318-331

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Front Chem, 2020, 23;8:184

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BMC Microbiol, 2020, 20(1):28

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Arch Insect Biochem Physiol, 2020, 103(4):e21649

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Cell Rep, 2020, 30(7):2195-2208

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Theranostics, 2020, 10(17):7747-7757

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Theranostics, 2020, 10(5):2188-2200

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Mol Cell, 2019, 73(4):788-802

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Mol Cell, 2019, 74(6):1250-1263

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Nat Commun, 2019, 10(1):5792

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Nat Commun, 2019, 10(1):4353

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Nat Commun, 2019, 10(1):5800

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Nucleic Acids Res, 2019, 19;47(16):8502-8520

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Autophagy, 2019, 1-13

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Autophagy, 2019, 10.1080/15548627.2019.1707488

PubMed: 31878840 ( click the link to review the publication )

Cancer Res, 2019, 10.1158/0008-5472.CAN-18-2486

PubMed: 31253668 ( click the link to review the publication )

Cell Death Differ, 2019, 26(5):843-859

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Int J Cancer, 2019, 10.1002/ijc.32425

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Mol Ther, 2019, 27(5):1039-1050

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EBioMedicine, 2019, 43:238-252

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J Bone Miner Res, 2019, 10.1002/jbmr.3716

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J Exp Clin Cancer Res, 2019, 38(1):428

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J Exp Clin Cancer Res, 2019, 38(1):84

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J Exp Clin Cancer Res, 2019, 38(1):463

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J Mol Cell Biol, 2019, 10.1093/jmcb/mjz093

PubMed: 31560394 ( click the link to review the publication )

Mol Cancer Ther, 2019, 18(5):900-908

PubMed: 30824609 ( click the link to review the publication )

Mol Neurobiol, 2019, 10.1007/s12035-019-1565-7

PubMed: 30963442 ( click the link to review the publication )

J Mol Med (Berl), 2019, 97(4):541-552

PubMed: 30806715 ( click the link to review the publication )
Pharmacol Res, 2019, 146:104281

PubMed: 31125601 ( click the link to review the publication )

Cancer Sci, 2019, 110(11):3442-3452

PubMed: 31432592 ( click the link to review the publication )

J Neurochem, 2019, 10.1111/jnc.14935

PubMed: 31811660 ( click the link to review the publication )

Front Cell Neurosci, 2019, 13:468

PubMed: 31708743 ( click the link to review the publication )

Sci Rep, 2019, 9(1):4360

PubMed: 30867438 ( click the link to review the publication )

PLoS Comput Biol, 2019, 15(2):e1006826

PubMed: 30785874 ( click the link to review the publication )

Front Genet, 2019, 10:422

PubMed: 31130994 ( click the link to review the publication )

Life Sci, 2019, 223:1-8

PubMed: 30862568 ( click the link to review the publication )

J Cell Biochem, 2019, 10.1002/jcb.29470

PubMed: 31692090 ( click the link to review the publication )

Cell Adh Migr, 2019, 13(1):285-292

PubMed: 31271097 ( click the link to review the publication )

Alcohol Clin Exp Res, 2019, 43(5):822-832

PubMed: 30860602 ( click the link to review the publication )

Oncol Rep, 2019, 41(6):3209-3218

PubMed: 31002353 ( click the link to review the publication )

Int J Mol Med, 2019, 44(5):1789-1800

PubMed: 31545402 ( click the link to review the publication )

Int J Mol Med, 2019, 43(1):285-293

PubMed: 30387821 ( click the link to review the publication )

Tuberculosis (Edinb), 2019, 118:101861

PubMed: 31526947 ( click the link to review the publication )

Reprod Fertil Dev, 2019, 31(3):473-481

PubMed: 30301509 ( click the link to review the publication )

Res Vet Sci, 2019, 126:207-212

PubMed: 31610471 ( click the link to review the publication )

Exp Ther Med, 2019, 17(6):4547-4553

PubMed: 31186678 ( click the link to review the publication )

Sci Adv, 2019, 5(3):eaav1118

PubMed: 30944854 ( click the link to review the publication )

Nat Biomed Eng, 2018, 2(8):578-588

PubMed: 31015631 ( click the link to review the publication )

J Clin Invest, 2018, 128(9):4098-4114

PubMed: 30124467 ( click the link to review the publication )

Cell Rep, 2018, 24(7):1722-1729

PubMed: 30110629 ( click the link to review the publication )

Mol Ther, 2018, 26(7):1828-1839

PubMed: 29730197 ( click the link to review the publication )

