1313019-65-6

Basic information

• Product Name: SC-1
• Synonyms: SC-1;N-[4-Chloro-3-(trifluoromethyl)phenyl]-N′-[4-(4-cyanophenoxy)phenyl]-urea
• CAS NO: 1313019-65-6
• Molecular Formula: C₂₁H₁₃ClF₃N₃O₂
• Molecular Weight: 431.8
• EINECS: -0
• Mol File: 1313019-65-6.mol

Chemical Properties

• Appearance: white to beige/
• Storage Temp.: 2-8°C
• Solubility: DMSO: soluble15mg/mL, clear
• CAS DataBase Reference: SC-1(CAS DataBase Reference)
• NIST Chemistry Reference: SC-1(1313019-65-6)
• EPA Substance Registry System: SC-1(1313019-65-6)

Safety Data

• Hazard Codes: Xi
• Statements: 36
• Safety Statements: 26
• WGK Germany: 3
• Hazardous Substances Data: 1313019-65-6(Hazardous Substances Data)

Upstream product

• 32315-10-9 bis(trichloromethyl) carbonate 
• 17076-69-6 4-amino-4'-cyanodiphenyl ether 
• 320-51-4 4-chloro-3-trifluoromethyl-aniline 

Relevant articles and documents

SORAFENIB ANALOGS AND USES THEREOF

The present invention provides, inter alia, compounds according to formula I. Also provided are pharmaceutical compositions and kits containing such compounds. Methods for using such compounds, compositions, and kits for treating a subject having system xc-, dysregulation for activating ferroptosis, for inhibiting system xc- in a cell, and for monitoring treatment of a subject having system xc- dysregulation are provided as well.

AGONISTS OF SRC HOMOLOGY-2 CONTAINING PROTEIN TYROSINE PHOSPHATASE-1 AND TREATMENT METHODS USING THE SAME

The present invention provides new compounds of formula I, II or III, which have Src homology-2 containing protein tyrosine phosphatase- 1 (SHP-1) agonist activity. Also provided are treatment methods using the compounds of formula I, II or III.

Sorafenib derivatives induce apoptosis through inhibition of STAT3 independent of Raf

STAT3 is a transcription factor that modulates survival-directed transcription. It is persistently activated in many human cancers. Literature has shown that sorafenib, Raf kinase inhibitor, reduces Phospho-STAT3 and induces cell death. A series of sorafenib derivatives were synthesized as new inhibitors for STAT3. Urea, sulfonamide, and carboxamide linkers brought out different SARs from the end of sorafenib. Urea and carboxamide linked derivatives showed greater inhibition against STAT3 activity than sulfonamide linked derivatives. In particular, 1-(4-chloro-3-(trifluoromethyl)phenyl)-3-(4- (4-cyanophenoxy)phenyl)urea (1), a urea linker, was as potent as sorafenib in reducing P-STAT3 level and cell death but no inhibition for Raf activity. Such result provides a new lead for the design of STAT3 inhibitors.