Disease relevance of Ansaid

• Flurbiprofen: a potent inhibitor of alveolar bone resorption in beagles [1].
• The nonsteroidal anti-inflammatory drug, flurbiprofen, a potent cyclooxygenase inhibitor, significantly decreases the resorption of alveolar bone in naturally occurring chronic destructive periodontal disease in beagles [1].
• Flurbiprofen and cutaneous vasculitis [2].
• The purposes of this investigation were (1) to develop an in vivo method of determining the myocardium at risk after experimental coronary occlusion; (2) to define the spatial geometry of the salvageable ischemic border zone; an (3) to assess the ability of flurbiprofen, an antiinflammatory agent, to protect ischemic myocardium from necrosis [3].
• E-7869 (R-flurbiprofen) inhibits progression of prostate cancer in the TRAMP mouse [4].

Psychiatry related information on Ansaid

• Activity of flurbiprofen and chemically related anti-inflammatory drugs in models of Alzheimer's disease [5].
• Neither L-NAME (10 mg kg-1) nor flurbiprofen (50 mg kg-1) either alone or in combination significantly altered mouse locomotor activity [6].

High impact information on Ansaid

• NSAIDs and enantiomers of flurbiprofen target gamma-secretase and lower Abeta 42 in vivo [7].
• In this study, 20 commonly used NSAIDs, dapsone, and enantiomers of flurbiprofen were analyzed for their ability to lower the level of the 42-amino-acid form of amyloid beta protein (Abeta42) in a human H4 cell line [7].
• This is not mediated by a cyclooxygenase product as inhibition by EGF is observed even in the presence of the cyclooxygenase inhibitor, flurbiprofen [8].
• No malignant tumors developed in the gastrointestinal tracts of animals treated with flurbiprofen or 16,16-dm-PGE2 alone or in controls [9].
• The flurbiprofen derivative inhibited collagen-induced platelet aggregation significantly more than the native NSAID [10].

Chemical compound and disease context of Ansaid

• The first gastric adenocarcinoma infiltrating the muscularis proper was detected after 139 days in an animal treated with a combination of MNNG and flurbiprofen [11].
• Esophageal adenocarcinoma cell lines were treated with various concentrations of NS-398 (selective for COX-2 inhibition) and flurbiprofen (selective for COX-1 inhibition) [12].
• The relative efficacy and safety of flurbiprofen (Ansaid, Upjohn) and indomethacin were compared in 29 patients with monoarticular gouty arthritis of less than 48 hours' duration [13].
• Comparative efficacy of oral flurbiprofen, intramuscular morphine sulfate, and placebo in the treatment of gynecologic postoperative pain [14].
• Double-blind comparison of flurbiprofen and sulindac for the treatment of osteoarthritis [15].

Biological context of Ansaid

• Incubation of human umbilical vein endothelial cells with serum from celecoxib- or flurbiprofen-treated rats resulted in suppressed proliferation and increased apoptosis, effects that were reversed by an antiendostatin antibody [16].
• Treatment with COX-1-selective concentrations of flurbiprofen did not affect cell growth in any of the three tumor cell lines [12].
• We have examined the kinetics, stoichiometry, and chemical nature of the interaction of three anti-inflammatory agents (indomethacin, flurbiprofen, and meclofenamic acid) with pure ovine prostaglandin H synthase [17].
• Pharmacokinetics of flurbiprofen [18].
• Following a single oral dose of 100 mg of flurbiprofen, drug bioavailability is equivalent using regimens of four 25-mg tablets, two 50-mg tablets, or one 100-mg tablet once daily [18].