Cancer Lett, 2018, 432:121-131

PubMed: 29890207 ( click the link to review the publication )
Mol Oncol, 2018, 12(5):724-755

PubMed: 29577611 ( click the link to review the publication )

Oncogenesis, 2018, 7(11):91

PubMed: 30467308 ( click the link to review the publication )

J Proteome Res, 2018, 17(4):1436-1451

PubMed: 29564889 ( click the link to review the publication )

Plant Cell Rep, 2018, 37(1):115-123

PubMed: 28939922 ( click the link to review the publication )

Exp Cell Res, 2018, 371(1):231-237

PubMed: 30107147 ( click the link to review the publication )

Int Immunopharmacol, 2018, 65:303-311

PubMed: 30342347 ( click the link to review the publication )

Oncol Rep, 2018, 39(4):1892-1900

PubMed: 29393444 ( click the link to review the publication )

Biochem Biophys Res Commun, 2018, 503(2):420-427

PubMed: 29649477 ( click the link to review the publication )

Cell Biochem Funct, 2018, 36(8):398-407

PubMed: 30484863 ( click the link to review the publication )

Med Sci Monit, 2018, 24:461-472

PubMed: 29363667 ( click the link to review the publication )

Sci Rep, 2018, 8(1):13072

PubMed: 30166563 ( click the link to review the publication )

Cell Res, 2017, 27(7):898-915

PubMed: 28497810 ( click the link to review the publication )

Mol Cell, 2017, 67(4):566-578

PubMed: 28803781 ( click the link to review the publication )

Cell Mol Immunol, 2017, 14(4):371-379

PubMed: 26388239 ( click the link to review the publication )

Oncogene, 2017, 36(12):1707-1720

PubMed: 27694895 ( click the link to review the publication )

Chemistry, 2017, 23(13):3107-3116

PubMed: 27922200 ( click the link to review the publication )

Cancer Epidemiol Biomarkers Prev, 2017, 26(9):1411-1419

PubMed: 28619831 ( click the link to review the publication )

Eur J Med Chem, 2017, 127:531-553

PubMed: 28109947 ( click the link to review the publication )

J Biol Chem, 2017, 292(31):12842-12859

PubMed: 28634230 ( click the link to review the publication )

J Pharmacol Exp Ther, 2017, 363(2):211-220

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J Diabetes Res, 2017, 2017:8208065

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Int J Parasitol Drugs Drug Resist, 2017, 7(1):51-60

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Connect Tissue Res, 2017, 58(1):64-75

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Biochem Biophys Res Commun, 2017, 485(2):454-460

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Oncotarget, 2017, 8(7):11937-11949

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Nat Commun, 2016, 7:10690

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Nucleic Acids Res, 2016, 45(3):1159-1176

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Clin Cancer Res, 2016, 22(8):1978-88

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Thorax, 2016, 633-45

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J Med Chem, 2016, 59(4):1613-33

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PLoS Pathog, 2016, 12(10):e1005950

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Free Radic Biol Med, 2016, 99:167-178

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Oxid Med Cell Longev, 2016, 2016:4085727

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Am J Pathol, 2016, 186(10):2701-8

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Mol Cell Biol, 2016, 36(22):2838-2854

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Int J Oncol, 2016, 48(6):2591-607

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BMC Cancer, 2016, 16(1):886

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Mol Cell Biochem, 2016, 415(1-2):197-205

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Oncotarget, 2016, 8(60):100975-100988

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Genet Mol Res, 2016, 15(4)

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Sci Rep, 2016, 6:21678

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Tumour Biol, 2016, 37(6):8293-304

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Tumour Biol, 2016, 37(8):10269-78

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Nat Commun, 2015, 3;6:10091

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EMBO Mol Med, 2015, 10.15252/emmm.201404396

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Cancer Lett, 2015, 356(2 Pt B):828-36

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Am J Transplant, 2015, 10.1111/ajt.13106

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Cell Death Dis, 2015, 6:e1586

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J Antimicrob Chemother, 2015, 10.1093/jac/dku549

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Mol Nutr Food Res, 2015, 59(2):189-202

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Mol Nutr Food Res, 2015, 59(2):189-202

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Am J Physiol Lung Cell Mol Physiol, 2015, 309(12):L1410-9

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Chem Biol Interact, 2015, 242:227-34

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Oncotarget, 2015, 6(18):15814-27

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EMBO J, 2014, 34(1):115-29

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Proc Natl Acad Sci USA, 2014, 111(3):E364-73

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PLoS Biol, 2014, 12(1):e1001758

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Cancer Lett, 2014, 10.1016/j.canlet.2014.10.034

