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Article ; Online: Protocols to assess the gastrointestinal side effects resulting from inhibition of cyclo-oxygenase isoforms.

Whittle, Brendan J R

Methods in molecular biology (Clifton, N.J.)

2010 Volume 644, Page(s) 189–200

Abstract: A prevalent unwanted action of cyclo-oxygenase (COX) inhibitors, as exemplified by the non-steroidal anti-inflammatory drugs (NSAIDs), is their potential to produce gastrointestinal side effects in clinical use. The injury provoked by such agents ... ...

Abstract	A prevalent unwanted action of cyclo-oxygenase (COX) inhibitors, as exemplified by the non-steroidal anti-inflammatory drugs (NSAIDs), is their potential to produce gastrointestinal side effects in clinical use. The injury provoked by such agents includes rapid superficial disruption to the surface layer of the gastric mucosa, the production of acute gastric erosions in the corpus region and the formation of ulcers in the antral region of the stomach. The small intestine is also adversely affected, with a developing enteropathy over a more protracted period that causes lesions and inflammation in the gut. From experimental work, the interactive mechanisms of such damage in the stomach differ distinctly from those that underlie the intestinal injury, yet the damage in both regions involves the inhibition of both COX-1 and COX-2 isoforms. This chapter outlines the in vivo methods that can be used to identify the potential for novel NSAIDs and selective COX-inhibitors to produce acute gastric corpus lesions and more-chronic antral ulcers in the rat, as well as causing small intestinal enteropathy. Such methods can also be utilized to evaluate the ability of novel agents to prevent the gastrointestinal injury provoked by NSAIDs or COX-inhibitors.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Cyclooxygenase Inhibitors/adverse effects ; Gastric Mucosa/drug effects ; Gastrointestinal Tract/drug effects ; Intestine, Small/drug effects ; Male ; Prostaglandin-Endoperoxide Synthases/metabolism ; Rats ; Rats, Wistar ; Stomach Ulcer/chemically induced
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase Inhibitors ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	2010
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-59745-364-6_16
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Article: New light on the anti-colitic actions of therapeutic aminosalicylates: the role of heme oxygenase.

Whittle, Brendan J R / Varga, Csaba

Pharmacological reports : PR

2010 Volume 62, Issue 3, Page(s) 548–556

Abstract: Although a variety of pharmaceutical preparations of aminosalicylate are commonly used in the clinic for the control of inflammatory bowel disease, the mechanisms underlying their therapeutic actions remain unclear. Recent in vivo and in vitro studies ... ...

Abstract	Although a variety of pharmaceutical preparations of aminosalicylate are commonly used in the clinic for the control of inflammatory bowel disease, the mechanisms underlying their therapeutic actions remain unclear. Recent in vivo and in vitro studies have demonstrated that 5-aminosalicylic acid (5-ASA), regarded as the active moiety in aminosalicylate preparations such as sulfasalazine, can induce the heat shock protein, heme oxygenase-1 (HO-1) and up-regulate HO enzyme activity in the colon. As HO-1 can produce endogenous anti-oxidant and anti-inflammatory moieties such as bilirubin and carbon monoxide (CO), these findings suggest a novel mechanism of action for aminosalicylates, acting as anti-colitic agents through the up-regulation of HO-1 enzyme expression and activity.
MeSH term(s)	Aminosalicylic Acids/metabolism ; Aminosalicylic Acids/pharmacology ; Aminosalicylic Acids/therapeutic use ; Animals ; Antioxidants/metabolism ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Colitis/drug therapy ; Colitis/enzymology ; Colitis/metabolism ; Colon/drug effects ; Colon/enzymology ; Colon/metabolism ; Heme Oxygenase-1/metabolism ; Humans ; Inflammatory Bowel Diseases/drug therapy ; Inflammatory Bowel Diseases/enzymology ; Inflammatory Bowel Diseases/metabolism ; Mesalamine/pharmacology ; Mesalamine/therapeutic use ; Mice ; Rats ; Up-Regulation
Chemical Substances	Aminosalicylic Acids ; Antioxidants ; Mesalamine (4Q81I59GXC) ; Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2010-07-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2186248-5
ISSN	1734-1140
ISSN	1734-1140
DOI	10.1016/s1734-1140(10)70312-1
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Article: COX-2 inhibitors, NO-NSAIDs and beyond.

