Trichostatin A (TSA)

Catalog No.S1045

Molecular Weight(MW): 302.4

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

Cited by 111 Publications

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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	MYXGeY5kfGmxbjDBd5NigQ>?	MljlNE44\|ryP	NYHmdnI1OjSq	NYDtZXlx\XSqYX7vcC=>	MXvlcohidmOnczDFUoFEKGGlZYT5cIF1cW:wIHHu[EBqdmO{ZXHz[ZMhTU6jQzDhZpVv\GGwY3WgbY4hfGinIITveIFtKGOnbHygcJl{[XSnIHHu[EBifCC2aHWgZ4VtdCC\|dYLmZYNm	M37WWFI2Pzh5MEe5
TE13	MXLGeY5kfGmxbjDBd5NigQ>?	M2X0[FAvO87:TR?=	M{f3NFI1cA>?		MV\1dE1z\We3bHH0[ZMhWkGVU1[1RUBt\X[nbB?=	M2PlTFI2PTd7Nk[1
TE13	M1SxfGFxd3C2b4Ppd{BCe3OjeR?=	NH7NZW8xNjQQvF2=	MnX2NlRp		MoPobY5pcWKrdIOgeIhmKGOnbHygdJJwdGmoZYLheIlwdg>?	MlTtNlU2Pzl4NkW=
MEFs	M4LhdmZ2dmO2aX;uJGF{e2G7	MlXiOe69VQ>?	NXTBdFV6OT[q		M4TrR4lv[3KnYYPld{B1cGViRWDFR{BifHSjY3jt[Y51NCCWaYKg[IVtcX[ncomgZY5lKHSqZTDl[oZq[2mnbnP5JI9nKHCnZHXzeIFtKG[xcn3heIlwdg>?	MkjkNlU1QDJ4M{S=
SW480	NV;3SHpiTnWwY4Tpc44hSXO\|YYm=	MYmwMlHPxE1?	MmC0OFhp	NWPoOYp[TE2VTx?=	M2G0eJJmfmW{c3XzJGVOXA>?	M{DsSFI2PDN2OUm3
PC3	M3fYNGZ2dmO2aX;uJGF{e2G7	NFnuSYUxNjIQvF2=	NX3KfXFjPDiq	MX3EUXNQ	NXrDUpBDemW4ZYLz[ZMhTU2W	NVj3THFbOjV2M{S5PVc>
SW480	NETIdZpHfW6ldHnvckBCe3OjeR?=	M3nnO\|AvOc7:TR?=	MoHoOFhp	Ml7SSG1UVw>?	NWLmOVhI[XS2ZX71ZZRmeyCrbo\hd4lwdiCjbnSgcYloemG2aX;u	MlLKNlU1OzR7OUe=
PC3	M2XUPWZ2dmO2aX;uJGF{e2G7	NYTETnJuOC5zzszN	NXTSTYJZPDiq	NFW4eZBFVVOR	NGK3fGZifHSnboXheIV{KGmwdnHzbY9vKGGwZDDtbYdz[XSrb36=	MkO1NlU1OzR7OUe=
SW480	Ml\VSpVv[3Srb36gRZN{[Xl?	NYHJbow4OC5zzszN	NX3ES25rPDiq	MVzEUXNQ	M3O3d4lv\HWlZYOgbY5kemWjc3Wgc4YhUESDQ{GgZY5lKEiGQVOyJI9vKFOudXeg[4Vv\XNicILvcY91\XJ?	NV;SVnFIOjV2M{S5PVc>
PC3	M4XDemZ2dmO2aX;uJGF{e2G7	MnfXNE4y\|ryP	NET3T2Q1QGh?	M17hZ2ROW09?	M1\z[4lv\HWlZYOgbY5kemWjc3Wgc4YhUESDQ{GgZY5lKEiGQVOyJI9vKFOudXeg[4Vv\XNicILvcY91\XJ?	NYnMU2JIOjV2M{S5PVc>
A431	M4HGV2Fxd3C2b4Ppd{BCe3OjeR?=	NGi5WlEzNzFyL{WwM\|ExOG6P	MXq0PIg>	MmOzSG1UVw>?	NX\kWm9HcW6qaXLpeJMhfGinIHPlcIwh\3Kxd4To	MXWyOVM4OTB4OR?=
A431	M2i1WmZ2dmO2aX;uJGF{e2G7	MYW1NI5O	MmPLNk83NzF{L{K0bC=>	M1n1RmROW09?	NUDYdVFG[WO2aY\heIV{KHB{MTDhcoQhcW6qaXLpeJMhSVSIMzDlfJBz\XO\|aX;u	NYr1PXdHOjV\|N{GwOlk>
MDA-MB-231	M1T0UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGmxVGgxNTZyMH7N	MkXNNlRp	NX[yXZFpTE2VTx?=	MnXLTWM2OCCxZjCxNFBvVQ>?	NGr2UIgzPTF7MkeyNS=>
MCF7	NWm2e\|JrT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MVmwMVYxOG6P	NYTxOpZwOjSq	MlvJSG1UVw>?	NE\MboFKSzVyIH;mJFc2dk1?	MV[yOVE6Ojd{MR?=
SKOV-3	MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M3fBWlEuOTEQvF2=	MVmyOIg>	NVTTXpdtTE2VTx?=	Mn7zTWM2OCCxZjC1MlbPxE1?	MWeyOVE3QTR7MR?=
A549	MlL5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MYexMVEx\|ryP	NVnFOoZvOjSq	MlnnSG1UVw>?	MnvqTWM2OCCxZjCzMlLPxE1?	NEXUcIMzPTF4OUS5NS=>
SKOV-3	NVjDWYtIT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NH:3UmoxNjFvMd88US=>	NHrvfGo1QGh?	NU\uVXZVTE2VTx?=	MXTJR\|UxKG:oIECuO:69VQ>?	M4fzc\|I2OTZ7NEmx
A549	MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MWiwMlEuOc7:TR?=	NHHjfFI1QGh?	MUHEUXNQ	MYnJR\|UxKG:oIECuNljPxE1?	M3:1OVI2OTZ7NEmx