Anatomical context of Ansaid

• Twenty-two open-chest dogs underwent left anterior descending coronary artery occlusion and were randomized to treated (flurbiprofen 1 mg/kg i.v. at 30 minutes and 4 hours after occlusion; n = 11) or control (saline; n = 11) groups [3].
• Demonstration of lateral and epicardial border zone salvage by flurbiprofen using an in vivo method for assessing myocardium at risk [3].
• RESULTS: HCT1026 was significantly more efficacious than the parent compound, flurbiprofen, at inhibiting osteoclast formation and bone resorption in vitro, and these effects could not be reproduced by combinations of flurbiprofen with a variety of NO donors [19].
• Flurbiprofen in the context of anti-IgE or LPS activation did not alter mast cell IL-6 or TNF-alpha production [20].
• In a series of three studies involving dental outpatients undergoing removal of impacted third molars, preoperative and postoperative administration of flurbiprofen (Ansaid, Upjohn) led to superior pain relief when compared with acetaminophen alone or in combination with oxycodone [21].

Associations of Ansaid with other chemical compounds

• The endothelium-dependent relaxation of canine arteries remains intact after treatment with cyclooxygenase inhibitors (indomethacin and flurbiprofen), and this argues against mediation by prostaglandins [22].
• The lipoxygenase inhibitor nordihydroguaiaretic acid had almost no effect in decreasing the response, while flurbiprofen, a cyclooxygenase inhibitor was very effective at 10(-6) M [23].
• Hp-induced PGE2 formation was abolished by indomethacin and flurbiprofen, whereas the stimulation of 45Ca release was only partially reduced [24].
• Km values for arachidonate (8 microM) and ID50 values for reversible inhibition by the cyclooxygenase inhibitors, flurbiprofen (5 microM), flufenamate (20 microM), and aspirin (20 mM), were also the same for both native and mutant PGG/H synthases; however, only the native enzyme was irreversibly inactivated by aspirin [25].
• From the crystal structure of sheep PGHS-1, it has been proposed that the carboxylic acid group of flurbiprofen is located in a favorable position for interacting with the arginine 120 residue of PGHS-1 (Picot, D., Loll, P. J., and Garavito, R. M. (1994) Nature 367, 243-249) [26].

Gene context of Ansaid

• Isothermal titration calorimetry established that only one monomer of the native PGHS-2 homodimer binds flurbiprofen tightly [27].
• Celecoxib and flurbiprofen impaired angiogenesis and delayed ulcer healing, as well as increasing serum endostatin levels relative to those of VEGF [16].
• Indomethacin and flurbiprofen abolished the formation of PGE(2) and partially reduced (45)Ca release stimulated by IL-11 [28].
• Kinetic studies suggested that dapsone activated CYP2C9-mediated flurbiprofen 4(')-hydroxylation by decreasing the K(m) (alpha=0.2) and increasing the V(max) (beta=1.9) [29].
• The IC(50) for S-flurbiprofen inhibition of gemcabene glucuronidation was similar in HLM (60.6 microM) compared with recombinant UGT2B7 (27.4 microM), consistent with a major role for UGT2B7 in gemcabene glucuronidation in HLM [30].

Analytical, diagnostic and therapeutic context of Ansaid

• R-flurbiprofen chemoprevention and treatment of intestinal adenomas in the APC(Min)/+ mouse model: implications for prophylaxis and treatment of colon cancer [31].
• Studies in cell lines and animal models have shown that flurbiprofen racemate, its R-enantiomer and its nitric oxide (NO)-releasing derivatives, HCT 1026 and NCX 2216, are effective on AD amyloid pathology [5].
• The structure of human P450 2C9 complexed with flurbiprofen was determined to 2.0 A by x-ray crystallography [32].
• Two investigators enrolled 26 women with metastatic breast carcinoma in a six-week, double-blind, placebo-controlled, crossover study of flurbiprofen (Ansaid, Upjohn) and placebo [33].
• Results show that both 50 mg of oral flurbiprofen and 10 mg of intramuscular morphine sulfate were significantly superior to placebo in 161 patients with respect to pain intensity after medication, pain relief scores, need for additional analgesia, and overall clinical evaluation of pain relief [34].

References