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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

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Nitric oxide release is not required to decrease the ulcerogenic profile of nonsteroidal anti-inflammatory drugs.

Sarthak Jain¹, Susan Tran, Mohamed A M El Gendy

¹Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta T6G 2N8 Canada.

Journal of Medicinal Chemistry

|December 14, 2011

Summary

New nonsteroidal anti-inflammatory drugs (NSAIDs) with ester modifications, not nitric oxide (NO) release, demonstrated potent anti-inflammatory effects with significantly reduced gastric toxicity. This challenges the necessity of NO in NO-NSAID design.

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Analytical Techniques for Assaying Nitric Oxide Bioactivity

Analytical Techniques for Assaying Nitric Oxide Bioactivity

Published on: June 18, 2012

Area of Science:

Medicinal Chemistry
Pharmacology
Drug Design

Background:

Nitric oxide-releasing nonsteroidal anti-inflammatory drugs (NO-NSAIDs) were designed to combine NSAID efficacy with reduced gastrointestinal toxicity.
The cytoprotective mechanism of NO-NSAIDs has been attributed to the release of nitric oxide (NO).

Purpose of the Study:

To evaluate the biological properties of novel NO-NSAIDs featuring a tyrosol linker.
To investigate the role of the NO-releasing moiety in the efficacy and safety profile of these compounds.

Main Methods:

In vitro screening of NSAID ester intermediates.
In vivo oral administration studies in animal models to assess anti-inflammatory activity and gastric toxicity.
Selective COX-2 inhibition assays.

Main Results:

NSAID ester intermediates, lacking the NO-releasing group, exhibited potent and selective COX-2 inhibition in vitro.
These intermediates demonstrated anti-inflammatory activity comparable to parent NSAIDs.
A marked reduction in gastric toxicity was observed with oral administration of the ester intermediates compared to traditional NSAIDs.

Conclusions:

The efficacy and reduced gastric toxicity of the tested NSAID ester intermediates suggest that nitric oxide release may not be essential for cytoprotection.
These findings challenge the established understanding of NO-NSAID mechanisms and support the potential of NSAID prodrugs without NO-releasing moieties.
The study advocates for a re-evaluation of NSAID prodrug design, potentially replacing current NSAID prodrugs with unprotected NSAIDs.