|1.||Ongini, Ennio: 4 articles (01/2012 - 05/2004)|
|2.||Monopoli, Angela: 2 articles (01/2012 - 01/2007)|
|3.||Moore, Philip K: 2 articles (08/2005 - 01/2004)|
|4.||Gasparini, Laura: 2 articles (02/2005 - 05/2004)|
|5.||Del Soldato, P: 2 articles (09/2004 - 09/2001)|
|6.||Ralston, S H: 2 articles (09/2004 - 09/2001)|
|7.||Hauss-Wegrzyniak, Beatrice: 2 articles (07/2003 - 10/2002)|
|8.||Wenk, Gary L: 2 articles (07/2003 - 10/2002)|
|9.||McGann, Kristin: 2 articles (07/2003 - 10/2002)|
|10.||Rosi, Susanna: 2 articles (07/2003 - 10/2002)|
09/01/2004 - "The aim of this study was to investigate the mechanism by which HCT1026 inhibits bone resorption. "
01/14/2009 - "This suggests that HCT1026 inhibits bone resorption by inhibiting the effects of RANKL. "
09/01/2001 - "These data indicate that HCT1026 is a potent inhibitor of bone resorption in vitro and protects against ovariectomy-induced bone loss in vivo by a novel mechanism that appears to be distinct from its NO donor properties and from its inhibitory effects on COX activity. "
09/01/2001 - "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. "
09/01/2001 - "Studies in vivo showed that HCT1026 protected against ovariectomy-induced bone loss by inhibiting osteoclastic bone resorption, whereas flurbiprofen at similar concentrations was ineffective. "
|2.||Encephalitis (Encephalitis, Rasmussen)
02/01/2005 - "The results suggest that HCT1026 may exert additional anti-inflammatory actions through PPAR-gamma activation, allowing a more effective control of microglial activation and brain inflammation."
10/25/2002 - "The current study investigated the ability of a nitric oxide (NO)-donating derivative of the nonsteroidal anti-inflammatory drug (NSAID) flurbiprofen, HCT1026, to reduce brain inflammation in young rats. "
09/01/2004 - "Comparison between flurbiprofen and its nitric oxide-releasing derivatives HCT-1026 and NCX-2216 on Abeta(1-42)-induced brain inflammation and neuronal damage in the rat."
07/01/2003 - "We investigated changes in the expression of adenosine type-2B (A2B) receptors and a related intracellular second messenger during chronic brain inflammation and following treatment with the non-steroidal anti-inflammatory drug flurbiprofen and its nitric oxide (NO)-donating derivative, HCT1026. "
01/02/2007 - "HCT 1026 acted by reducing inflammation, preventing muscle damage, and preserving the number and function of satellite cells. "
09/01/2001 - "We conclude that HCT1026 may be of clinical value in the prevention and treatment of inflammatory diseases such as rheumatoid arthritis, which are characterized by joint inflammation as well as periarticular and systemic bone loss."
04/01/2005 - "(3) In the final studies, we treated mice with flurbiprofen and an NO-donating derivative of flurbiprofen (HCT 1026) for several months (from 6 till 14 months of age), and studied the A pathology and inflammation in the brain. "
05/01/1997 - "The number of small intestinal ulcers, pointed and longitudinal, was significantly reduced with nitroxybutyl-flurbiprofen apart from the number of longitudinal ulcers with the highest dose. "
10/01/2002 - "The absence of a delaying effect of HCT-1026 on ulcer healing may be related to the maintenance of a more favorable balance in serum levels of pro- and antiangiogenic growth factors."
05/01/1997 - "A dose-response study with flurbiprofen (single doses of 5, 10, 20, and 40 mg/kg) and equimolar doses of nitroxybutyl-flurbiprofen was performed; assessing their effect on intestinal permeability (at 18-20 hours), with 51Cr EDTA, and the number of pointed (< 5 mm) and longitudinal (> 5 mm) small intestinal ulcers at 24 hours. "
10/01/2002 - "HCT-1026 did not delay ulcer healing nor impair angiogenesis, and also did not change the ratio of serum endostatin to VEGF. "
05/01/2004 - "In addition, a topical formulation of nitroflurbiprofen is under development for the potential treatment of dermatological disorders, including contact urticaria. "
05/01/2004 - "By 1999, nitroflurbiprofen was in phase IIa trials for urinary incontinence, Paget's disease and osteoporosis, and phase II trials of the topical formulation were underway in contact urticaria by March 2002. "
|2.||Nitric Oxide (Nitrogen Monoxide)
|3.||Edetic Acid (EDTA)
|4.||Interleukin-1beta (Interleukin 1 beta)
|5.||Bone Density Conservation Agents
|6.||Sarcoglycans (beta Sarcoglycan)
|9.||Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)
|10.||Intercellular Signaling Peptides and Proteins (Growth Factors)