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Merck

R7532

Sigma-Aldrich

RRD-251 hydrochloride

≥98% (HPLC)

Synonym(e):

(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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About This Item

Empirische Formel (Hill-System):
C8H8Cl2N2S· HCl
CAS-Nummer:
Molekulargewicht:
271.59
MDL-Nummer:
UNSPSC-Code:
12352200
PubChem Substanz-ID:
NACRES:
NA.77

Assay

≥98% (HPLC)

Form

powder

Lagerbedingungen

desiccated

Farbe

white to off-white

Löslichkeit

DMSO: >10 mg/mL
H2O: >2 mg/mL

Lagertemp.

room temp

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

InChIKey

COMNQRICZGJVLE-UHFFFAOYSA-N

Biochem./physiol. Wirkung

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.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3


Analysenzertifikate (COA)

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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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