1034681-37-2

Basic information

• Product Name: 4-nitro-N-(4-(trifluoromethyl)phenyl)benzothioamide
• Synonyms: 4-nitro-N-(4-(trifluoromethyl)phenyl)benzothioamide
• CAS NO: 1034681-37-2
• Molecular Weight: 326.299
• Mol File: 1034681-37-2.mol
• Article Data: 6

Chemical Properties

• CAS DataBase Reference: 4-nitro-N-(4-(trifluoromethyl)phenyl)benzothioamide(CAS DataBase Reference)
• NIST Chemistry Reference: 4-nitro-N-(4-(trifluoromethyl)phenyl)benzothioamide(1034681-37-2)
• EPA Substance Registry System: 4-nitro-N-(4-(trifluoromethyl)phenyl)benzothioamide(1034681-37-2)

Safety Data

• Hazardous Substances Data: 1034681-37-2(Hazardous Substances Data)

Upstream product

• 1237737-81-3 N-(phenyl)-3-methyl-4-nitrothiobenzamide 
• 7607-41-2 4-nitro-N-(4-(trifluoromethyl)phenyl)benzamide 
• 62-23-7 4-nitro-benzoic acid 
• 455-14-1 4-trifluoromethylphenylamine 

Downstream Products

• 877603-41-3 2-(4-nitrophenyl)-6-trifluoromethyl-benzothiazole 
• 221524-47-6 4-[6-(trifluoromethyl)-1,3-benzothiazol-2-yl]aniline 
• 1257095-87-6 C₂₈H₁₆F₆N₄O₄S₂ 

Relevant articles and documents

Synthesis and biological evaluation of thiobenzanilides as anticancer agents

A series of novel thiobenzanilides is described. These compounds have been previously found to show strong biological activity such as antimycotic and antifungal actions. This is the first demonstration on the mechanism of the anticancer effect of thiobenzanilide agents (4a-c) on human melanoma A375 cells. The cytotoxic studies of compounds 4a-c on human melanoma A375 cells indicate thiobenzanilides induced higher cytotoxicity than nitrobenzanilides (3a-c). In addition, DNA flow cytometric analysis shows that 4a-c displays a significant G2/M phase arrest, which progresses to early apoptosis as detected by flow cytometry after double-staining with annexin V and propidium iodide (PI). Because cellular apoptosis is often preceded by the disruption of mitochondrial function, the assessment of mitochondrial function in 4a-c-treated cells is worthy of investigation. Our data revealed that treatment of A375 cells with 4a-c resulted in the loss of mitochondrial membrane potential (ΔΨmt), a reduction of ATP synthesis, increased reactive oxygen species (ROS) generation, and activation of caspase-3. Thus, we suggest that 4a-c agents are potent inducers of cell apoptosis in A375 cells.

Synthesis of 2-(4-aminophenyl) benzothiazole derivatives and use thereof

The present invention provides a method of preparing a compound of formula 6 comprising: (a) reacting a compound of formula 1 with a compound of formula 2 to form a compound of formula 3 wherein X of formula 2 is Cl or OH; (b) treating the compound formula 3 with Lawesson's reagent to form a compound of formula 4 (c) reacting a compound of formula 4 with potassium ferricyanide to produce a compound of formula 5 and (d) performing catalytic reduction of nitro group of the compound of formula 5 with palladium on charcoal to generate the compound of formula 6, wherein R1 of formulae 1-6 is H, C1-10 alkyl, C1-10 alkoxy or C1-10 haloalkyl, and R2 of formulae 1-6 is H or C1-10 alkyl. The present invention also provides a photodynamic therapy to a patient having at least one tumor comprising the steps of: administering a compound of formula 6 (wherein R1 and R2 are defined as the above) in a pharmaceutically acceptable carrier to the patient; waiting for a sufficient time to allow the administered compound to be taken up by a target tissue having the at least one tumor; and irradiating a region of the patient containing the target tissue; wherein growth of the tumor is inhibited.

Synthesis, and biological evaluation of 2-(4-aminophenyl)benzothiazole derivatives as photosensitizing agents

Photodynamic therapy (PDT) employing exogenous photosensitizers is currently being approved for treatment of basal cell carcinoma (BCC). 2-(4-Aminophenyl)benzothiazoles (6) consist of chromophoric structure and absorb light in the UVA (315-400 nm). These results encouraged us to design and synthesize a diversity of 2-phenylbenzothiazoles (6). Studies on the apoptotic mechanism involved in photosensitive effects induced by UVA-activated 6 in BCC cells are carried out in the present article. 6-UVA-treated cells displayed several features of apoptosis, including an increase in the sub-G1 population, a significantly increased annexin V binding, and activation of caspase-3. 6-UVA induced a decrease in mitochondrial membrane potential (Δψ mt) and ATP via enhanced ROS generation and promoted phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK expression. These results suggest that 6-UVA elicits photosensitive effects in mitochondria processes which involve ERK and p38 activation, and ultimately lead to BCC cell apoptosis.