Whittle, Brendan J R

IDrugs : the investigational drugs journal

2002 Volume 5, Issue 7, Page(s) 623–625

Language	English
Publishing date	2002-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2086568-5
ISSN	2040-3410 ; 1369-7056
ISSN (online)	2040-3410
ISSN	1369-7056
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Article: Evolution of COX isozymes and their inhibitors - William Harvey Research Conference.

Whittle, Brendan J R

IDrugs : the investigational drugs journal

2002 Volume 5, Issue 12, Page(s) 1113–1117

Language	English
Publishing date	2002-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2086568-5
ISSN	2040-3410 ; 1369-7056
ISSN (online)	2040-3410
ISSN	1369-7056
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Article ; Online: Nitric oxide-modulating agents for gastrointestinal disorders.

Whittle, Brendan J R

Expert opinion on investigational drugs

2005 Volume 14, Issue 11, Page(s) 1347–1358

Abstract: Almost 20 years after the identification of the biological role of nitric oxide (NO), the full therapeutic potential of novel agents that mimic the activity of NO or interfere with its synthesis has yet to be realised for utilities involving the ... ...

Abstract	Almost 20 years after the identification of the biological role of nitric oxide (NO), the full therapeutic potential of novel agents that mimic the activity of NO or interfere with its synthesis has yet to be realised for utilities involving the gastrointestinal tract. New utilities for classical NO donors, which were used as vasodilators for decades, in the treatment of motility disorders have been explored and a product for treating anal fissure was recently launched. New classes of compounds incorporating a NO-donating moiety into standard non-steroidal anti-inflammatory drugs, the NO-non-steroidal anti-inflammatory drugs (NO-NSAIDs) or COX-inhibiting nitric oxide donors (CINODs) have also been developed. These have been shown to exhibit reduced gastrointestinal injury in experimental models, and reports on their efficacy and safety in Phase I and II studies are now available. Modulation of the inducible NO synthase isoform that generates excessive NO that can lead to subsequent cytotoxic moieties, such as peroxynitrite, may have therapeutic possibilities in a range of inflammatory diseases of the gut. Likewise, agents that promote the decomposition of peroxynitrite or removal of its other component, superoxide, may also prove to be of use. Further targets for pharmaceutical exploitation are likely to come from both genomic and molecular insights into the processes that regulate the NO system.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Aspirin/analogs & derivatives ; Aspirin/therapeutic use ; Enteritis/etiology ; Esophagus/drug effects ; Esophagus/physiology ; Fissure in Ano/drug therapy ; Gastric Emptying/drug effects ; Gastrointestinal Diseases/drug therapy ; Gastrointestinal Motility/drug effects ; Humans ; Naproxen/analogs & derivatives ; Naproxen/therapeutic use ; Nitrates/therapeutic use ; Nitric Oxide/physiology ; Nitric Oxide/therapeutic use ; Nitric Oxide Donors/therapeutic use ; Nitric Oxide Synthase Type II/drug effects ; Peroxynitrous Acid/physiology
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; N-acetyl-S-(alpha-methyl-4-(2-methylpropyl)benzeneacetyl)cysteine 4-(nitrooxy)butyl ester ; Nitrates ; Nitric Oxide Donors ; naproxen-n-butyl nitrate ; Peroxynitrous Acid (14691-52-2) ; Nitric Oxide (31C4KY9ESH) ; Naproxen (57Y76R9ATQ) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2005-09-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1182884-5
ISSN	1744-7658 ; 0967-8298 ; 1354-3784
ISSN (online)	1744-7658
ISSN	0967-8298 ; 1354-3784
DOI	10.1517/13543784.14.11.1347
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Article: Mechanisms underlying intestinal injury induced by anti-inflammatory COX inhibitors.

Whittle, Brendan J R

European journal of pharmacology

2004 Volume 500, Issue 1-3, Page(s) 427–439

Abstract: By far the most attention has been paid to the deleterious actions of nonsteroidal anti-inflammatory drugs (NSAIDs), including isoform selective agents that inhibit cyclooxygenase (COX), on the upper gastrointestinal tract, particularly the gastric and ... ...

