7150-23-4

Basic information

• Product Name: BUTTPARK 182\12-94
• Synonyms: 6-Methoxynicotinamide;3-PYRIDINECARBOXAMIDE, 6-METHOXY-;6-METHOXYPYRIDINE-3-CARBOXAMIDE;BUTTPARK 182\12-94;JBSNF-000088
• CAS NO: 7150-23-4
• Molecular Formula: C₇H₈N₂O₂
• Molecular Weight: 152.152
• Mol File: 7150-23-4.mol

Chemical Properties

• Boiling Point: 301.6 °C at 760 mmHg
• Flash Point: 136.2 °C
• Appearance: /
• Density: 1.213 g/cm³
• Vapor Pressure: 0.00104mmHg at 25°C
• Refractive Index: 1.55
• Storage Temp.: -20°C Freezer
• Solubility: DMSO (Slightly), Methanol (Slightly)
• PKA: 15.17±0.50(Predicted)
• CAS DataBase Reference: BUTTPARK 182\12-94(CAS DataBase Reference)
• NIST Chemistry Reference: BUTTPARK 182\12-94(7150-23-4)
• EPA Substance Registry System: BUTTPARK 182\12-94(7150-23-4)

Safety Data

• Hazardous Substances Data: 7150-23-4(Hazardous Substances Data)

Usage

Uses

Since BUTTPARK 182\12-94 is not a recognized chemical substance, it is not possible to list its uses based on the materials provided. However, if it is indeed a product or code from a specific industry, its applications would depend on the context in which it is used. It is recommended to consult the source of this term or contact relevant industry experts for a detailed explanation and to refer to Material Safety Data Sheets (MSDS) or similar documents for information on substances used in a professional or industrial context.
Used in [Application Industry]:
BUTTPARK 182\12-94 is used as [application type] for [application reason]

InChI:InChI=1/C7H8N2O2/c1-11-6-3-2-5(4-9-6)7(8)10/h2-4H,1H3,(H2,8,10)

Upstream product

• 67-56-1 methanol 
• 98-92-0 nicotinamide 
• 26218-80-4 6-methoxy-nicotinic acid methyl ester 
• 15871-85-9 6-methoxynicotinonitrile 

Downstream Products

• 6628-77-9 6-methoxy-pyridin-3-ylamine 

Relevant articles and documents

Nicotinamide N-methyltransferase in endothelium protects against oxidant stress-induced endothelial injury

Nicotinamide N-methyltransferase (NNMT, EC 2.1.1.1.) plays an important role in the growth of many different tumours and is also involved in various non-neoplastic disorders. However, the presence and role of NNMT in the endothelium has yet to be specifically explored. Here, we characterized the functional activity of NNMT in the endothelium and tested whether NNMT regulates endothelial cell viability. NNMT in endothelial cells (HAEC, HMEC-1 and EA.hy926) was inhibited using two approaches: pharmacological inhibition of the enzyme by NNMT inhibitors (5-amino-1-methylquinoline – 5MQ and 6-methoxynicotinamide – JBSF-88) or by shRNA-mediated silencing. Functional inhibition of NNMT was confirmed by LC/MS/MS-based analysis of impaired MNA production. The effects of NNMT inhibition on cellular viability were analyzed in both the absence and presence of menadione. Our results revealed that all studied endothelial lines express relatively high levels of functionally active NNMT compared with cancer cells (MDA-MB-231). Although the aldehyde oxidase 1 enzyme was also expressed in the endothelium, the further metabolites of N1-methylnicotinamide (N1-methyl-2-pyridone-5-carboxamide and N1-methyl-4-pyridone-3-carboxamide) generated by this enzyme were not detected, suggesting that endothelial NNMT-derived MNA was not subsequently metabolized in the endothelium by aldehyde oxidase 1. Menadione induced a concentration-dependent decrease in endothelial viability as evidenced by a decrease in cell number that was associated with the upregulation of NNMT and SIRT1 expression in the nucleus in viable cells. The suppression of the NNMT activity either by NNMT inhibitors or shRNA-based silencing significantly decreased the endothelial cell viability in response to menadione. Furthermore, NNMT inhibition resulted in nuclear SIRT1 expression downregulation and upregulation of the phosphorylated form of SIRT1 on Ser47. In conclusion, our results suggest that the endothelial nuclear NNMT/SIRT1 pathway exerts a cytoprotective role that safeguards endothelial cell viability under oxidant stress insult.

Novel nicotinamide analog as inhibitor of nicotinamide N-methyltransferase

Nicotinamide N-methyltransferase (NNMT) has been linked to obesity and diabetes. We have identified a novel nicotinamide (NA) analog, compound 12 that inhibited NNMT enzymatic activity and reduced the formation of 1-methyl-nicotinamide (MNA), the primary metabolite of NA by ～80% at 2 h when dosed in mice orally at 50 mg/kg.

Photochemical Alkylation, Hydroxyalkylation, and Alkoxylation of Pyridinecarboxamides in Alcohol

The UV-irradiation of 2- and 4-pyridinecarboxamides in alcohol brings about alkylation and/or hydroxyalkylation in the pyridine ring.In the irradiation of 3-pyridinecarboxamide in the presence of sulfuric acid, ionic reaction (alkoxylation at the 2- and 6-position) and radical reaction (alkylation at the 4- and 6-position) occur in parallel.The effects of quenchers indicate that two alkylation products originate from one excited triplet state which is quenched by energy-transfer mechanism and that two alkoxylation products originate from the excited singlet state.

SIMULTANEOUS PARTICIPATION OF SEVERAL EXCITED STATES IN PHOTOCHEMICAL METHOXYLATION AND METHYLATION OF 3-PYRIDINECARBOXAMIDE IN METHANOL

The UV-irradiation of 3-pyridinecarboxamide in methanol in the presence of sulfuric acid brings about methoxylation (ionic reaction) at the 2- and 6-position and methylation (radical reaction) at the 4- and 6-position.The effects of quenchers indicate that two methylation products originate from one excited triplet state which is quenched by energy transfer mechanism and that two methoxylation products originate from two different excited singlet states which are quenched by electron transfer mechanism.