Trichostatin A (TSA)

Name: Trichostatin A (TSA)
Brand: Selleck Chemicals
SKU: S1045
Rating: 5 (113 reviews)

For research use only. Not for use in humans.

Catalog No.S1045

113 publications

Molecular Weight(MW): 302.4

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 113 publications

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

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

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

PubMed: 30661930 ( click the link to review the publication )

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

PubMed: 29088702 ( click the link to review the publication )

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

PubMed: 29056338 ( click the link to review the publication )

Nat Biotechnol, 2015, 10.1038/nbt.3130

PubMed: 25751058 ( click the link to review the publication )

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

PubMed: 25314079 ( click the link to review the publication )

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

PubMed: 30704899 ( click the link to review the publication )

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

PubMed: 31054974 ( click the link to review the publication )

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

PubMed: 30704899 ( click the link to review the publication )

Nat Commun, 2019, 10(1):5792

PubMed: 31857589 ( click the link to review the publication )

Nat Commun, 2019, 10(1):4353

PubMed: 31554795 ( click the link to review the publication )

Nat Commun, 2019, 10(1):5800

PubMed: 31863007 ( click the link to review the publication )

Sci Adv, 2019, 5(3):eaav1118

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

Autophagy, 2019, 1-13

PubMed: 30957628 ( click the link to review the publication )

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

PubMed: 29988076 ( click the link to review the publication )

Int J Cancer, 2019, 10.1002/ijc.32425

PubMed: 31111958 ( click the link to review the publication )

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

PubMed: 30852137 ( click the link to review the publication )

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

PubMed: 30852137 ( click the link to review the publication )

EBioMedicine, 2019, 43:238-252

PubMed: 31047858 ( click the link to review the publication )

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

PubMed: 31112333 ( click the link to review the publication )

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

PubMed: 31665064 ( click the link to review the publication )

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

PubMed: 30777099 ( click the link to review the publication )
J Exp Clin Cancer Res, 2019, 38(1):463

PubMed: 31718704 ( click the link to review the publication )

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 )

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 )

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 )

Sci Rep, 2018, 8(1):13072

PubMed: 30166563 ( 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 )

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 )

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 )

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

PubMed: 27922200 ( 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

PubMed: 28860353 ( click the link to review the publication )

J Diabetes Res, 2017, 2017:8208065

PubMed: 28191472 ( click the link to review the publication )

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

PubMed: 28110187 ( click the link to review the publication )

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

PubMed: 27404795 ( click the link to review the publication )

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

PubMed: 28192116 ( click the link to review the publication )

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

PubMed: 28060760 ( click the link to review the publication )

Nat Commun, 2016, 7:10690

PubMed: 26891683 ( click the link to review the publication )
Nucleic Acids Res, 2016, 45(3):1159-1176

PubMed: 28180300 ( click the link to review the publication )

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

PubMed: 26634271 ( click the link to review the publication )

Thorax, 2016, 633-45

PubMed: 27071418 ( click the link to review the publication )

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

PubMed: 26681404 ( click the link to review the publication )

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

PubMed: 27498117 ( click the link to review the publication )

Oxid Med Cell Longev, 2016, 2016:4085727

PubMed: 27746856 ( click the link to review the publication )

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

PubMed: 27555113 ( click the link to review the publication )

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

PubMed: 27573019 ( click the link to review the publication )

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

PubMed: 27082124 ( click the link to review the publication )

BMC Cancer, 2016, 16(1):886

PubMed: 27842508 ( click the link to review the publication )

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

PubMed: 27000860 ( click the link to review the publication )

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

PubMed: 29254139 ( click the link to review the publication )

Genet Mol Res, 2016, 15(4)

PubMed: 27819724 ( click the link to review the publication )

Sci Rep, 2016, 6:21678

PubMed: 26902929 ( click the link to review the publication )

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

PubMed: 26729194 ( click the link to review the publication )

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

PubMed: 26831669 ( click the link to review the publication )