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Mol Cell Biol, 2014, 34(22):4143-64

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Toxicol Appl Pharmacol, 2014, 274(1):7-16

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Life Sci, 2014, 99(1-2):31-6

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Biochem Biophys Res Commun, 2014, 445(2):320-6

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Sci Rep, 2014, 4:4663

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Science, 2014, 344(6183):1252304

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Neuropsychopharmacology, 2013, 38(9):1674-84

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Plant J, 2013, 74(5):815-28

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Cytokine, 2013, 65(2):121-5

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Purity & Quality Control

Choose Selective HDAC Inhibitors

Biological Activity

Description

Trichostatin A (TSA) is an HDAC inhibitor with IC50 of ~1.8 nM in cell-free assays.

Targets

HDAC ^[1]
(Cell-free assay)

~1.8 nM

In vitro

Trichostatin A inhibits the proliferation of eight breast carcinoma cell lines including MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, and SK-BR-3 with mean IC50 of 124.4 nM (range, 26.4-308.1 nM), with more potency against cell lines that express ERα than the ERα-negative cell lines. Trichostatin A inhibits HDAC activity similarly in all the breast cancer cell lines with mean IC50 of 2.4 nM (range, 0.6-2.6 nM), and results in pronounced histone H4 hyperacetylation. ^[1] Unlike Trapoxin (TPX) and Chlamydocin which potently inhibit HDAC1 or HDAC4 but not HDAC6, Trichostatin A inhibits these HDACs to a similar extent with IC50 of 6 nM, 38 nM, and 8.6 nM, respectively. ^[2] Trichostatin A (100 ng/mL) treatment induces the expression of transforming growth factor β type II receptor (TβRII) in MIA PaCa-2 cells through the recruitment of p300 and PCAF into a Sp1-NF-Y HDAC complex that binds the DNA element of TβRII promoter, which is associated with a concomitant acetylation of Sp1 and an overall decrease in the amount of HDAC associated with the complex. ^[4]

