247080-48-4

Upstream product

• 137-07-5 2-amino-benzenethiol 
• 35675-46-8 3-methyl-4-nitro-benzoyl chloride 
• 1237737-81-3 N-(phenyl)-3-methyl-4-nitrothiobenzamide 
• 349406-90-2 N-(phenyl)-3-methyl-4-nitrobenzamide 
• 62-53-3 aniline 
• 3113-71-1 3-methyl-4-nitrobenzoic acid 

Downstream Products

• 178804-04-1 2-(4'-amino-3'-methylphenyl)-benzothiazole 
• 877603-41-3 2-(4-nitrophenyl)-6-trifluoromethyl-benzothiazole 
• 1446322-34-4 N-(4-(benzo[d]thiazol-2-yl)-2-methylphenyl)hydroxylamine 
• 1446322-22-0 C₁₆H₁₄N₂O₂S 
• 1446322-39-9 4-(benzo[d]thiazol-2-yl)-4-hydroxy-2-methylcyclohexa-2,5-dienone 
• 1446322-43-5 2-azido-4-(benzo[d]thiazol-2-yl)-6-methylaniline 
• 1446322-28-6 C₁₄H₁₁N₂S⁽¹⁺⁾ 

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.

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 ANTITUMOR ACTIVITY OF NOVEL BIS(BENZYLIDENE-BENZENAMINE)DISULFIDES

Novel synthetic bis(benzylidene-benzenamine)disulfides and the preparation method are disclosed in the present invention. These compounds are afforded with the oxidizing reagent at low temperature and short time period via intra-molecular coupling reactio

Synthesis of sulfur-sulfur bond formation from thioamides promoted by 2,3-dichloro-5,6-dicyanobenzoquinone

A mild and efficient synthesis of sulfur-sulfur bond formation from thioformanilides with 2,3-dichloro-5,6-dicyanobenzoquinone (DDQ) is described. Functionality on the aromatic ring plays a key role in the formation of a sulfur-sulfur bond.

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.

A novel practical synthesis of benzothiazoles via Pd-catalyzed thiol cross-coupling

A convenient synthesis of substituted benzothiazoles from 2-bromoanilides has been accomplished. The various 2-bromoanilides were reacted with an alkyl thiolate in high yields using a palladium catalyst. The resulting sulfides were easily converted to the corresponding benzothiazoles via the simultaneous generation of thiols and condensation under basic or acidic conditions.

Antitumor benzothiazoles. 8.1 Synthesis, metabolic formation, and biological properties of the C- and N-oxidation products of antitumor 2-(4- aminophenyl)-benzothiazoles

2-(4-Aminophenyl)benzothiazoles 1 and their N-acetylated forms have been converted to C and N-hydroxylated derivatives to investigate the role of metabolic oxidation in the mode of action of this series of compounds. 2-(4- Amino-3-methylphenyl)benzothiazole (1a, DF 203, NSC 674495) is a novel and potent antitumor agent with selective growth inhibitory properties against human cancer cell lines. Very low IC50 values (14C]1a derived radioactivity was observed in the sensitive MCF-7 cell line but not in the insensitive MDA-MB-435 cell line. The mechanism of growth inhibition by 1a, which is unknown, may be dependent on the differential metabolism of the drug to an activated form by sensitive cell lines only and its covalent binding to an intracellular protein. However, the 6-hydroxy derivative 6c is not the 'active' metabolite since, like all other C- and N-hydroxylated benzothiazoles examined in this study, it is devoid of antitumor properties in vitro.