Abstract	By far the most attention has been paid to the deleterious actions of nonsteroidal anti-inflammatory drugs (NSAIDs), including isoform selective agents that inhibit cyclooxygenase (COX), on the upper gastrointestinal tract, particularly the gastric and duodenal mucosa. However, recent studies confirm a relatively high incidence of serious clinical events, especially with the more-established drugs of this class, involving the small intestine. Pathogenic factors that have been proposed from early studies in such enteropathy have included the enterohepatic circulation of the nonsteroidal anti-inflammatory drugs, inhibition of cyclooxygenase, surface epithelial changes and focal microvascular events. More recent work has concerned the role of infiltrating inflammatory cells, the relative roles of cyclooxygenase isoforms, COX-1 and COX-2 and the key involvement of inducible nitric oxide (NO) synthase and its product in combination with superoxide, peroxynitrite. In the present review, evidence for the underlying involvement of each these processes, and their sequential integration in the development of the intestinal injury and ulceration promoted by nonsteroidal anti-inflammatory drugs has been considered.
MeSH term(s)	Animals ; Cyclooxygenase Inhibitors/adverse effects ; Gastrointestinal Diseases/chemically induced ; Humans ; Ulcer/chemically induced
Chemical Substances	Cyclooxygenase Inhibitors
Language	English
Publishing date	2004-10-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2004.07.042
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Article: Cyclooxygenase and nitric oxide systems in the gut as therapeutic targets for safer anti-inflammatory drugs.

Whittle, Brendan J R

Current opinion in pharmacology

2004 Volume 4, Issue 6, Page(s) 538–545

Abstract: After a decade of intense pharmacological and drug development activity by the pharmaceutical industry, compounds derived from two key strategies for reducing gastrointestinal effects of non-steroidal anti-inflammatory drugs (NSAIDs) have been subjected ... ...

Abstract	After a decade of intense pharmacological and drug development activity by the pharmaceutical industry, compounds derived from two key strategies for reducing gastrointestinal effects of non-steroidal anti-inflammatory drugs (NSAIDs) have been subjected to rigorous clinical appraisal. Despite the undoubted therapeutic and commercial success of the selective cyclooxygenase (COX)-2 inhibitors, known as the coxibs, with second-generation compounds already approved and launched, some concerns over their full gastrointestinal profile still linger, while the cardiovascular safety of this class has become a key issue. Likewise, Phase II evaluation of compounds incorporating a nitric oxide (NO)-donating moiety into standard NSAIDs (the NO-NSAIDs or CINODs) has created recent controversy over the full clinical profile of these compounds. Other approaches such as NO-COX-2 inhibitors and dual COX-lipoxygenase inhibitors are already warranting interest. It might therefore be too early to predict the eventual winning strategy for safer anti-inflammatory drugs.
MeSH term(s)	Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Anti-Inflammatory Agents, Non-Steroidal/antagonists & inhibitors ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Cyclooxygenase 1 ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/adverse effects ; Cyclooxygenase Inhibitors/therapeutic use ; Drug Industry/trends ; Gastrointestinal Diseases/enzymology ; Gastrointestinal Tract/drug effects ; Gastrointestinal Tract/metabolism ; Humans ; Membrane Proteins ; Multicenter Studies as Topic ; Nitric Oxide/physiology ; Nitric Oxide/therapeutic use ; Prostaglandin-Endoperoxide Synthases/drug effects ; Prostaglandin-Endoperoxide Synthases/physiology ; Prostaglandin-Endoperoxide Synthases/therapeutic use
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; Membrane Proteins ; Nitric Oxide (31C4KY9ESH) ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS1 protein, human (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	2004-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2004.08.003
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Zs.A 5608: Show issues

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Article: Nitric oxide and the gut injury induced by non-steroidal anti-inflammatory drugs.

Whittle, Brendan J R

Inflammopharmacology

2003 Volume 11, Issue 4, Page(s) 415–422

Abstract: Nitric oxide (NO) can protect the gastrointestinal tract from injury, including that provoked by non-steroidal anti-inflammatory drugs (NSAIDs). This protective profile of NO, which predominantly reflects actions on the microcirculation, is mimicked by ... ...

Abstract	Nitric oxide (NO) can protect the gastrointestinal tract from injury, including that provoked by non-steroidal anti-inflammatory drugs (NSAIDs). This protective profile of NO, which predominantly reflects actions on the microcirculation, is mimicked by NO donors. Moreover, the NO-donating agents know as the NO-NSAIDs or CINODs (cyclo-oxygenase-inhibiting nitric oxide-donating drugs) exhibit reduced gut injury in experimental models, which is considered to reflect these local beneficial actions of NO. NSAIDs cause chronic inflammatory lesions in the small intestine in experimental models. This injury results from initial COX inhibition and other local events, with translocation of indigenous luminal bacteria, leading to induction of NO synthase isoform, iNOS, and subsequent production of the cytotoxic moiety, peroxynitrite from NO and superoxide. Agents that inhibit iNOS or superoxide production can attenuate such intestinal injury. In the absence of reactive oxygen moieties, NO may play a beneficial role in the resolution of inflammatory damage to the gut, thus reconciling the potential opposing properties of NO in tissue inflammation and injury.
Language	English
Publishing date	2003
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1080058-x
ISSN	1568-5608 ; 0925-4692
ISSN (online)	1568-5608
ISSN	0925-4692
DOI	10.1163/156856003322699582
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Zs.A 3274: Show issues

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Article: ONO-1714 (Ono).

