Some<unk> s are used in a single dose to treat pain after surgery. Etoricoxib appears as good as, if not better than, other pain medications. Celecoxib appears to be about as useful as ibuprofen. NSAIDs are often used in treatment of acute gout attacks.<unk> s appear to work as well as nonselective NSAIDS, such as Aspirin. They have not been compared to other treatment options such as colchicine or glucocorticoids. Cancer<unk> -2 appears to be related to cancers and abnormal growths in the intestinal tract. Overexpression of<unk> -2 produces excess prostaglandins which have been shown to increase the possibility of colorectal cancer.<unk>  inhibitors have been shown to reduce the occurrence of cancers and pre-cancerous growths. The National Cancer Institute has done some studies on<unk> -2 and cancer. The FDA has approved Celebrex for treatment of familial adenomatous polyposis (FAP).<unk> s are currently being studied in breast cancer and appear to be beneficial. Neuropsychiatric disorders<unk> s have been found to be effective in suppressing inflammatory neurodegenerative pathways, with beneficial results in animal studies for major depressive disorder as well as schizophrenia. These need to be confirmed in human clinical trials. Other targets The inhibition of<unk> -2 is paramount for the anti-inflammatory and analgesic function of the selective<unk>  celecoxib. However, with regard to this drug's promise for the therapy of advanced cancers, it is unclear whether the inhibition of<unk> -2 plays a dominant role, and this has become a controversial and intensely researched issue. In recent years, several additional intracellular components (besides<unk> -2) were discovered that appear to be important for mediating the anticancer effects of celecoxib in the absence of<unk> -2. Moreover, a recent study with various malignant tumor cells showed that celecoxib could inhibit the growth of these cells, even though some of these cancer cells didn't even contain<unk> -2. Additional support for the idea that other targets besides<unk> -2 are important for celecoxib's anticancer effects has come from studies with chemically modified versions of celecoxib. Several dozen analogs of celecoxib were generated with small alterations in their chemical structures. Some of these analogs retained<unk> y activity, whereas many others didn't. However, when the ability of all these compounds to kill tumor cells in cell culture was investigated, it turned out that the antitumor potency did not at all depend on whether or not the respective compound could inhibit<unk> -2, showing that inhibition of<unk> -2 was not required for the anticancer effects. One of these compounds,<unk> ,5-dimethyl-celecoxib, which entirely lacks the ability to inhibit<unk> -2, actually turned out to display stronger anticancer activity than celecoxib itself and this anticancer effect could also be verified in highly drug-resistant tumor cells and in various animal tumor models. Adverse effects Analysis of clinical trial data revealed that there was a significant increase in the rate of vascular events with<unk> s compared with placebo; "vascular events" are non-fatal myocardial infarction (MI) or heart attack, non-fatal stroke, and death from a vascular event such as MI or stroke. These results led Merck to voluntarily withdraw (rofecoxib) from the market in September<unk> 004 and to regulatory authorities imposing a boxed warning on the label of celecoxib. Traditional NSAIDs were also found to have cardiovascular risks, leading to similar boxed warnings. The cause of the cardiovascular problems became, and remains, a subject of intensive research. As of<unk> 012 results have been converging on the hypothesis that the adverse cardiovascular effects are most likely due to inhibition of<unk> -2 in blood vessels, which leads to a decrease in the production of prostacyclin in them. Prostacyclin usually prevents platelet aggregation and vasoconstriction, so its inhibition can lead to excess clot formation and higher blood pressure.
COX-2 inhibitor
Arachidonate 5-lipoxygenase inhibitor
Reuptake inhibitor
CDK inhibitor
Endopeptidase inhibitor
Histone deacetylase inhibitor
Protein kinase inhibitor
TNF inhibitor