EMBO Mol Med, 2015, 10.15252/emmm.201404396

PubMed: 25872941 ( click the link to review the publication )

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

PubMed: 25449774 ( click the link to review the publication )

Am J Transplant, 2015, 10.1111/ajt.13106

PubMed: 25708614 ( click the link to review the publication )

Cell Death Dis, 2015, 6:e1586

PubMed: 25569103 ( click the link to review the publication )

J Antimicrob Chemother, 2015, 10.1093/jac/dku549

PubMed: 25558076 ( click the link to review the publication )

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

PubMed: 25303559 ( click the link to review the publication )

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

PubMed: ( click the link to review the publication )

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

PubMed: 26498249 ( click the link to review the publication )
Chem Biol Interact, 2015, 242:227-34

PubMed: 26482938 ( click the link to review the publication )

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

PubMed: 26158412 ( click the link to review the publication )

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

PubMed: 25398909 ( click the link to review the publication )

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

PubMed: 24395801 ( click the link to review the publication )

PLoS Biol, 2014, 12(1):e1001758

PubMed: 24409098 ( click the link to review the publication )

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

PubMed: ( click the link to review the publication )

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

PubMed: 25202123 ( click the link to review the publication )

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

PubMed: 24200994 ( click the link to review the publication )

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

PubMed: 24486299 ( click the link to review the publication )

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

PubMed: 24530917 ( click the link to review the publication )

Sci Rep, 2014, 4:4663

PubMed: 24722541 ( click the link to review the publication )

Science, 2014, 344(6183):1252304

PubMed: 24727982 ( click the link to review the publication )

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

PubMed: 23474591 ( click the link to review the publication )

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

PubMed: 23464703 ( click the link to review the publication )

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

PubMed: 24373940 ( click the link to review the publication )

Genes Brain Behav, 2013, 13(1):69-86

PubMed: 24286462 ( click the link to review the publication )

Epigenetics, 2012, 7(10):1161-72

PubMed: 22965008 ( click the link to review the publication )

