Quaternary Pyridinium Compounds

Shaw, Elliott

doi:10.1002/9780470186657.ch1

Cited by 6 publications

(1 citation statement)

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“…The pyridinium compounds (chloride salts): MNA, 1‐propylnicotinamide (PNA), 1,N′‐dimethylnicotinamide (MNA‐Me), 1‐methyl‐N′,N′‐diethylnicotinamide (MNA‐Et 2 ), 1‐(2‐hydroxyethyl)nicotinamide [(EtOH)NA] and 1‐methyl‐3‐acetylpyridine (MAP) were synthesized by alkylation of the corresponding 3‐substituted pyridine derivatives with the appropriate reagent (methyl iodide, n‐propyl iodide or 2‐iodoethanol) in methanol solution, as described by Shaw (1961). The resulting iodide salts were converted to chlorides in aqueous solutions using freshly precipitated silver chloride and then purified by repeated crystallization from acetone–methanol.…”

Section: Methodsmentioning

confidence: 99%

1‐Methylnicotinamide (MNA), a primary metabolite of nicotinamide, exerts anti‐thrombotic activity mediated by a cyclooxygenase‐2/prostacyclin pathway

Chłopicki¹,

Swieş²,

Mogielnicki³

et al. 2007

British J Pharmacology

175

156

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Background and purpose: 1-methylnicotinamide (MNA) has been considered to be an inactive metabolite of nicotinamide. Here we assessed the anti-thrombotic activity of MNA in vivo. Experimental approach: Antithrombotic action of MNA was studied in normotensive rats with extracorporeal thrombus formation (thrombolysis), in renovascular hypertensive rats with intraarterial thrombus formation (arterial thrombosis) and in a venous thrombosis model in rats (venous thrombosis). Key results: MNA (3-100 mg kg À1 ) induced a dose-dependent and sustained thrombolytic response, associated with a rise in 6-keto-PGF 1a in blood. Various compounds structurally related to MNA were either inactive or weaker thrombolytics. Rofecoxib (0.01-1 mg kg À1 ), dose-dependently inhibited the thrombolytic response of MNA, indomethacin (5 mg kg À1 ) abolished it, while L-NAME (5 mg kg À1 ) were without effect. MNA (3-30 mg kg À1 ) also reduced arterial thrombosis and this effect was abrogated by indomethacin (2.5 mg kg À1 ) as well as by rofecoxib (1 mg kg À1 ). MNA, however, did not affect venous thrombosis. In vitro MNA did not modify platelet aggregation nor induce vasodilation. Conclusions and implications: MNA displayed a profile of anti-thrombotic activity in vivo that surpasses that of closely related compounds. MNA inhibited platelet-dependent thrombosis by a mechanism involving cyclooxygenase-2 and prostacyclin. Our findings suggest that endogenous MNA, produced in the liver by nicotinamide N-methyltransferase, could be an endogenous activator of prostacyclin production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system.

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Section: Methodsmentioning

confidence: 99%

1‐Methylnicotinamide (MNA), a primary metabolite of nicotinamide, exerts anti‐thrombotic activity mediated by a cyclooxygenase‐2/prostacyclin pathway

Chłopicki¹,

Swieş²,

Mogielnicki³

et al. 2007

British J Pharmacology

175

156

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Chemical constitution and activity of bipyridyliium herbicides. Part VIII. 4‐Bromo‐6,7‐dihydrodipyrido[1,2‐α:2′,1′‐c]‐pyrazinediium dibromide and related compounds

Pojer

Summers

1974

Journal of Heterocyclic Chem

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On the mode of formation of 1,6-dihydro-NAD in NADH preparations

Godtfredsen

Ottesen

Andersen³

1979

Carlsberg Res. Commun.

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The identity of the product obtained by sodium borohydride reduction of NAD § as 1,6-dihydro-NAD has been verified by 13C NMR spectroscopy. The behaviour of this compound during chromatography on Sephadex G-15 has been found identical with that of the humidity induced inhibitor detected in NADH preparations and postulated to be identical with 1,6-dihydro-NAD. Evidence is presented that this inhibitor is responsible for the bulk of the inhibitory effect developed in moist NADH preparations and that it is generated through a bimolecular reaction between NADH and NAD + which in essence is a NAD + catalyzed double bond rearrangement of NADH effected by transfer of hydride anions from NADH to NAD + . One implication of these findings, that removal of NAD + from NADH preparations should convey increased stability to the reduced cofactor, has been verified. The structure of the lactate dehydrogenase inhibitors described in the literature is discussed.Abbreviations: NADH = 1,4-dihydro-nicotinamide adenine dinucleotide, LDH = lactate dehydrogenase, ADPR = adenosine 5'-diphosphoribose, NAD + = nicotinamide adenine dinucleotide, 1,6-dihydro-NAD = 1,6-dihydronicotinamide adenine dinucleotide, TMS = tetramethyl silane, compound 2 = 4-phosphoryloxy-1,4-dihydro-nicotinamide adenine dinucleotide.

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Quaternary Pyridinium Compounds

Abstract: 65 agonists (e.g., clonidine) to block the release of acetyl-Other approaches to OP antidotes have dealt with choline from presynaptic nerve terminals (Buccafusco, changes in the heteroaromatic ring system in order to

Cited by 6 publications

References 370 publications

1‐Methylnicotinamide (MNA), a primary metabolite of nicotinamide, exerts anti‐thrombotic activity mediated by a cyclooxygenase‐2/prostacyclin pathway

1‐Methylnicotinamide (MNA), a primary metabolite of nicotinamide, exerts anti‐thrombotic activity mediated by a cyclooxygenase‐2/prostacyclin pathway

Chemical constitution and activity of bipyridyliium herbicides. Part VIII. 4‐Bromo‐6,7‐dihydrodipyrido[1,2‐α:2′,1′‐c]‐pyrazinediium dibromide and related compounds

On the mode of formation of 1,6-dihydro-NAD in NADH preparations

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