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Formulation	Activity Description	PMID
HEK 293	NH3vZoFHfW6ldHnvckBCe3OjeR?=	NHTVeo8xNjgQvF2=	NHPq[IgzPGh?	MlLM[ZRp[W6xbB?=	MlG1[Y5p[W6lZYOgSW5iSyCjY3X0fYxifGmxbjDhcoQhcW6lcnXhd4V{KEWQYVOgZYJ2dmSjbnPlJIlvKHSqZTD0c5RidCClZXzsJIx6e2G2ZTDhcoQh[XRidHjlJINmdGxic4Xy[oFk\Q>?	MYKyOVc5PzB5OR?=
TE13	MXfGeY5kfGmxbjDBd5NigQ>?	MmrzNE4{\|ryP	NGTkOHozPGh?		MV\1dE1z\We3bHH0[ZMhWkGVU1[1RUBt\X[nbB?=	MW[yOVU4QTZ4NR?=
TE13	MoexRZBweHSxc3nzJGF{e2G7	NFf5SHAxNjQQvF2=	M{nNR\|I1cA>?		MWPpcohq[mm2czD0bIUh[2WubDDwdo9tcW[ncnH0bY9v	Mo\nNlU2Pzl4NkW=
MEFs	M3zle2Z2dmO2aX;uJGF{e2G7	NX7RbZRLPc7:TR?=	M3e4RVE3cA>?		NHHsZ4ZqdmO{ZXHz[ZMhfGinIFXQSWMh[XS2YXPocYVvfCxiVHnyJIRmdGm4ZYL5JIFv\CC2aHWg[YZncWOrZX7jfUBw\iCyZXTld5RidCCob4LtZZRqd25?	M3LUNFI2PDh{NkO0
SW480	NV\iOJYzTnWwY4Tpc44hSXO\|YYm=	NYGwRVh3OC5zzszN	M2rFbFQ5cA>?	MlT4SG1UVw>?	NY\LbYZHemW4ZYLz[ZMhTU2W	M1\Ge\|I2PDN2OUm3
PC3	MWTGeY5kfGmxbjDBd5NigQ>?	MVqwMlHPxE1?	MkKwOFhp	M4TZNWROW09?	MWHy[ZZmenOnczDFUXQ>	MonKNlU1OzR7OUe=
SW480	Mn;USpVv[3Srb36gRZN{[Xl?	M{TqPVAvOc7:TR?=	MUC0PIg>	NFLuRnhFVVOR	NYm2fnZF[XS2ZX71ZZRmeyCrbo\hd4lwdiCjbnSgcYloemG2aX;u	M3zTU\|I2PDN2OUm3
PC3	M2DZWGZ2dmO2aX;uJGF{e2G7	NH3vNnUxNjIQvF2=	MWi0PIg>	Mli1SG1UVw>?	NHGydW9ifHSnboXheIV{KGmwdnHzbY9vKGGwZDDtbYdz[XSrb36=	MkDkNlU1OzR7OUe=
SW480	MnXFSpVv[3Srb36gRZN{[Xl?	NFT0PYkxNjIQvF2=	M4jnUVQ5cA>?	NWf6WlF[TE2VTx?=	NHz6VFlqdmS3Y3XzJIlv[3KnYYPlJI9nKEiGQVOxJIFv\CCKRFHDNkBwdiCVbIXnJIdmdmW\|IIDyc41wfGW{	NGHFXI8zPTR\|NEm5Oy=>
PC3	NF;U[3ZHfW6ldHnvckBCe3OjeR?=	Mm[2NE4y\|ryP	MkPaOFhp	Ml7hSG1UVw>?	M1jjR4lv\HWlZYOgbY5kemWjc3Wgc4YhUESDQ{GgZY5lKEiGQVOyJI9vKFOudXeg[4Vv\XNicILvcY91\XJ?	NWDZV5d6OjV2M{S5PVc>
A431	MoHGRZBweHSxc3nzJGF{e2G7	NV2yWFhSOi9zMD:1NE8yODCwTR?=	Ml;tOFhp	NIizXINFVVOR	Ml6wbY5pcWKrdIOgeIhmKGOnbHyg[5Jwf3Sq	MUCyOVM4OTB4OR?=
A431	NWS2bWVETnWwY4Tpc44hSXO\|YYm=	NIrxW3E2OG6P	NX3MdXRVOi94L{GyM\|I1cA>?	MnK1SG1UVw>?	NEjuSGhi[3SrdnH0[ZMheDJzIHHu[EBqdmirYnn0d{BCXEZ\|IHX4dJJme3Orb36=	NGLqTVMzPTN5MUC2PS=>
MDA-MB-231	M3z2Xmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MYKwMVYxOG6P	NH7UN2ozPGh?	MlTMSG1UVw>?	MULJR\|UxKG:oIEGwNI5O	MUeyOVE6Ojd{MR?=
MCF7	NGfGeW1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MWGwMVYxOG6P	NXPKdnBvOjSq	NWXQTJIyTE2VTx?=	NXHLO2hmUUN3MDDv[kA4PW6P	NV;lZoRlOjVzOUK3NlE>
SKOV-3	M4i0Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NIG5eHMyNTFyzszN	NXPkeWJtOjSq	MmP2SG1UVw>?	MlXyTWM2OCCxZjC1MlbPxE1?	M3nqXFI2OTZ7NEmx
A549	NYHTbXVHT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M{jNTlEuOTEQvF2=	NEHVcJMzPGh?	Mn3RSG1UVw>?	NGnjNHhKSzVyIH;mJFMvOs7:TR?=	M3LsXFI2OTZ7NEmx
SKOV-3	MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NW\nVJBROC5zLUJOwG0>	Mo\WOFhp	NH6zTpVFVVOR	M4XYNmlEPTBib3[gNE44\|ryP	NWfwT4piOjVzNkm0PVE>
A549	MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MWGwMlEuOc7:TR?=	MVO0PIg>	MX\EUXNQ	NYLOUIlJUUN3MDDv[kAxNjJ6zszN	NVzKdZJiOjVzNkm0PVE>
SKOV-3	MknzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M{fkZ\|AvODFvMD65{txO	NV:4ZYhPPzKq	MXPEUXNQ	MW\JR\|UxKG:oIECuN\|LPxE1?	MoKzNlUyPjl2OUG=
A549	MmGzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M3TMUFAvODFvMD65{txO	MlHyO\|Jp	NYj2OZg4TE2VTx?=	NXPUeVV5UUN3MDDv[kAxNjB4zszN	MWqyOVE3QTR7MR?=
HeLa	NGG2ZpRHfW6ldHnvckBCe3OjeR?=	NVmwNnVIOjVybl2=	MU[xOog>	MmjzSG1UVw>?	NWfWVGRHcW6lcnXhd4V{KEO\UEHBNUBuWk6DIHX4dJJme3Orb39CpC=>	Mo\0NlUyOTZ4OEi=
