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RITA CAS NO.213261-59-7
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- Min.Order: 100 Gram
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- Available Specifications:
≥98.0%(100-500)Gram≥98.0%(1000-5000)Gram
- Product Details
Keywords
- RITA
- 5,5'-(2,5-FURANDIYL)BIS-2-THIOPHENEMETHANOL;RITA;p53 Activator III;RITA (NSC 652287);(5,5'-(furan-2,5-diyl)bis(thiophene-5,2-diyl))diMethanol;RITA, >99%;2-Thiophenemethanol, 5,5'-(2,5-furandiyl)bis-;5
- 213261-59-7
Quick Details
- ProName: RITA
- CasNo: 213261-59-7
- Molecular Formula: C14H12O3S2
- Appearance: off white powder
- Application: CAS：213261-59-7； 5,5'-(2,5-FURANDIYL)...
- DeliveryTime: 3 months
- PackAge: 100g,500g,1kg,25kg
- Port: shang hai
- ProductionCapacity: 1000 Metric Ton/Month
- Purity: 98%
- Storage: Dry seal
- Transportation: shipping
- LimitNum: 100 Gram
Superiority
We are committed to provide excellence in researching, manufacturing and drug discovery process.
Our research team of scientists consists of western-trained Ph.D.s with experience and capabilities in drug R&D methodologies and medicinal chemistry.
Details
RITA(NSC 652287) induced both DNA-protein and DNA-DNA cross-links with no detectable DNA single-strand breaks. RITA, a drug that, like nutlin-3, can disrupt the p53/Mdm2 interaction.
IC50 Value: 54nM in MCF-7 cells [4]
Target: MDM-2/p53
in vitro: [2,2':5',2"-terthiopene] 5,5"-diyldimethanol (1f) displayed promising antiproliferative activity compared to RITA (IC50=28 nM in MCF-7 cells and 100 nM in colon cancer HCT116 cells, vs. 54 and 0.10 nM, respectively, for RITA) [4]. NSC 652287 induced both DNA-protein and DNA-DNA cross-links with no detectable DNA single-strand breaks. These DNA-protein cross-links (DPC) persisted for at least 12 h after drug removal and their frequency was correlated with cytotoxicity in the renal cell lines studied. The most sensitive renal carcinoma cell line, A498, exhibited cell cycle arrest in G(0)-G(1) and G(2)-M at 10 nM NSC 652287, with increased p53 and p21(WAF1) protein. At higher concentrations, NSC 652287 still induced p53 elevation but with p21(WAF1) reduction and massive apoptosis [1]. RITA induced prominent accumulation and reactivation of p53 in a wild-type TP53-bearing HNC cell line. RITA showed maximal growth suppression in tumor cells showing MDM2-dependent p53 degradation. RITA promoted apoptosis in association with upregulation of p21, BAX, and cleaved caspase-3; notably, the apoptotic response was blocked by pifithrin-α, demonstrating its p53 dependence. With increasing concentrations, RITA strongly induced apoptosis rather than G2-phase arrest [2]. By Western blot analysis we further confirmed that RITA induced activation of p53 in conjunction with up-regulation of phosphorylated ASK-1, MKK-4 and c-Jun [3].
in vivo: