Evidence map›Paper›PMID 17641676›Full record

ArticleBritish journal of pharmacology2007

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

S Chlopicki, J Swies, A Mogielnicki, W Buczko, M Bartus, M Lomnicka, J Adamus, J Gebicki

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 198 citations in OpenAlex.

  1. Pooled it
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  5. NAD Metabolism Regulates Proliferation of Macrophages in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2025
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34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

S ChlopickiDepartment of Experimental Pharmacology, Chair of Pharmacology, Jagiellonian University Medical College, Krakow, Poland. s.chlopicki@cyfronet.krakow.pl
J Swies
A Mogielnicki
W Buczko
M Bartus
M Lomnicka
J Adamus
J Gebicki
Jagiellonian University · PLLodz University of Technology · PLMedical University of Białystok · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purpose1-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

resultsMNA (3-100 mg kg(-1)) induced a dose-dependent and sustained thrombolytic response, associated with a rise in 6-keto-PGF(1alpha) in blood. Various compounds structurally related to MNA were either inactive or weaker thrombolytics. Rofecoxib (0.01-1 mg kg(-1)), dose-dependently inhibited the thrombolytic response of MNA, indomethacin (5 mg kg(-1)) abolished it, while L-NAME (5 mg kg(-1)) were without effect. MNA (3-30 mg kg(-1)) also reduced arterial thrombosis and this effect was abrogated by indomethacin (2.5 mg kg(-1)) as well as by rofecoxib (1 mg kg(-1)). 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.

Indexed as

AnimalsAortaCyclooxygenase 2Cyclooxygenase 2 InhibitorsEpoprostenolFibrinolytic AgentsHypertensionIn Vitro TechniquesLactonesMaleMesenteric ArteriesNiacinamidePlatelet AggregationProstaglandinsRatsRats, WistarCyclooxygenase 2Cyclooxygenase 2 InhibitorsEpoprostenolFibrinolytic AgentsLactonesN(1)-methylnicotinamideNiacinamideProstaglandinsrofecoxibSulfones

Identifiers

PMID17641676
PMCPMC1978255
OpenAlexW1988122231

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.