102625-99-0

Basic information

• Product Name: (3,4-dimethoxypyridin-2-yl)methyl acetate
• Synonyms: (3,4-Dimethoxypyridin-2-yl)methyl acetate; 2-pyridinemethanol, 3,4-dimethoxy-, acetate (ester)
• CAS NO: 102625-99-0
• Molecular Formula: C₁₀H₁₃NO₄
• Molecular Weight: 211.2145
• Mol File: 102625-99-0.mol

Chemical Properties

• Boiling Point: 279.381°C at 760 mmHg
• Flash Point: 122.766°C
• Density: 1.151g/cm³
• Vapor Pressure: 0.004mmHg at 25°C
• Refractive Index: 1.497
• PKA: 4.83±0.10(Predicted)
• CAS DataBase Reference: (3,4-dimethoxypyridin-2-yl)methyl acetate(CAS DataBase Reference)
• NIST Chemistry Reference: (3,4-dimethoxypyridin-2-yl)methyl acetate(102625-99-0)
• EPA Substance Registry System: (3,4-dimethoxypyridin-2-yl)methyl acetate(102625-99-0)

Safety Data

• Hazardous Substances Data: 102625-99-0(Hazardous Substances Data)

Usage

Uses

Used in Pharmaceutical Synthesis:
(3,4-dimethoxypyridin-2-yl)methyl acetate is used as a reagent in the synthesis of (pyridinylmethyl)piperazinyl-substituted dibenzothiazepines and (azabenzimidazolylthio)alkoxy-substituted dihydroquinolinones. These compounds are of interest for their potential therapeutic applications, particularly in the treatment of schizophrenia. The presence of the pyridine ring and methoxy groups in (3,4-dimethoxypyridin-2-yl)methyl acetate allows for the formation of these complex structures, which may exhibit beneficial pharmacological properties.
Used in the Synthesis of Pantoprazole:
(3,4-dimethoxypyridin-2-yl)methyl acetate also serves as a synthetic intermediate or impurity in the synthesis of pantoprazole (P183000), an antiulcerative and gastric pump inhibitor. Pantoprazole is a proton pump inhibitor used to treat various gastrointestinal conditions, such as gastroesophageal reflux disease (GERD), peptic ulcers, and Zollinger-Ellison syndrome. The role of (3,4-dimethoxypyridin-2-yl)methyl acetate in the synthesis process highlights its importance in the production of this widely used medication.

Upstream product

• 108-24-7 acetic anhydride 
• 72830-07-0 3,4-dimethoxy-2-methylpyridine N-oxide ? 
• 118-71-8 Maltol 
• 4780-14-7 3-methoxy-2-methyl-4-pyrone 
• 76015-11-7 3-methoxy-2-methylpyridin-4(1H)-one 
• 107512-34-5 4-Chloro-3-methoxy-2-methyl-pyridine 
• 107512-35-6 3,4-dimethoxy-2-methylpyridine 
• 15931-25-6 3-methoxy-2-methyl-4-nitropyridine 1-oxide 
• 35392-65-5 3-methoxy-2-methylpyridine 1-oxide 
• 122307-41-9 4-chloro-3-methoxy-2-methylpyridine N-oxide 

Downstream Products

• 102625-64-9 pantoprazole sulfide 
• 102625-70-7 5-(difluoromethoxy)-2-[[(3,4-dimethoxy-2-pyridyl)methyl]sulfinyl]-1H-benzimidazole 
• 169905-10-6 2-(chloromethyl)-3,4-dimethoxypyridine 
• 72830-09-2 2-Chloromethyl-3,4-dimethoxy-pyridine; hydrochloride 
• 72830-08-1 2-hydroxymethyl-3,4-dimethoxypyridine 

Relevant articles and documents

Diversified synthesis of novel quinoline and dibenzo thiazepine derivatives using known active intermediates

The novel drug development to control resisting infections in conventional drug therapy is a need of today. Few antiulcer relative derivatives developed by approaching convergent synthesis. The derivatives synthesized successfully are dibenzo thiazepine-pyridine (SLN11-SLN15) and benzimidazole-hydroquinoline based derivatives (SLN16-SLN20). It involved the coupling through microwave, sonication and conventional techniques at final step. The efficient technology identified as sonication technique basically time and yield. The reported compounds were structural characterized by elemental analysis and spectral studies such as 1H, 13C NMR and MS.

