73590-60-0

Usage

Uses

Used in Pharmaceutical Industry:
2-[[(4-Methoxy-3,5-dimethyl-2-pyridinyl)methyl]sulfinyl]-1H-benzimidazole is used as an impurity in the synthesis of Esomeprazole, an anti-ulcerative drug. It plays a role in the production process of this medication, which is designed for the treatment of acid-related diseases. The presence of 2-[[(4-Methoxy-3,5-dimethyl-2-pyridinyl)methyl]sulfinyl]-1H-benzimidazole as an impurity is significant in ensuring the quality and efficacy of the final pharmaceutical product.

Upstream product

• 86604-78-6 (4-methoxy-3,5-dimethylpyridin-2-yl)methanol 
• 84006-10-0 (chloromethyl)-4-methoxy-3,5-dimethylpyridine 
• 134469-07-1 Benzimidazol-2-thiol 
• 73590-87-1 2-[(3,5-dimethyl-4-methoxy-2-pyridinylmethyl)thio]-1H-benzimidazole 

Downstream Products

• 64-19-7 acetic acid 

Relevant academic research and scientific papers

Enhanced Antigiardial Effect of Omeprazole Analog Benzimidazole Compounds

Giardiasis is a diarrheal disease that is highly prevalent in developing countries. Several drugs are available for the treatment of this parasitosis; however, failures in drug therapy are common, and have adverse effects and increased resistance of the parasite to the drug, generating the need to find new alternative treatments. In this study, we synthesized a series of 2-mercaptobenzimidazoles that are derivatives of omeprazole, and the chemical structures were confirmed through mass, 1H NMR, and 13C NMR techniques. The in vitro efficacy compounds against Giardia, as well as its effect on the inhibition of triosephosphate isomerase (TPI) recombinant, were investigated, the inactivation assays were performed with 0.2 mg/mL of the enzyme incubating for 2 h at 37 ?C in TE buffer, pH 7.4 with increasing concentrations of the compounds. Among the target compounds, H-BZM2, O2N-BZM7, and O2N-BZM9 had greater antigiardial activity (IC50: 36, 14, and 17 μM on trophozoites), and inhibited the TPI enzyme (K2: 2.3, 3.2, and 2.8 M?1 s?1) respectively, loading alterations on the secondary structure, global stability, and tertiary structure of the TPI protein. Finally, we demonstrated that it had low toxicity on Caco-2 and HT29 cells. This finding makes it an attractive potential starting point for new antigiardial drugs.

Proton pump inhibitors selectively suppress MLL rearranged leukemia cells via disrupting MLL1-WDR5 protein-protein interaction

Genetic rearrangements of the mixed lineage leukemia (MLL) leading to oncogenic MLL-fusion proteins (MLL-FPs). MLL-FPs occur in about 10% of acute leukemias and are associated with dismal prognosis and treatment outcomes which emphasized the need for new therapeutic strategies. In present study, by a cell-based screening in-house compound collection, we disclosed that Rabeprazole specially inhibited the proliferation of leukemia cells harboring MLL-FPs with little toxicity to non-MLL cells. Mechanism study showed Rabeprazole down-regulated the transcription of MLL-FPs related Hox and Meis1 genes and effectively inhibited MLL1 H3K4 methyltransferase (HMT) activity in MV4-11 cells bearing MLL-AF4 fusion protein. Displacement of MLL1 probe from WDR5 protein suggested that Rabeprazole may inhibit MLL1 HMT activity through disturbing MLL1-WDR5 protein-protein interaction. Moreover, other proton pump inhibitors (PPIs) also indicated the inhibition activity of MLL1-WDR5. Preliminary SARs showed the structural characteristics of PPIs were also essential for the activities of MLL1-WDR5 inhibition. Our results indicated the drug reposition of PPIs for MLL-rearranged leukemias and provided new insight for further optimization of targeting MLL1 methyltransferase activity, the MLL1-WDR5 interaction or WDR5.

