RITA (NSC 652287)

Catalog No.S2781

RITA (NSC 652287) Chemical Structure

Molecular Weight(MW): 292.37

RITA (NSC 652287) induces both DNA-protein and DNA-DNA cross-links with no detectable DNA single-strand breaks, and also inhibits MDM2-p53 interaction by targeting p53.

Size Price Stock Quantity  
In DMSO USD 200 In stock
USD 170 In stock
USD 270 In stock
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  • To determine the number of viable cells, cells were serum starved for 8 hours and treated with 25 nM RITA and stimulated with 1ug/mL SDF1α for 48 hours in serum-free media. After 48 hours, cells were harvested and counted by trypan blue exclusion, using standard methods.

    Oncogene 2014 10.1038/onc.2014.37. RITA (NSC 652287) purchased from Selleck.

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Biological Activity

Description RITA (NSC 652287) induces both DNA-protein and DNA-DNA cross-links with no detectable DNA single-strand breaks, and also inhibits MDM2-p53 interaction by targeting p53.
Features Inducer of DNA cross-links, not a DNA intercalator.
Mdm2 [1] p53 [3]
In vitro

RITA shows a highly selective pattern of differential cytotoxic activity in the tumor cell lines, due to cellular accumulation to the cytosolic (S100) fraction. RITA also inhibits the growth of other renal cell lines including ACHN and UO-31 with IC50 of 13 μM and 37 μM, respectively. [1] RITA (10 nM) causes cell cycle arrest with accumulation of cells at the G2-M phase and induces DNA fragmentation and apoptosis at 100 nM, both with evaluated p53 protein levels. RITA (30 nM) also induces both DNA-protein and DNA-DNA cross-links in A498 cells. Meanwhile RITA has no effects on top1-mediated relaxation of supercoiled SV40 DNA. [2] RITA significantly suppresses the growth of HCT116 cells (97%) but only slightly inhibits the growth of HCT116 TP53-/- cells (13%). RITA is much more efficient at growth suppression in wild-type p53-expressing tumor cell lines than in cell lines lacking p53 and those expressing mutant p53. RITA binds full-length p53 but not glutathione S-transferase (GST) protein or HDM-2 (a key regulator of p53 is strongly supported by the rescue of embryonic lethality of MDM2). RITA blocks p53−HDM-2 interaction and p53 ubiquitination. RITA substantially decreases the amount of HDM-2 that is co-precipitated with p53, although both proteins are upregulated. RITA prevents interactions between the purified GST-p53 and 6XHis-tagged His-HDM-2 proteins. [3] RITA is shown to induce apoptosis by promoting p53Ser46 phosphorylation. [4] RITA induces activation of p53 in conjunction with up-regulation of phosphorylated ASK-1, MKK-4 and c-Jun. RITA induces the activation of JNK signaling. [5] But On the contrary, another results by nuclear magnetic resonance (NMR) show that RITA does not block the formation of the complex between p53 (residues 1-312) and the N-terminal p53-binding domain of MDM2 (residues 1-118), which is highly probable that the binding of RITA requires native conformation of p53. [6]

In vivo RITA is well tolerated in mice after intraperitoneal administration, with no observable weight loss at doses up to 10 mg/kg during 1 month. After five injections of 0.1 mg/kg of RITA, the growth of the HCT116 tumors is suppressed by 40%, without apparent effects on the HCT116 TP53-/- tumors. At a dose of 1 or 10 mg/kg, RITA shows strong antitumor activity. Five 1 mg/kg injections of RITA results in a more than twofold decrease in the growth rate of p53-positive xenografts without any effect on p53-null xenografts. HCT116 tumors are 90% smaller in mice treated with 10 mg/kg of RITA than in control untreated mice. RITA inhibits the tumor growth in a wild-type p53−dependent manner. [3]


Cell Research:[1]
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  • Cell lines: HCT116 cells and HCT116 TP53-/- cells
  • Concentrations: 0.1 nM - 1 mM, 10 mM stocked in DMSO
  • Incubation Time: 48 hours
  • Method: Examination to assess susceptibility of cells to RITA (0.1 nM - 1 mM) is done using the XTT assay. Cells are inoculated into 96-well flat-bottom plates at a density of 1500 cells per well and incubated for 24 hours at 37 °C in a humidified 5% CO2 5% air atmosphere. Serial concentrations of RITA in DMSO are added to the wells, and sensitivity is determined 48 hours after the addition of RIT
    (Only for Reference)
Animal Research:[3]
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  • Animal Models: SCID mice carrying HCT116 and HCT116 TP53-/- xenografts
  • Formulation: Phosphate buffered saline
  • Dosages: 0.1 mg/kg, 1 mg/kg or 10 mg/kg
  • Administration: Administered via i.v. or i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 58 mg/mL (198.37 mM)
Ethanol 8 mg/mL (27.36 mM)
Water Insoluble
In vivo Add solvents individually and in order:
30% propylene glycol, 5% Tween 80, 65% D5W
30 mg/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

Molecular Weight 292.37


CAS No. 213261-59-7
Storage powder
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00571987 Completed Cancer of the Breast University of Arkansas|Angiodynamics, Inc. September 2004 Phase 1|Phase 2
NCT00690703 Completed Non Small Cell Lung Cancer|Pulmonary Metastases Angiodynamics, Inc. July 2001 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID