R7532
RRD-251 hydrochloride
≥98% (HPLC)
别名:
(2,4-Dichlorophenyl)carbamimidothioic acid methyl ester hydrochloride, 2-(2,4-Dichlorobenzyl)-2-thiopseudourea hydrochloride, Rb/Raf-1 disruptor 251 hydrochloride, S-(2,4-Dichlorobenzyl)-isothiouronium hydrochloride
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关于此项目
经验公式（希尔记法）:
C8H8Cl2N2S· HCl
化学文摘社编号:
分子量:
271.59
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
产品名称
RRD-251 hydrochloride, ≥98% (HPLC)
InChI key
COMNQRICZGJVLE-UHFFFAOYSA-N
SMILES string
Cl.NC(=N)SCc1ccc(Cl)cc1Cl
InChI
1S/C8H8Cl2N2S.ClH/c9-6-2-1-5(7(10)3-6)4-13-8(11)12;/h1-3H,4H2,(H3,11,12);1H
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
color
white to off-white
solubility
DMSO: >10 mg/mL
H2O: >2 mg/mL
storage temp.
room temp
Quality Level
Biochem/physiol Actions
RRD-251 hydrochloride is a reversible, potent, and selective disruptor of Rb/Raf-1 interaction.
RRD-251 hydrochloride is a reversible, potent, and selective disruptor of Rb/Raf-1 interaction. The retinoblastoma tumor suppressor protein (Rb) controls the G1-S boundary by repressing the transcriptional activity of the E2F family of transcription factors. Raf-1 kinase binds and phosphorylates Rb early in the G1 phase. RRD-251 significantly inhibits angiogenesis and tumor growth in vivo in an Rb-dependent manner. RRD-251 does not inhibit the binding of B-Raf to Rb and Raf-1 to Mek1/2. Also, RRD-251 does not affect the kinase activities associated with cyclin D, cyclin E, or Raf-1.
存储类别
11 - Combustible Solids
wgk
WGK 3
Sandeep Singh et al.
Molecular cancer therapeutics, 9(12), 3330-3341 (2010-12-09)
Metastatic melanoma is an aggressive cancer with very low response rate against conventional chemotherapeutic agents such as dacarbazine (DTIC). Inhibitor of Rb-Raf-1 interaction RRD-251 was tested against the melanoma cell lines SK-MEL-28, SK-MEL-5, and SK-MEL-2. RRD-251 was found to be
Debora Stelitano et al.
Oncotarget, 8(40), 67422-67438 (2017-10-06)
GTSE1 over-expression has been reported as a potential marker for metastasis in various types of malignancies, including breast cancer. Despite this, the transcriptional regulation of this protein and the causes of its misregulation in tumors remain largely unknown. The aims
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