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    Romidepsin (FK228, FR901228, Depsipeptide, NSC630176)
    Romidepsin (FK228, FR901228, Depsipeptide, NSC630176)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0261
    CAS #: 128517-07-7Purity ≥98%

    Description: Romidepsin (formerly FK-228, FR-901228, Depsipeptide, NSC-630176; trade name Istodax) is a novel, potent and naturally occuring bicyclic depsipeptide antibiotic isolated from the bacterium Chromobacterium violaceum with potential anticancer activity. Romidepsin acts as a potent histone deacetylase (HDAC1/2) inhibitor with IC50 of 36 nM and 47 nM in cell-free assays, respectively. After intracellular activation, romidepsin binds to and inhibits HDAC, resulting in alterations in gene expression and the induction of cell differentiation, cell cycle arrest, and apoptosis. The US FDA approved romidepsin for the treatment of cutaneous T-cell lymphoma (CTCL) in November 2009 and approved romidepsin for other peripheral T-cell lymphomas (PTCLs) in June 2011.

    ReferencesCancer Res. 2002 Sep 1;62(17):4916-21; Biochem Pharmacol. 2002 Oct 1;64(7):1079-90; Int J Cancer. 2002 Jan 20;97(3):290-6.

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    Molecular Weight (MW)540.7
    CAS No.128517-07-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 10 mg/mL (18.5 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)1% DMSO+30% polyethylene glycol+1% Tween 80: 18mg/mL
    SynonymNSC 630176;FK228; FK 228; FK-228; FR901228; FR-901228; FR 901228; NSC-630176; NSC-630176; depsipeptide; US trade name: Istodax.

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    In Vitro

    In vitro activity: 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

    Kinase Assay: 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.

    Cell Assay: Cells are exposed to various concentrations of Romidepsin for 72 hours in 96-well plates. 20 μL of 5 mg/mL MTT solution in PBS is added to each well for 4 hours. After removal of the medium, 170 μL of DMSO is added to each well to dissolve the formazan crystals. The absorbance at 540 nm is determined. In addition, cells are incubated with trypan blue, and the numbers of blue (dead) cells and transparent (live) cells are counted in a hemocytometer. For cell cycle analysis, cells are incubated for 30 minutes in propidium iodide staining solution containing 0.05 mg/mL propidium iodide, 1 mM EDTA, 0.1% Triton X-100, and 1 mg/mL RNase A in PBS. The suspension is then passed through a nylon mesh filter and analyzed on a Becton Dickinson FACScan.

    In VivoRomidepsin 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).
    Animal model Nude mice inoculated i.p. with U-937 cells
    Formulation & DosageDissolved in DMSO and then diluted in saline; 1 mg/kg; i.p. injection.

    Cancer Res. 2002 Sep 1;62(17):4916-21; Biochem Pharmacol. 2002 Oct 1;64(7):1079-90; Int J Cancer. 2002 Jan 20;97(3):290-6.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    Romidepsin (FK228, Depsipeptide)


    Romidepsin (FK228, Depsipeptide)


    Romidepsin (FK228, Depsipeptide)


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