Whittle, Brendan J R

IDrugs : the investigational drugs journal

2002 Volume 5, Issue 6, Page(s) 590–593

Abstract: Ono Pharmaceuticals is developing ONO-1714, a selective inducible NO synthase modulator, for the potential treatment of sepsis and hypotension. By March 1999, ONO-1714 had entered phase I trials [354023]. By June 2002, a phase II trial in hypotension ... ...

Abstract	Ono Pharmaceuticals is developing ONO-1714, a selective inducible NO synthase modulator, for the potential treatment of sepsis and hypotension. By March 1999, ONO-1714 had entered phase I trials [354023]. By June 2002, a phase II trial in hypotension during dialysis was ongoing in Japan and clinical pharmacology trials were underway in the UK [446138]. In August 1999, Lehmann Brothers gave ONO-1714 a 10% probability of reaching the market with an expected launch in 2004. Sales were expected to peak at 50 million US dollars in 2012 [349228].
Language	English
Publishing date	2002-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2086568-5
ISSN	2040-3410 ; 1369-7056
ISSN (online)	2040-3410
ISSN	1369-7056
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Article: Gastrointestinal effects of nonsteroidal anti-inflammatory drugs.

Whittle, Brendan J R

Fundamental & clinical pharmacology

2003 Volume 17, Issue 3, Page(s) 301–313

Abstract: Non-steroidal anti-inflammatory drugs (NSAIDs) causes extensive damage to the gastrointestinal (GI) tract. The underlying mechanisms of gastric injury include topical irritant actions that disrupt the epithelial barrier, as well as the inhibition of ... ...

Abstract	Non-steroidal anti-inflammatory drugs (NSAIDs) causes extensive damage to the gastrointestinal (GI) tract. The underlying mechanisms of gastric injury include topical irritant actions that disrupt the epithelial barrier, as well as the inhibition of cyclo-oxygenase (COX), which is predominantly the COX-1 isoform in the mucosa. This damage can be attenuated by antisecretory agents or by mucosal protective agents such as the synthetic prostanoids or nitric oxide (NO) donors. Compounds designed to attenuate topical irritancy, or have protective agents incorporated, such as NO-containing NSAIDs, the CINODs (cyclo-oxygenase-inhibiting NO-donating drugs) show reduced mucosal injury. NSAIDs also cause injury in the small intestine, which appears to result from initial COX inhibition, with subsequent translocation of indigenous bacteria, induction of NO synthase and production of the cytotoxic moiety, peroxynitrite. The COX-2 selective agents, the coxibs, which inhibit prostanoid biosynthesis at inflammatory sites, but not the endogenous protective prostanoids in the gut formed by COX-1, have proved so far to be a successful therapeutic approach to reducing NSAIDs GI damage. The clinical outcome of the use of the second generation of coxibs, and the newer NO NSAIDs is now awaited.
MeSH term(s)	Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Clinical Trials as Topic ; Cyclooxygenase 1 ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/adverse effects ; Cyclooxygenase Inhibitors/metabolism ; Drug Design ; Gastric Mucosa/drug effects ; Gastric Mucosa/pathology ; Gastrointestinal Diseases/chemically induced ; Gastrointestinal Diseases/pathology ; Gastrointestinal Diseases/prevention & control ; Humans ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/pathology ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/metabolism ; Membrane Proteins ; Nitric Oxide Donors/adverse effects ; Nitric Oxide Donors/pharmacology ; Nitric Oxide Donors/therapeutic use ; Prostaglandin-Endoperoxide Synthases/metabolism ; Prostaglandins/metabolism
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; Isoenzymes ; Membrane Proteins ; Nitric Oxide Donors ; Prostaglandins ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS1 protein, human (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	2003-04-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639134-5
ISSN	1472-8206 ; 0767-3981
ISSN (online)	1472-8206
ISSN	0767-3981
DOI	10.1046/j.1472-8206.2003.00135.x
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