7607-41-2

Upstream product

• 455-14-1 4-trifluoromethylphenylamine 
• 122-04-3 4-nitro-benzoyl chloride 
• 62-23-7 4-nitro-benzoic acid 

Downstream Products

• 90234-12-1 4-(Propane-2-sulfonylamino)-N-(4-trifluoromethyl-phenyl)-benzamide 
• 1034681-37-2 4-nitro-N-(4-(trifluoromethyl)phenyl)benzothioamide 
• 1257095-87-6 C₂₈H₁₆F₆N₄O₄S₂ 
• 1621378-26-4 7-(trifluoromethyl)-3-(4-aminophenyl)-1-phenyl-1,2-dihydrobenzo[1,2,4]triazin-2-yl 
• 1621378-27-5 7-(trifluoromethyl)-3-(4-(N-BOC-pyrrolidine-2-carboxamido)phenyl)-1-phenyl-1,2-dihydrobenzo[1,2,4]triazin-2-yl 
• 1621378-28-6 7-(trifluoromethyl)-3-(4-(hexylamino)phenyl)-1-phenyl-1,2-dihydrobenzo[1,2,4]triazin-2-yl 
• 1621377-87-4 N'-phenyl-N-[4-(trifluoromethyl)phenyl]-4-nitrobenzenecarbohydrazonamide 
• 1621377-73-8 7-(trifluoromethyl)-3-(4-nitrophenyl)-1-phenyl-1,2-dihydrobenzo[1,2,4]triazin-2-yl 
• 1621377-99-8 4-nitro-N-(4-(trifluoromethyl)phenyl)benzimidoyl chloride 
• 221524-47-6 4-[6-(trifluoromethyl)-1,3-benzothiazol-2-yl]aniline 
• 877603-41-3 2-(4-nitrophenyl)-6-trifluoromethyl-benzothiazole 

Relevant academic research and scientific papers

Design, synthesis and antimetastatic evaluation of 1-benzothiazolylphenylbenzotriazoles for photodynamic therapy in oral cancer cells

We have designed and synthesized a new series of 1-benzothiazolylphenylbenzotriazoles 9a-p and studied their antimetastatic mechanism involved in photosensitive effects induced by UVA in oral cancer cell Ca9-22. Our results revealed that the compounds plus UVA significantly suppressed migration and invasion, as detected by wound healing assay and Boyden chamber assay. Quantitative RT-PCR assay indicated that compound 9i plus UVA induced an antimetastatic effect through up-regulation of syndecan-1 and TIMP-3 and down-regulation of heparanase, MMP-2 and MMP-9 mRNA expressions. Western blot analysis showed that Ca9-22 treated with 9i plus UVA resulted in decreased levels of p-EGFR and p-ERK, MMP-2 and MMP-9, and an increased level of TIMP-3. These results are the first to report the function of UVA-activated 1-benzothiazolylphenylbenzotriazoles in tumor metastasis and their underlying molecular mechanism, and thus suggest that compound 9i plus PDT may serve as a potential ancillary modality for the treatment of oral cancer.

Functional group transformations in derivatives of 1,4-dihydrobenzo[1,2,4] triazinyl radical

Transformations of functional groups OCOPh, OCH2Ph, I, NO 2, and CO2Me in Blatter's radical derivatives 1-5 were investigated in order to develop synthetic tools for incorporation of the benzo[1,2,4]triazinyl system into c

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 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.

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.

Cyclooxygenase-1-selective inhibitors are attractive candidates for analgesics that do not cause gastric damage. Design and in vitro/in vivo evaluation of a benzamide-type cyclooxygenase-1 selective inhibitor

Although cyclooxygenase-1 (COX-1) inhibition is thought to be a major mechanism of gastric damage by nonsteroidal anti-inflammatory drugs (NSAIDs), some COX-1-selective inhibitors exhibit strong analgesic effects without causing gastric damage. However, it is not clear whether their analgesic effects are attributable to COX-1-inhibitory activity or other bioactivities. Here, we report that N-(5-amino-2-pyridinyl)-4-(trifluoromethyl)benzamide (18f, TFAP), which has a structure clearly different from those of currently available COX-1-selective inhibitors, is a potent COX-1-selective inhibitor (COX-1 IC 50 = 0.80 ± 0.05 μM, COX-2 IC50 = 210 ± 10 μM). This compound causes little gastric damage in rats even at an oral dose of 300 mg/kg, though it has an analgesic effect at as low a dose as 10 mg/kg. Our results show that COX-1-selective inhibitors can be analgesic agents without causing gastric damage.

Synthesis and Antiviral Activity of Sulfonamidobenzophenone Oximes and Sulfonamidobenzamides

To find antiviral agents, various sulfonamidobenzophenone oximes (II) were synthesized from the appropriate m-sulfonamidobenzophenones by hydroxylamine reaction.The reaction products were generally obtained as syn/anti mixtures which were separable by fractional crystallization.The anti isomer had more potent antipoliovirus activity than the syn isomer.Various sulfonamidobenzamides (III) which were structurally related to II were synthesized by the reaction of amino-substituted benzamides with sulfuryl chloride or amines with (aminosulfonyl)benzoyl chloride.Antiviral activity was examined by the plaque-inhibition test.Compounds 5, 36, and 69 exhibited strong antipicornavirus activity.The structure-activity relationships are discussed.