CNE2	MnPkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MmXjNVAxNTZyMH7N	NVPLOFN4OjRxNEivO\|Jp		NInjeXJqdmirYnn0d{B1cGVicILvcIln\XKjdHnvckBqdiCjIITpcYUuKGGwZDDkc5NmNWSncHXu[IVvfCCvYX7u[ZI>	Mkn3NlQ6Pjl7MEG=
PC3	NVG0bmpXT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NV\zO3ZEOTByLUGwNFBvVQ>?	NGWxZmMzPGh?		NWeyR5RTUUN3MDDv[kA{ODCwTR?=	M37yWFI1QDV2NkW4
LNCaP	M1[yOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NV71epNsOTByLUGwNFBvVQ>?	MYKyOIg>		NFPWOWpKSzVyIH;mJFMxOG6P	NFvNZ3AzPDh3NE[1PC=>
HeLa	MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NWHGRXlJOs7:TR?=	M4e5cFQ5cA>?		MlfS[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHHic5V1KDJ3JR?=	M4nLTFI1QDR4MUO1
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MCF-7	MmjUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MojHNlUuPDByIH7N	NF7lemI1QCCq		MXfJR\|UxKG:oIEKyNE41dk1?	NVrX[G9ZOjNyNUWxPVg>
ECC-1	Mn\DS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NVL5NHRNOTByIH7N	MkO2NlQhcA>?	NIXZRWhmfGijbn;s	MWrpcoNz\WG\|ZYOgeIhmKHC{b4DvdpRqd25ib3[gZZBweHSxdHnjJI52[2ynaTD0c{A{PSV?	Mln2NlMxOjh6MEO=
HEC-1A	MlrGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MmrQNVAxKG6P	M{[3XlI1KGh?	MmT1[ZRp[W6xbB?=	NV3RW3hscW6lcnXhd4V{KHSqZTDwdo9xd3K2aX;uJI9nKGGyb4D0c5Rq[yCwdXPs[YkhfG9iM{ml	NI\3[48zOzB{OEiwNy=>
NHAC-kn	M{XPVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NYe0dmN7OTBxMUCwM\|UxOCCwTR?=	NHnVdnUyOiCq	MVXEUXNQ	NYrZOItqUUN3MDDv[kA2ODCwTR?=	M3XZU\|I{ODF5OEex
A549	NEjJPYZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M1L3N\|I2OCCwTR?=	M3r2dVYuPzJiaB?=	NFTocXdFVVOR	NFLOXZdk[XW\|ZYOgZUBoemWjdHXyJIlvcGmkaYTvdpkh\W[oZXP0JINwdWKrbnWge4l1cCCWWGSgc5Ih\XKub4Tpcolj	Mn[3NlI6QTR5OEC=
MG-63	MoPRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NULkTYtkOzByIH7N	MWOxNkBp	NITiRY5FVVOR	NHjlXmtqdmirYnn0d{B1cGViY3XscEBoem:5dHigeI8hQDZn	NWDCcGcyOjJ5OUmzN\|g>
MG-63	MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NIPhOlM{ODBibl2=	NGnrT3EzPCCq	NVvhTWZETE2VTx?=	M4HHZYlvcGmkaYTzJJRp\SClZXzsJIdzd3e2aDD0c{A3PyV?	MVKyNlc6QTN\|OB?=
MG-63	MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MXezNFAhdk1?	NI[y[2E1QCCq	MlWzSG1UVw>?	MX;pcohq[mm2czD0bIUh[2WubDDndo94fGhidH:gOVYm	MUSyNlc6QTN\|OB?=
HL60	NImxSopIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MU[xOVAuOzVyIH7N	M13pPVI1KGh?		NE\x[5NqdmO{ZXHz[ZMh[2WubDDhdI9xfG:\|aYRCpJdp\W5iY3;uZ4VvfHKjdHnvcpMhcGmpaHXyJJRp[W5iMkWwJI5O	NUXiWo1GOjJ5NUO3N\|k>
U937	M3nDR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M3r3PVE2OC1\|NUCgcm0>	M1K3fFI1KGh?		NIrHbGhqdmO{ZXHz[ZMh[2WubDDhdI9xfG:\|aYRCpJdp\W5iY3;uZ4VvfHKjdHnvcpMhcGmpaHXyJJRp[W5iMkWwJI5O	NHjh[YQzOjd3M{ezPS=>
SCC-6	M4PkZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MoPRNlAxNTN{MECgcm0>	MkDqNVIwOjRxNEigbC=>	MojQSG1UVw>?	NFnUZZhqdmirYnn0d{B1cGVicILvcIln\XKjdHnvckBw\iCVQ1OtOkBk\WyuczDpckBiKGSxc3WtJIFv\CC2aX3lMYRmeGWwZHXueEBu[W6wZYK=	MUOyNlU2OjN{MR?=
U87	M4S5TGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGHOWGIyODBvM{CwJI5o	M4fYSFI1KGh?		MVXpcohq[mm2czD0bIUh[2WubDDndo94fGhidH:gO\|ImKCCjdDCyNFBv\w>?	MnfXNlIzPzB6NEm=
K562	M{P5ZmZ2dmO2aX;uJGF{e2G7	NUfrfodYOSEQvF2=	NIn1bYcyOiCq	NWexfHlUTE2VTx?=	NYjMZ4JU\W6qYX7j[ZMhfGinIHX4dJJme3Orb36gc4YhWlWQWEOgbY5lfWOnZDDifUA2NWG8YT3D[HI>	MWGyNlE4QTF7OB?=
Reh	MYfGeY5kfGmxbjDBd5NigQ>?	MVWwMlMwOSEQvF2=	M3jaUlEzKGh?	M2TFe2ROW09?	Mn3S[Y5p[W6lZYOgeIhmKGW6cILld5Nqd25ib3[gVnVPYDNiaX7keYNm\CCkeTC1MYF7[S2FZGK=	M1zFXFIzOTd7MUm4