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	Moq1SpVv[3Srb36gRZN{[Xl?	MmXVNE44\|ryP	MnfwNlRp	NHzad2tmfGijbn;s	M2jCXYVvcGGwY3XzJGVP[UNiYXPleJlt[XSrb36gZY5lKGmwY4LlZZNmeyCHTnHDJIFjfW6mYX7j[UBqdiC2aHWgeI91[WxiY3XscEBtgXOjdHWgZY5lKGG2IITo[UBk\WyuIIP1doZi[2V?	MlznNlU4QDdyN{m=
TE13	NVLUPIszTnWwY4Tpc44hSXO\|YYm=	NFTKfGYxNjQQvF2=	MYiyOIg>		NXO4bodofXBvcnXneYxifGW\|IGLBV3NHPUFibHX2[Yw>	NEHjVoczPTV5OU[2OS=>
TE13	NWXOd4pOSXCxcITvd4l{KEG\|c3H5	MUOwMlPPxE1?	MX[yOIg>		MWrpcohq[mm2czD0bIUh[2WubDDwdo9tcW[ncnH0bY9v	MUeyOVU4QTZ4NR?=
MEFs	MkPwSpVv[3Srb36gRZN{[Xl?	NWLEdJVqPc7:TR?=	NEi3RoYyPmh?		MYXpcoNz\WG\|ZYOgeIhmKEWSRVOgZZR1[WOqbXXueEwhXGm{IHTlcIl3\XK7IHHu[EB1cGViZX\mbYNq\W6leTDv[kBx\WSnc4ThcEBnd3KvYYTpc44>	M{nZWFI2PDh{NkO0
SW480	NYP1UIlGTnWwY4Tpc44hSXO\|YYm=	M{XLRlAvOc7:TR?=	MlKwOFhp	NXTPXmMxTE2VTx?=	MlLydoV3\XK\|ZYOgSW1V	MWSyOVQ{PDl7Nx?=
PC3	MVfGeY5kfGmxbjDBd5NigQ>?	NVXIVGx6OC5zzszN	MlLiOFhp	NGe3cHZFVVOR	M1zpdpJmfmW{c3XzJGVOXA>?	NUHGS25rOjV2M{S5PVc>
SW480	NGG1U5BHfW6ldHnvckBCe3OjeR?=	Mlq1NE4y\|ryP	NWrMR41pPDiq	NYficVVSTE2VTx?=	MnvnZZR1\W63YYTld{Bqdn[jc3nvckBidmRibXnndoF1cW:w	MW[yOVQ{PDl7Nx?=
PC3	NWnTWY11TnWwY4Tpc44hSXO\|YYm=	NIj2fZMxNjIQvF2=	NED4NlQ1QGh?	MXfEUXNQ	NVzGSGo{[XS2ZX71ZZRmeyCrbo\hd4lwdiCjbnSgcYloemG2aX;u	MknDNlU1OzR7OUe=
SW480	MUDGeY5kfGmxbjDBd5NigQ>?	MlXtNE4y\|ryP	NXnZdZFxPDiq	NH[1OHZFVVOR	NFLBPIpqdmS3Y3XzJIlv[3KnYYPlJI9nKEiGQVOxJIFv\CCKRFHDNkBwdiCVbIXnJIdmdmW\|IIDyc41wfGW{	NX\iS3dtOjV2M{S5PVc>
PC3	Mm\QSpVv[3Srb36gRZN{[Xl?	MkXVNE4y\|ryP	MnHsOFhp	M4LvcmROW09?	MWHpcoR2[2W\|IHnuZ5Jm[XOnIH;mJGhFSUNzIHHu[EBJTEGFMjDvckBUdHWpIHflcoV{KHC{b33veIVz	NIO0co8zPTR\|NEm5Oy=>
A431	MX;BdI9xfG:\|aYOgRZN{[Xl?	NUjPU5AxOi9zMD:1NE8yODCwTR?=	NGjZUFU1QGh?	MlTXSG1UVw>?	MWXpcohq[mm2czD0bIUh[2WubDDndo94fGh?	M3y4ZlI2OzdzME[5
A431	NXzTTIF2TnWwY4Tpc44hSXO\|YYm=	NUHUW4p{PTCwTR?=	MoXPNk83NzF{L{K0bC=>	NGTZO5FFVVOR	MkPTZYN1cX[jdHXzJJAzOSCjbnSgbY5pcWKrdIOgRXRHOyCneIDy[ZN{cW:w	NYjIXJpyOjV\|N{GwOlk>
MDA-MB-231	MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NYO2TZpsOC14MEDuUS=>	NGXIV2YzPGh?	NXzGTGlXTE2VTx?=	MWHJR\|UxKG:oIEGwNI5O	Mo\CNlUyQTJ5MkG=
MCF7	NGfEVZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NYf0VpJOOC14MEDuUS=>	NEPhRnMzPGh?	NYL5do1KTE2VTx?=	NYruOFlZUUN3MDDv[kA4PW6P	NWfqelVKOjVzOUK3NlE>
SKOV-3	NYj6dXJUT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NGfPRoUyNTFyzszN	NYXXT5piOjSq	MXTEUXNQ	M1LGXGlEPTBib3[gOU43\|ryP	NYO5NWptOjVzNkm0PVE>
A549	MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MnHJNU0yOM7:TR?=	MYOyOIg>	MV7EUXNQ	M1;HRmlEPTBib3[gN{4z\|ryP	M1\qbFI2OTZ7NEmx
SKOV-3	NGDaPJdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M4nkdVAvOS1zzszN	NITpO3o1QGh?	Mnr3SG1UVw>?	M1\SfWlEPTBib3[gNE44\|ryP	NIfYcGgzPTF4OUS5NS=>