SKOV-3	MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{HrZlAvODFvMD65{txO	MnTOO\|Jp	NX33U4NFTE2VTx?=	M1X4c2lEPTBib3[gNE4{Os7:TR?=	M1XtU\|I2OTZ7NEmx
A549	M2L4RWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGLCXVcxNjBzLUCuPe69VQ>?	MoPSO\|Jp	NHLBUm9FVVOR	MVTJR\|UxKG:oIECuNFbPxE1?	MkD0NlUyPjl2OUG=
HeLa	NVqwR3JtTnWwY4Tpc44hSXO\|YYm=	MYqyOVBvVQ>?	MWixOog>	MlroSG1UVw>?	MYXpcoNz\WG\|ZYOgR3lROUFzIH3SUmEh\XiycnXzd4lwdsLi	Mk\sNlUyOTZ4OEi=
CNE2	NY[yTZA2T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MoLuNVAxNTZyMH7N	M4PqW\|I1NzR6L{eybC=>		M2\4SYlvcGmkaYTzJJRp\SCycn;sbYZmemG2aX;uJIlvKGFidHnt[U0h[W6mIHTvd4Uu\GWyZX7k[Y51KG2jbn7ldi=>	NFHKbWkzPDl4OUmwNS=>
PC3	Moj5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MkDGNVAxNTFyMEDuUS=>	M2rIUlI1cA>?		MWjJR\|UxKG:oIEOwNI5O	MlrQNlQ5PTR4NUi=
LNCaP	MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NYTPSnhOOTByLUGwNFBvVQ>?	M4LuclI1cA>?		MkLTTWM2OCCxZjCzNFBvVQ>?	NUPDSHlkOjR6NUS2OVg>
HeLa	NWHJc3RyT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NHPwSIoz\|ryP	NX22Xms{PDiq		NInnSGFl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgZYJwfXRiMkWl	NV\zSng5OjR6NE[xN\|U>
HMEC-1	MXnGeY5kfGmxbjDBd5NigQ>?	MnvzN\|Axdk1?	M{C2dFI1cA>?		MnzZbY5kemWjc3XzJIV5eHKnc4Ppc44hd2cEoG\FS2ZTO8LibWLORS=>	MUmyOFcyODZ\|MR?=
HeLa	NGjBeYVHfW6ldHnvckBCe3OjeR?=	MYexcW0>	MXqwMlVp		MmP1ZYJwdGm\|aHXzJJRp\SC2b4ThcEBJTEGFIHHjeIl3cXS7	MonnNlQ4ODd2N{S=
ACP02	M2TLemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MoTUNlUxNzN3MD:1NFBvVQ>?	NXjl[WdEOjSq		NULqTJl7\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JI9nKGGycILvfIlu[XSnbImgO\|DDqCViYYSgNlUxyqCwTR?=	MV:yOFY3QDV2Nx?=
ACP03	MljCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NXjUZ5VQOjVyL{O1NE82ODCwTR?=	M1y0clI1cA>?		NVfkOZUz\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JI9nKGGycILvfIlu[XSnbImgO\|DDqCViYYSgNlUxyqCwTR?=	MUSyOFY3QDV2Nx?=
U87 GBM	MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MlLvNVAxNzNyMD:1NFAhdk1?	MmnQO\|IhcA>?	M174V\|ExOCViZYToZY5wdA>?	M1e0V5Jm\HWlZYOgcYVidiClZXzsJI52dWKncjDifUA{OSxiNUSsJIFv\CB3ONMgKS=>	Mkm0NlQ1PjR6NEG=
U87 GBM	NYDTc2x[TnWwY4Tpc44hSXO\|YYm=	Ml3wNVAxNzVyMDDOcS=>	MV60PEBp	MoXaNVAxLSCndHjhco9t	MWnJcoR2[2W\|IGPlcoV{[2WwY3WtUIls\SCDbITldoF1cW:wczDpckBPfWOuZXHyJG1wenCqb3zv[5k>	M{W1dVI1PDZ2OESx
RPE	NGjDT\|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NXvjRXkzOC5{L{CuOE8xNjhxMTFOwG0>	M2TqNlI1NzR6L{eyJIg>	MVfEUXNQ	MkDnbY5pcWKrdIOgeIhmKHC{b3zp[oVz[XSrb36gZpkh[2WubDDjfYNt\SCjcoLld5Q>	NVrzVZE{OjR2NU[2NFI>
HT29	NH7tSVRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M2X6TFE5OCCwTR?=	NXq0N5prPzJiaB?=		NIPTR5pKSzVyIH;mJFE5OCCwTR?=	NH[2RpEzPDN4OEK2OS=>
hMSCs	NYPCNGs4TnWwY4Tpc44hSXO\|YYm=	MVi2MlI2KG6P	NVPIfHpqOjRiaB?=	M3;tcWROW09?	MUXzeIFjcWyrenXzJGhqe3SxbnWgRYNmfHmuYYTpc44h[W6mIITo[UBGgHC{ZYPzbY9vKG:oIGDseZJqeG:2ZX70JGdmdmW\|	NHm5SnozPDNzMkO1Oi=>
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HL60	MkO3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NXjQSYV6OTVyLUO1NEBvVQ>?	NHL2e2YzPCCq		M4TPO4lv[3KnYYPld{Bk\WyuIHHwc5B1d3Orc9Mge4hmdiClb37j[Y51emG2aX;ud{BpcWeqZYKgeIhidiB{NUCgcm0>	NGfuSpozOjd3M{ezPS=>