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	EGFR / STAT3 ; PubMed: 31289542 Oncol Lett Expression of EGFR and STAT3 in PC3 cells treated with TSA. PC3 cells were plated in 6-cm dishes, and 0.25, 0.5 or 1 µM TSA was added for 24 h. DMSO was added into the control group wells. Cells were collected and lysed with lysis buffer and the protein expression analyzed via western blotting. Cyclin D1 / CDK6 / CDK4 / p-RB / RB; PubMed: 31289542 Oncol Lett Expression of cyclin D1, CDK6, CDK4 and RB, and the phosphorylation of RB, was detected in PC3 cells treated with TSA for 24 h. MMP-1 / MMP-3 / MMP-13 / TIMP-1; PubMed: 27431944 Mol Med Rep Chondrocytes were pretreated with increasing concentrations of TSA for 2 h, followed by stimulation with 5 ng/ml IL-1β for 24 h. Acetyl-H3 (Lys27) / H3 (96C10) / Acetyl-H4(Lys8) / H4(L64C1); PubMed: 27431944 Mol Med Rep Chondrocytes were treated with increasing concentrations of TSA for 24 h. α-H3Ac / α-H4Ac / α-H3K9Ac / α-H3K9 S10 / α-H3K4 me / α-H3K4 me2 / α-H3K9 me2; PubMed: 23802098 Front Oncol Histone acetylation occurs directly at the promoter region of IL-23R. The ChIP assay demonstrates that TSA treatment results in an increase in the acetylation of histone H3 and H4. A549 cells were cultured in the presence or absence of TSA (250 ng/mL) for a period of 24 h. Subsequently, a ChIP assay was performed using the following antibodies; pan acetyl-histone H3 (H3Ac), pan acetyl-histone H4 (H4Ac), acetyl-histone H3 Lys 9 (H3K9Ac), acetyl-histone H3 Lys 9/14 (H3K9/14ac), acetyl-histone H3 Lys 9 phosphoSer10 (H3K9S10), methyl-histone H3 Lys 4 (H3K4Me), di methyl-histone H3 Lys 4 (H3K4Me2), and di methyl-histone H3 Lys 9 (H3K9Me2). Input DNA serves as a positive control as recommended by the manufacturer (Diagenode). A no antibody control was included to test for non-specific binding (UT, untreated; TSA, Trichostatin A).	31289542 27431944 23802098
Immunofluorescence	α-C/EBPβ / α-HP1α ; PubMed: 21122806 Exp Cell Res 3T3-L1 preadipocytes were grown on coverslips for three days and induced to differentiate by treatment with MDI (48 h) in the presence of vehicle (-TSA) or 87 nM Trichostatin A (+TSA). Under these experimental conditions: A-H Cells were fixed and permeabilized in cold methanol, subjected to IIF with the indicated antibodies, and nuclei were counterstained with DAPI. Scale bar, 5 μm. α-HDAC1 ; PubMed: 29045501 PLoS One MCF-7 cells were treated with indicated concentrations of trichostatin A (optical sections E-H, respectively) for 12 hours, fixed, permeabilized and optical sections were obtained by laser scanning confocal microscopy. Fluorescence signal for HDAC1 is shown in green (left panels), DAPI staining is shown in blue (middle panels), and merged optical sections are shown in the right panels. α-tubulin / acetylated histone 3; PubMed: 27957719 Neurotherapeutics Immunocytochemistry for acetylated α-tubulin (red) and acetylated histone 3 (green) on N2a cells treated with 1 μM TSA, ACY-738, and ACY-775.	21122806 29045501 27957719
Growth inhibition assay	Cell viability (A549 cells); PubMed: 27571418 PLoS One Cytotoxicity of histamine determined by MTT assay in A549 cells. Cell viability (MDA-MB-231 cells); PubMed: 27548148 Int J Mol Sci The human breast cancer cells (MDA-MB-231) were incubated with various concentrations of TSA (0–300 nM) for 24 h. Cell viability was measured by WST-8. Cell viability (PC3 cells); PubMed: 31289542 Oncol Lett PC3 cells were plated in a 96-well plate and treated with different doses of TSA (0, 0.25, 0.5 and 1 µM) for 72 h; an MTT assay was used to measure the effects of TSA on PC3 cell proliferation.	27571418 27548148 31289542