A549	NWHxW5FQT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MoTrNE4yNTIQvF2=	NE\VUnk1QGh?	NHvJZmJFVVOR	MVfJR\|UxKG:oIECuNljPxE1?	M{K4eFI2OTZ7NEmx
SKOV-3	MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVOwMlAyNTBwOd88US=>	NV7GPZRlPzKq	MXHEUXNQ	NELJOYNKSzVyIH;mJFAvOzMQvF2=	NX\0bFZLOjVzNkm0PVE>
A549	NXHBXWMyT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NHnrZ3cxNjBzLUCuPe69VQ>?	NVHvSnViPzKq	NWjx[YJJTE2VTx?=	NIrkOoxKSzVyIH;mJFAvODcQvF2=	MoHTNlUyPjl2OUG=
HeLa	MljPSpVv[3Srb36gRZN{[Xl?	NWK0dJJKOjVybl2=	M3vWbFE3cA>?	NFjGUZFFVVOR	NHzTS\|JqdmO{ZXHz[ZMhS1mSMVGxJI1TVkFiZYjwdoV{e2mxbtMg	M3faNFI2OTF4Nki4
CNE2	M4jzbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MlnoNVAxNTZyMH7N	NWHKWlI4OjRxNEivO\|Jp		NVzHXll1cW6qaXLpeJMhfGinIIDyc4xq\mW{YYTpc44hcW5iYTD0bY1mNSCjbnSg[I9{\S2mZYDlcoRmdnRibXHucoVz	MkDXNlQ6Pjl7MEG=
PC3	MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NGPZUlYyODBvMUCwNI5O	NHHKVpUzPGh?		NGXXNmZKSzVyIH;mJFMxOG6P	M{f6PFI1QDV2NkW4
LNCaP	NVfYcGdHT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NELOZnUyODBvMUCwNI5O	M3LDTVI1cA>?		NIq3TWtKSzVyIH;mJFMxOG6P	MUKyOFg2PDZ3OB?=
HeLa	Mmi5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	Moj0Nu69VQ>?	M2LNZlQ5cA>?		M3jES4Rm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDhZo92fCB{NTW=	MlnWNlQ5PDZzM{W=
HMEC-1	MYnGeY5kfGmxbjDBd5NigQ>?	MXmzNFBvVQ>?	MWKyOIg>		MnrGbY5kemWjc3XzJIV5eHKnc4Ppc44hd2cEoG\FS2ZTO8LibWLORS=>	M33tNlI1PzFyNkOx
HeLa	NHHKeJNHfW6ldHnvckBCe3OjeR?=	MmXYNY1O	Mn3ZNE42cA>?		Ml;BZYJwdGm\|aHXzJJRp\SC2b4ThcEBJTEGFIHHjeIl3cXS7	MWmyOFcxPzR5NB?=
ACP02	NHPmZ2dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NWe2XJI6OjVyL{O1NE82ODCwTR?=	M1TsO\|I1cA>?		MYPk[YNz\WG\|ZYOgZ4VtdCC4aXHibYxqfHlib3[gZZBxem:6aX3heIVtgSB5MNMgKUBifCB{NUFCpI5O	NILzUJEzPDZ4OEW0Oy=>
ACP03	NHm2OmxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MnLTNlUxNzN3MD:1NFBvVQ>?	M1frflI1cA>?		Mkn4[IVkemWjc3XzJINmdGxidnnhZoltcXS7IH;mJIFxeHKxeHntZZRmdHliN{FCpEUh[XRiMkWwxsBvVQ>?	MX6yOFY3QDV2Nx?=
U87 GBM	NHr3UZNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MWGxNFAwOzByL{WwNEBvVQ>?	MUm3NkBp	MWKxNFAmKGW2aHHuc4w>	MoXMdoVlfWOnczDt[YFvKGOnbHygcpVu[mW{IHL5JFMyNCB3NDygZY5lKDV6wrCl	M33DSFI1PDZ2OESx
U87 GBM	NVL5PIN6TnWwY4Tpc44hSXO\|YYm=	MWixNFAwPTByIF7t	M1P5S\|Q5KGh?	NYTLUoFVOTByJTDleIhidm:u	MVHJcoR2[2W\|IGPlcoV{[2WwY3WtUIls\SCDbITldoF1cW:wczDpckBPfWOuZXHyJG1wenCqb3zv[5k>	NVG3doJ7OjR2NkS4OFE>
RPE	NEPGUZhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MWCwMlIwOC52L{CuPE8yKM7:TR?=	MWiyOE81QC95MjDo	NELUWJRFVVOR	NXrvSW94cW6qaXLpeJMhfGinIIDyc4xq\mW{YYTpc44h[nliY3XscEBkgWOuZTDhdpJme3R?	M4\wSFI1PDV4NkCy
HT29	NWjX[IFpT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M2ToVlE5OCCwTR?=	NGHzV2M4OiCq		Mli5TWM2OCCxZjCxPFAhdk1?	M2fGUVI1OzZ6Mk[1