Structure-activity relationship of omeprazole and analogues as Helicobacter pylori urease inhibitors

Helicobacter pylori urease belongs to a family of highly conserved urea- hydrolyzing enzymes. A common feature of these enzymes is the presence of two Lewis acid nickel ions and a reactive cysteine residue in the active site. The H+/K+-ATPase inhibitor omeprazole is a prodrug of a sulfenamide which covalently modifies cysteine residues on the luminal side of the H+/K+- ATPase of gastric parietal cells. Omeprazole and eight analogues were selected based on their chemical, electronic, and kinetic properties, and each was incubated with viable H. pylori in phosphate-buffered saline at pH 7.4 for 30 min, after which 100 mM urea was added and the amount of ammonia formed analyzed after a further 10 min. Inhibition between 0% and 100% at a 0.1 mM concentration was observed for the different analogues and could be expressed as a function of the pK(a)-value of the pyridine, the pK(a)-value of the benzimidazole, the overall lipophilicity, and, most importantly, the rate of sulfenamide formation, in a quantitative structure-activity relationship. The inhibition was potentiated by a lower pH (favoring the formation of the sulfenamide) but abolished in the presence of β- mercaptoethanol (a scavenger of the sulfenamide). Structural analogues incapable of yielding the sulfenamide did not inhibit ammonia production. Treatment of Helicobacter felis-infected mice with 230 μmol/kg flurofamide b.i.d. for 4 weeks, known to potently inhibit urease activity in vivo, as a means of eradicating the infection, was tested and compared with the effect of 125 μmol/kg omeprazole b.i.d. for 4 weeks. Neither treatment proved efficacious.

(H+,K+)-ATPase inhibiting 2-[(2-pyridylmethyl)sulfinyl]benzimidazoles. 4. A novel series of dimethoxypyridyl-substituted inhibitors with enhanced selectivity. The selection of pantoprazole as a clinical candidate

[(Pyridylmethyl)sulfinyl]benzimidazoles 1 (PSBs) are a class of highly potent antisecretory (H+,K+)-ATPase inhibitors which need to be activated by acid to form their active principle, the cyclic sulfenamide 4. Selective inhibitors of the (H+,K+)-ATPase in vivo give rise to the nonselective thiophile 4 solely at low pH, thus avoiding interaction with other thiol groups in the body. The propensity to undergo the acid-catalyzed transformation is dependent on the nucleophilic/electrophilic properties of the functional groups involved in the formation of 2 since this step is both rate-determining and pH-dependent. The aim of this study was to identify compounds with high (H+,K+)-ATPase inhibitory activity in stimulated gastric glands possessing acidic pH, but low reactivity (high chemical stability) at neutral pH as reflected by in vitro (Na+,K+)-ATPase inhibitory activity. The critical influence of substituents flanking the pyridine 4-methoxy substituent present in all derivatives was carefully studied. The introduction of a 3-methoxy group gave inhibitors possessing a combination of high potency, similar to omeprazole and lansoprazole, but increased stability. As a result of these studies, compound 1a (INN pantoprazole) was selected as a candidate drug and is currently undergoing phase III clinical studies.

2--1H-thienoimidazoles. A Novel Class of Gastric H+/K+-ATPase Inhibitors

2-thienoimidazoles were synthesized and investigated as potential inhibitors of gastric H+/K+-ATPase.The isomers of the two possible thienoimidazole series were found to be potent inhibitors of gastric acid secretion in vitro and in vivo.Structure-activity relationships indicate that especially lipophilic alkoxy, benzyloxy, and phenoxy substituents with additional electron-demanding properties in the 4-position of the pyridine moiety combined with an unsubstituted thienoimidazole lead to highly active compounds with a favorable chemical stability.Various substitution patterns in the thienoimidazole moiety result in lower biological activity.The heptafluorobutyloxy derivative saviprazole (HOE 731, 5d) was selected for further development and is currently undergoing clinical evaluation.Comprehensive pharmacological studies indicate a pharmacodynamic profile different to omeprazole, the first H+/K+-ATPase blocker introduced on the market.

Fluoroalkoxy substituted benzimidazoles useful as gastric acid secretion inhibitors

Dialkoxypyridines of formula I STR1 wherein R1 is 1-3C-alkyl which is completely or predominantly substituted by fluorine, or a chlorodifluoromethyl radical and R1' is hydrogen, halo, trifluoromethyl, 1-3C-alkyl, or 1-3C-alkoxy which is optionally completely or predominantly substituted by fluorine, or R1 and R1', together with the oxygen atom to which R1 is bonded, are 1-2C-alkylenedioxy, which is optionally completely or partly substituted by fluorine, or chlorotrifluoroethylenedioxy, R3 is 1-3C-alkoxy, one of R2 and R4 is 1-3C-alkoxy and the other is a hydrogen atom or 1-3C-alkyl and n is 0 or 1, and salts thereof are new compounds with a pronounced protective action on the stomach. Processes for preparing these compounds, medicaments containing them and their use, as well as intermediate compounds and their use for preparing the subject dialkoxypyridines, are disclosed.

Picoline derivative useful as gastric acid secretion inhibitors

Picoline derivatives of the formula I STR1 wherein the substituents have the meanings given in the description, and their salts are new compounds having a pronounced protective action on the stomach.