In vivo

Administration of Trichostatin A at 0.5 mg/kg for 4 weeks displays potent antitumor activity in the N-methyl-N-nitrosourea carcinogen-induced rat mammary carcinoma model, without any measurable toxicity at doses up to 5 mg/kg. ^[1] Single intraperitoneal doses of 10 mg/kg Trichostatin A in nontransgenic and spinal muscular atrophy (SMA) model mice results in increased levels of acetylated H3 and H4 histones and modest increases in survival motor neuron (SMN) gene expression. Administration of Trichostatin A at 10 mg/kg/day improves survival, attenuates weight loss, and enhances motor behavior in the SMA model mice. ^[5]

Protocol

Kinase Assay: ^[1]	- Collapse In vitro HDAC activity: Total cellular extracts are prepared from each breast cancer cell line (MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, or SK-BR-3). A 20 μL crude cell extract (~2.5 ×10⁵ cells), in the presence of varying concentrations of Trichostatin A in 0.1% (v/v) ethanol or 0.1% (v/v) ethanol as vehicle control, are incubated for 60 minutes at 25 °C with 1 μL (~1.5 × 10⁶ cpm) of [³H]acetyl-labeled histone H4 peptide substrate (NH2-terminal residues 2-20) that has been acetylated with [³H]acetic acid, sodium salt (3.7 GBq/mmol) by an in vitro incorporation method. Each 200 μL reaction is quenched with 50 μL of 1 M HCl/0.16 M acetic acid and extracted with 600 μL of ethyl acetate, and released [³H]acetate is quantified by scintillation counting. IC50 values are determined graphically using nonlinear regression to fit inhibition data to the appropriate dose-response curve.
Cell Research: ^[1]	- Collapse Cell lines: MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, and SK-BR-3 Concentrations: Dissolved in absolute ethanol, final concentrations ~10 μM Incubation Time: 96 hours Method: Cells are exposed to various concentrations of Trichostatin A for 96 hours. After treatment, cell proliferation is estimated using the sulforhodamine B colorimetric assay. Cell viability is determined by trypan blue exclusion. (Only for Reference)
Animal Research: ^[1]	- Collapse Animal Models: Inbred virgin female (Ludwig/Wistar/Olac) rats bearing tumors induced with NMU Dosages: ~5 mg/kg/day Administration: Injection s.c. (Only for Reference)

References

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Solubility (25°C)

In vitro	DMSO	23 mg/mL (76.05 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+2% Tween 80+ddH2O For best results, use promptly after mixing.	3mg/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 Download Trichostatin A (TSA) SDF

Molecular Weight	302.4
Formula	C₁₇H₂₂N₂O₃
CAS No.	58880-19-6
Storage	3 years-20°C powder 2 years-80°C in solvent
Synonyms	N/A
Smiles	CC(C=C(C)C=CC(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

Dosage

mg/kg

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Step 2: Enter the in vivo formulation (Different batches have different solubility ratios, please contact Selleck to provide you with the correct ratio)

% DMSO+ % + % Tween 80+ % ddH₂O

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Calculation results:

Working concentration： mg/ml；

Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL， Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation：Take DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH₂O，mix and clarify.

Note：1.Please make sure the liquid is clear before adding the next solvent.
2.Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.

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 (mg) = Concentration (mM) × Volume (mL) × 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).

