Romidepsin (FK228, Depsipeptide)
Catalog No.S3020 Synonyms: FR 901228, NSC 630176
Molecular Weight(MW): 540.7
Romidepsin (FK228, depsipeptide) is a potent HDAC1 and HDAC2 inhibitor with IC50 of 36 nM and 47 nM in cell-free assays, respectively.
Cited by 15 Publications
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An HIV-Gag-SLYNTVATL-specific CTL clone was labeled with Alexa-Fluor555 conjugated cholera toxin subunit B either cultured with 500 nM SAHA or 25 nM romidepsin for 20 hours, or maintained as an untreated control. These effector cells were combined with SLYNTVATL peptide pulsed target cells, matched on the restricting allele, in a collagen matrix medium containing sytox green viability dye. These mixtures were then plated in three separate wells of an 8-well cover slip and imaged by time-lapse brightfield and fluorescent microscopy. A. Shown are representative fields of view from the no treatment (upper panel), 500 nM SAHA (middle panel), and 25 nM romidepsin (lower panel) conditions advancing in time from left to right. Time stamps are given in hh[ratio]mm format. Clones described in the results are indicated with yellow arrows and killed target cells are indicated with white arrows in the upper right panel.
PLoS Pathog 2014 10(8), e1004287. Romidepsin (FK228, Depsipeptide) purchased from Selleck.
PLZF-RARa–nonexpressing and -expressing PLZFRARβ3 cells were treated with 5 nmol/L romidepsin for the indicated time points. Induction of the DNA DSB marker γH2AX was measured by Western blotting. β-Actin was used as a loading control.
Mol Cancer Ther 2013 12(8), 1591-604. Romidepsin (FK228, Depsipeptide) purchased from Selleck.
Effects of combination of bort/romidepsin on HDAC6 inhibition and activation of ER stress signaling. HA cells were treated with combination of 15 nM bortezomib and 5 nM romidepsin or either drug alone for 24 hr. Expression of CHOP/GADD153 (green signals) and cleaved PARP (red signals) was detected by immunoﬂuorescent staining. DAPI (blue signals) stained the cell nuclei.
Int J Cancer 2014 135(12):2950-61. Romidepsin (FK228, Depsipeptide) purchased from Selleck.
Purity & Quality Control
Choose Selective HDAC Inhibitors
|Description||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.|
Unlike TSA, the active form redFK of Romidepsin strongly inhibits HDAC1 and HDAC2 with IC50 of 1.6 nM and 3.9 nM, respectively, but is relatively weak in inhibiting HDAC4 and HDAC6 with IC50 25 nM and 790 nM, respectively. Romidepsin is 17-23 times weaker than redFK in inhibiting these HDACs with IC50 of 36 nM, 47 nM, 510 nM, and 14 μM, respectively. Romidepsin treatment in HeLa cells induces histone acetylation and p21 expression with EC50 of 3.0 nM, more strongly than redFK with EC50 of 11 nM due to the instability of redFK.  In addition to G2/M arrest, Romidepsin treatment causes cyclin D1 downregulation and a p53-independent p21 induction, leading to inhibition of CDK and dephosphorylation of Rb resulting in growth arrest in the early G1 phase.  Romidepsin is 100 times more potent than TSA and 1,000,000 times more potent than butyrate in inhibiting the proliferation of the A549 cells.  Romidepsin inhibits the growth of U-937, K562, and CCRF-CEM cells with IC50 of 5.92 nM, 8.36 nM, and 6.95 nM, respectively.  Romidepsin promotes apoptosis in chronic lymphocytic leukemia (CLL) cells at a concentration corresponding to that at which H3 and H4 acetylation and HDAC inhibition occurs, selectively involving activation of caspase 8 and effector caspase 3, as well as down-regulation of c-FLIP protein.  In 11 of 13 (85%) renal cell carcinoma cell lines and in 16 of 37 (43%) other cancer cell lines, Romidepsin treatment up-regulates tumor death receptors, and potentiates natural killer (NK)-mediated tumor killing.  Romidepsin exhibits concentration-dependent cytotoxicity against a panel of mantle cell lymphoma (MCL) cell lines. 
|In vivo||Romidepsin treatment potently inhibits the neovascularization of chick embryo and that of adult mice in the Matrigel plug assay. Administration of Romidepsin at 0.1-1 mg/kg twice a week significantly prolongs the survival of mice bearing U-937 lymphoma, with median survival times of 30.5 (0.56 mg/kg) and 33 days (0.32 mg/kg), respectively (vs. 20 days in control mice). |
HDAC-inhibitory activity:For the enzyme assay, 10 μL of [3H]acetyl-labeled histones (25,000 cpm/10 μg) are added to 90 μL of the HDAC enzyme fraction extracted from 293T cells overexpressing HDAC1 or HDAC2 in the presence of increasing concentrations of Romidepsin, and the mixture is incubated at 37 °C for 15 minutes. The enzyme reaction is linear for at least 1 hour. The reaction is stopped by the addition of 10 μL of concentrated HCl. The released [3H]acetic acid is extracted with 1 mL of ethylacetate, and 0.9 mL of the solvent layer is taken into 5 mL of aqueous counting scintillant II solution for determination of radioactivity. The IC50 values are determined from at least three independent dose-response curves.
-  Furumai R, et al. Cancer Res, 2002, 62(17), 4916-4921.
-  Sandor V, et al. Br J Cancer, 2000, 83(6), 817-825.
-  Blagosklonny MV, et al. Mol Cancer Ther, 2002, 1(11), 937-941.
-  Kwon HJ, et al. Int J Cancer, 2002, 97(3), 290-296.
-  Sasakawa Y, et al. Biochem Pharmacol, 2002, 64(7), 1079-1090.
-  Aron JL, et al. Blood, 2003, 102(2), 652-628.
-  Lundqvist A, et al. Cancer Res, 2006, 66(14), 7317-7325.
-  Dai Y, et al. Clin Cancer Res, 2008, 14(2), 549-558.
-  Paoluzzi L, et al. Clin Cancer Res, 2010, 16(2), 554-565.
|In vitro||DMSO||10 mg/mL (18.49 mM)|
|In vivo||Add solvents to the product individually and in order:
2% DMSO+30% PEG 300+5%Tween 80+ddH2O
For best results, use promptly after mixing.
* 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.
|Synonyms||FR 901228, NSC 630176|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT00048334||Completed||Neoplasms||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||October 26, 2002||Phase 1|
|NCT00094978||Terminated||Carcinoma, Small Cell|Carcinoma, Non-Small-Cell Lung|Esophageal Neoplasms|Mesothelioma||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||October 25, 2004||Phase 1|
|NCT01445340||Terminated||Mycosis Fungoides|Cutaneous T-Cell Lymphoma|Neoplasms||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||April 21, 2007||Phase 1|
|NCT02616965||Not yet recruiting||Cutaneous T-cell Lymphoma (CTCL)||Fox Chase Cancer Center|Seattle Genetics, Inc.|Celgene Corporation||April 2017||Phase 1|
|NCT02850016||Recruiting||Human Immunodeficiency Virus (HIV)||Rockefeller University|University Hospital of Cologne|Aarhus University Hospital||December 2016||Phase 2|
|NCT02757248||Withdrawn||PTCL|CTCL||Anne Beaven, MD|National Comprehensive Cancer Network|Boehringer Ingelheim|Duke University||November 2016||Phase 1|
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