Nitrate prodrugs able to release nitric oxide in a controlled and selective way and their use for prevention and treatment of inflammatory, ischemic and proliferative diseases

New pharmaceutical compounds of general formula (I): F-(X)q where q is an integer from 1 to 5, preferably 1; -F is chosen among drugs described in the text, -X is chosen among 4 groups -M, -T, -V and -Y as described in the text. The compounds of general formula (I) are nitrate prodrugs which can release nitric oxide in vivo in a controlled and selective way and without hypotensive side effects and for this reason they are useful for the preparation of medicines for prevention and treatment of inflammatory, ischemic, degenerative and proliferative diseases of musculoskeletal, tegumental, respiratory, gastrointestinal, genito-urinary and central nervous systems.

N-substituted derivatives of 2-(pyridylalkenesulfinyl) benzimidazoles as gastric antisecretory agents

The present invention provides novel N-substituted derivatives 2-(pyridylalkylenesulfinyl)benzimidazoles with gastric acid inhibiting effects.

(Bezimidazol-2-yl)-pyridinium compounds

(Benzimidazol-2-yl)-pyridinium compounds of the formula STR1 wherein A is --SR9, --SO3- or --S--SO3- ; R1 and R3 each is hydrogen or (C1 -C7)-alkyl; R2 is hydrogen, (C1 -C7)-alkyl, (C1 -C7)-alkoxy or a negatively charged oxygen atom; R4 is hydrogen or a negative charge; R5, R6, R7 and R8 each is hydrogen, (C1 -C7)-alkyl, aryl, halogen, cyano, nitro, formyl, (C2 -C7)-alkanoyl, arylcarbonyl, carboxy, carboxy-(C1 -C7)-alkyl, (C1 -C7)-alkoxycarbonyl, aryloxycarbonyl, aryl-(C1 -C7)-alkoxycarbonyl, (C1 -C7)-alkoxycarbonyl-(C1 -C7)-alkyl, carbamoyl, mono- or di-(C1 -C7)-alkylcarbamoyl, pyrrolidinocarbonyl, piperidinocarbonyl, carbamoyl-(C1 -C7)-alkyl, mono- or di-(C1 -C7)-alkylcarbamoyl-(C1 -C7)-alkyl, pyrrolidinocarbonyl-(C1 -C7)-alkyl, piperdinocarbonyl-(C1 -C7)-alkyl, hydroxy, (C1 -C7)-alkoxy, (C2 -C7)-alkanoloxy, aryloxy, arylcarbonyloxy, (C1 -C7)-alkoxycarbonyloxy, aryl-(C1 -C7)-alkoxycarbonyloxy, aryloxycarbonyloxy, carbamoyloxy, mono- or di-(C1 -C7)-alkylcarbamoyloxy, pyrrolidinocarbonyloxy, piperidinocarbonyloxy, hydroxy-(C1 -C7)-alkyl, trifluoromethyl, di-(C1 -C7)-alkoxymethyl or (C2 -C3)-alkylenedioxymethyl or two of these substituents which are adjacent jointly and together with the carbon atoms to which they are attached are a 5-, 6- or 7-membered ring; and R9 is (C1 -C20)-alkyl, (C3 -C7)-cycloalkyl, (C3 -C7)-alkenylalkyl, (C3 -C7)-alkynylalkyl, substituted (C3 -C7)- alkenyl-alkyl, aryl, aryl-(C1 -C7)-alkyl, hydroxy- (C2 -C7)-alkyl, (C1 -C7)-alkoxy- (C2 -C7)-alkyl, (C1 -C7)-alkoxycarbonyl- (C1 -C7)-alkyl, carboxy-(C1 -C7)-alkyl, di-(C1 -C7)-alkoxycarbonyl-(C2 -C7)-alkyl, dicarboxy-(C2 -C7)-alkyl, carboxy-(C1 -C7)-alkylcarbamoyl-(C1 -C7)-alkyl, optionally N-substituted amino-(C2 -C7)-alkyl, optionally N-substituted amino-carboxy-(C2 -C7)-alkyl, optionally N-substituted amino-(C1 -C7)-alkoxycarbonyl-(C2 -C7)-alkyl, heteroaryl, heteroaryl-(C1 -C7)-alkyl or a residue derived from a cysteine-containing oligopeptide by elimination of the SH group; provided that when there is a net single positive charge there is an external anion, or a pharmaceutically acceptable acid addition salt thereof.