18331-34-5

Basic information

• Product Name: 5-Benzylidene-3-ethyl rhodanine
• Synonyms: 5-Benzylidene-3-ethyl rhodanine;3-Ethyl-5-benzylidene-2-thioxothiazolidin-4-one
• CAS NO: 18331-34-5
• Molecular Formula: C₁₂H₁₁NOS₂
• Molecular Weight: 249.35184
• Mol File: 18331-34-5.mol
• Article Data: 2

Chemical Properties

• Melting Point: 150 °C
• Boiling Point: 372.8°Cat760mmHg
• Flash Point: 179.3°C
• Appearance: /
• Density: 1.34g/cm³
• Vapor Pressure: 9.34E-06mmHg at 25°C
• Refractive Index: 1.692
• Storage Temp.: 2-8°C
• PKA: -2.75±0.20(Predicted)
• CAS DataBase Reference: 5-Benzylidene-3-ethyl rhodanine(CAS DataBase Reference)
• NIST Chemistry Reference: 5-Benzylidene-3-ethyl rhodanine(18331-34-5)
• EPA Substance Registry System: 5-Benzylidene-3-ethyl rhodanine(18331-34-5)

Safety Data

• Hazardous Substances Data: 18331-34-5(Hazardous Substances Data)

Usage

InChI:InChI=1/C12H11NOS2/c1-2-13-11(14)10(16-12(13)15)8-9-6-4-3-5-7-9/h3-8H,2H2,1H3/b10-8+

Upstream product

• 7648-01-3 3-ethylrhodanin 
• 100-52-7 benzaldehyde 
• 1725-45-7 5-ethoxymethylene-3-ethyl-2-thioxo-thiazolidin-4-one 
• 75-15-0 carbon disulfide 
• 7223-30-5 3-phenyl-propynoic acid amide 
• 98142-13-3 3-ethyl-5-chloromethylene-2-thioxo-thiazolidin-4-one 
• 71-43-2 benzene 

Downstream Products

• 64656-52-6 5-benzylidene-3,3'-diethyl-2'-thioxo-dihydro-[2,5']bithiazolylidene-4,4'-dione 

Relevant articles and documents

Novel rhodanine derivatives induce growth inhibition followed by apoptosis

We have designed and synthesized three novel compounds, 5-isopropylidiene derivatives of 3-dimethyl-2-thio-hydantoin (ITH-1), 3-ethyl-2-thio-2,4- oxazolidinedione (ITO-1), and 5-benzilidene-3-ethyl rhodanine (BTR-1), and have tested their chemotherapeutic properties. Our results showed that all three compounds induced cytotoxicity in a time- and concentration-dependent manner on leukemic cell line, CEM. Among the compounds tested, BTR-1 was 5- to 7-fold more potent than ITH-1 and ITO-1 when compared by trypan blue and MTT assays. IC50 value of BTR-1 was estimated to be a block at S phase. BTR-1 treatment led to increased level of ROS production and DNA strand breaks suggesting activation of apoptosis for induction of cell death.