The Serial Dilution Calculator Equation

Serial Dilutions
Concertration (start):
Dilution-folds:

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

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 (data from https://clinicaltrials.gov, updated on 2020-09-01)

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT03901053	Recruiting	Device: Reaktiv AFO\|Device: PhatBrace AFO	Foot Injuries and Disorders	Jason Wilken\|Minneapolis Veterans Affairs Medical Center\|Walter Reed National Military Medical Center\|Henry M. Jackson Foundation for the Advancement of Military Medicine\|Center for Veterans Research and Education\|University of Delaware\|Johns Hopkins Bloomberg School of Public Health\|University of Iowa	February 27 2020	Not Applicable
NCT03887650	Recruiting	Drug: Liposomal Bupivicaine 1.3%\|Drug: Bupivacaine 0.5%	Post-operative Pain\|Total Shoulder Arthroplasty\|Osteoarthritis of the Shoulder\|Pain Management	Hartford Hospital	January 14 2019	Phase 4
NCT03838926	Recruiting	Drug: Trichostatin A	Relapsed or Refractory Hematologic Malignancies	Vanda Pharmaceuticals	September 27 2018	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.

Frequently Asked Questions

Question 1:
I would like to obtain the enantiomers of TSA, as separate chemicals: R-TSA and S-TSA. Do you have any ideas?
Answer:
Our S1045 Trichostatin A (TSA) is R enantiomer.

HDAC Signaling Pathway Map

HDAC Inhibitors with Unique Features

Selective HDAC Inhibitor

RGFP966 : HDAC3-selective, IC50=80 nM.
Selective HDAC Inhibitor

Rocilinostat (ACY-1215) : HDAC5-selective, IC50=5 nM.
Most Potent HDAC Inhibitor

Quisinostat (JNJ-26481585) : HDAC1, IC50=0.11 nM; HDAC2, IC50=0.33 nM.
FDA-approved HDAC Inhibitor

Vorinostat (SAHA, MK0683) : Approved by FDA against cutaneous T cell lymphoma.
Newest HDAC Inhibitor

RG2833 (RGFP109) ^New : Brain-penetrant HDAC inhibitor with IC50 of 60 nM and 50 nM for HDAC1 and HDAC3, respectively.

Related HDAC Products

LMK-235 ^New

LMK-235 is a selective inhibitor of HDAC4 and HDAC5 with IC50 of 11.9 nM and 4.2 nM, respectively.
CAY10603 ^New

CAY10603 is a potent and selective HDAC6 inhibitor with IC50 of 2 pM, >200-fold selectivity over other HDACs.
Domatinostat (4SC-202) ^New

4SC-202 is a selective class I HDAC inhibitor with IC50 of 1.20 μM, 1.12 μM, and 0.57 μM for HDAC1, HDAC2, and HDAC3, respectively. Also displays inhibitory activity against Lysine specific demethylase 1 (LSD1). Phase 1.
Panobinostat (LBH589)

Panobinostat (LBH589, NVP-LBH589) is a novel broad-spectrum HDAC inhibitor with IC50 of 5 nM in a cell-free assay. Panobinostat (LBH589) induces autophagy and apoptosis. Panobinostat effectively disrupts HIV latency in vivo. Phase 3.
Vorinostat (SAHA)

Vorinostat (suberoylanilide hydroxamic acid, SAHA, MK0683) is an HDAC inhibitor with IC50 of ~10 nM in a cell-free assay. Vorinostat abrogates productive HPV-18 DNA amplification.
Entinostat (MS-275)

Entinostat (MS-275, SNDX-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. Entinostat induces autophagy and apoptosis. Phase 3.
Romidepsin (FK228, Depsipeptide)

Romidepsin (FK228, depsipeptide) is a potent HDAC1 and HDAC2 inhibitor with IC50 of 36 nM and 47 nM in cell-free assays, respectively. Romidepsin (FK228/depsipeptide) controls growth and induces apoptosis in neuroblastoma tumor cells.

Features:More effective than other classical HDAC inhibitors such as TSA, TPX, and butyrate.
RGFP966

RGFP966 is an HDAC3 inhibitor with IC50 of 0.08 μM in cell-free assay, exhibits > 200-fold selectivity over other HDAC.
Tubastatin A

Tubastatin A is a potent and selective HDAC6 inhibitor with IC50 of 15 nM in a cell-free assay. It is selective against all the other isozymes (1000-fold) except HDAC8 (57-fold). Tubastatin A promotes autophagy and increases apoptosis.
Mocetinostat (MGCD0103)

Mocetinostat (MGCD0103, MG0103) is a potent HDAC inhibitor with most potency for HDAC1 with IC50 of 0.15 μM in a cell-free assay, 2- to 10- fold selectivity against HDAC2, 3, and 11, and no activity to HDAC4, 5, 6, 7, and 8. Mocetinostat (MGCD0103) induces apoptosis and autophagy. Phase 2.

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Trichostatin A (TSA)