U937	M2XURWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M3fOS\|E2OC1\|NUCgcm0>	Mn;wNlQhcA>?		MYTpcoNz\WG\|ZYOgZ4VtdCCjcH;weI9{cXQEoIfo[Y4h[2:wY3XueJJifGmxboOgbIlocGW{IIToZY4hOjVyIH7N	MXKyNlc2Ozd\|OR?=
SCC-6	NIrJ[YdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MnnsNlAxNTN{MECgcm0>	MlPBNVIwOjRxNEigbC=>	Mk[zSG1UVw>?	MWHpcohq[mm2czD0bIUheHKxbHnm[ZJifGmxbjDv[kBUS0NvNjDj[YxteyCrbjDhJIRwe2VvIHHu[EB1cW2nLXTldIVv\GWwdDDtZY5v\XJ?	M{Ll[lIzPTV{M{Kx
U87	NIO4bJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NFr0fI0yODBvM{CwJI5o	NV6xfotNOjRiaB?=		NELCVpdqdmirYnn0d{B1cGViY3XscEBoem:5dHigeI8hPzJnIDDheEAzODCwZx?=	M2TTfFIzOjdyOES5
K562	MnnLSpVv[3Srb36gRZN{[Xl?	M4O3bVEh\|ryP	NF;tc3oyOiCq	MmL4SG1UVw>?	M{nPZYVvcGGwY3XzJJRp\SCneIDy[ZN{cW:wIH;mJHJWVlh\|IHnu[JVk\WRiYomgOU1igmFvQ3TS	MVuyNlE4QTF7OB?=
Reh	M1XmOmZ2dmO2aX;uJGF{e2G7	NHTUSWYxNjNxMTFOwG0>	MUSxNkBp	NHTtWFlFVVOR	MXHlcohidmOnczD0bIUh\XiycnXzd4lwdiCxZjDSWW5ZOyCrbnT1Z4VlKGK7IEWtZZpiNUOmUh?=	Mnq5NlIyPzlzOUi=

... 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

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C1=C0/X	C1:	LOG(C1):
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C4=C3/X	C4:	LOG(C4):
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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

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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,Domatinostat) ^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, MK0683)

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)

Cited by 111 Publications

Purity & Quality Control

Choose Selective HDAC Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download Trichostatin A (TSA) SDF

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Molarity Calculator

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

Dilution Calculator

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)

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Total Molecular Weight: g/mol

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Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-10-14)

Tech Support

Frequently Asked Questions

HDAC Signaling Pathway Map

HDAC Inhibitors with Unique Features

Related HDAC Products

Choose Your Country or Region

By Signaling Pathways

By product type

Trichostatin A (TSA)

Cited by 111 Publications

Purity & Quality Control

Choose Selective HDAC Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download Trichostatin A (TSA) SDF

Bio Calculators

Molarity Calculator

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

Dilution Calculator

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

Instructions to calculate molar mass (molecular weight) of a chemical compound:

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-10-14)

Tech Support

Frequently Asked Questions

HDAC Signaling Pathway Map

HDAC Inhibitors with Unique Features

Related HDAC Products

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)