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HL60	NILzelJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NX7uSpZwOTVyLUO1NEBvVQ>?	MnPONlQhcA>?		NXnWbXQ2cW6lcnXhd4V{KGOnbHygZZBweHSxc3nzxsB4cGWwIHPvcoNmdnS{YYTpc45{KGirZ3jldkB1cGGwIEK1NEBvVQ>?	M1fRR\|IzPzV\|N{O5
U937	MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NIHqNoYyPTBvM{WwJI5O	M{PYeVI1KGh?		NETPRlVqdmO{ZXHz[ZMh[2WubDDhdI9xfG:\|aYRCpJdp\W5iY3;uZ4VvfHKjdHnvcpMhcGmpaHXyJJRp[W5iMkWwJI5O	NI\3VGYzOjd3M{ezPS=>
SCC-6	NYnqRXZmT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MmXnNlAxNTN{MECgcm0>	NWPhZlg2OTJxMkSvOFghcA>?	NELsWoVFVVOR	NYOye4N1cW6qaXLpeJMhfGinIIDyc4xq\mW{YYTpc44hd2ZiU1PDMVYh[2WubIOgbY4h[SCmb4PlMUBidmRidHnt[U1l\XCnbnTlcpQhdWGwbnXy	MXGyNlU2OjN{MR?=
U87	MmX4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M4PIbVExOC1\|MECgcoc>	NFXvdHEzPCCq		MVLpcohq[mm2czD0bIUh[2WubDDndo94fGhidH:gO\|ImKCCjdDCyNFBv\w>?	NFvnPG8zOjJ5MEi0PS=>
K562	NWXDZWtWTnWwY4Tpc44hSXO\|YYm=	M3;tdFEh\|ryP	NEC1dnQyOiCq	M164bmROW09?	M3PBT4VvcGGwY3XzJJRp\SCneIDy[ZN{cW:wIH;mJHJWVlh\|IHnu[JVk\WRiYomgOU1igmFvQ3TS	MnXQNlIyPzlzOUi=
Reh	MWXGeY5kfGmxbjDBd5NigQ>?	MXOwMlMwOSEQvF2=	NV;HTGRUOTJiaB?=	MnHTSG1UVw>?	M3zzcYVvcGGwY3XzJJRp\SCneIDy[ZN{cW:wIH;mJHJWVlh\|IHnu[JVk\WRiYomgOU1igmFvQ3TS	NVf4bVh2OjJzN{mxPVg>

... 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 Formulation: Dissolved in DMSO 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
Storage	2 years -80°C in solvent
Synonyms	N/A

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)

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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 )

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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):
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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

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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 2019-10-14)

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT03901053	Not yet 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	June 2019	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) is a novel broad-spectrum HDAC inhibitor with IC50 of 5 nM in a cell-free assay. Phase 3.
Vorinostat (SAHA)

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

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.
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.

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).
Mocetinostat (MGCD0103)

Mocetinostat (MGCD0103) 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. Phase 2.

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Trichostatin A (TSA)