As with most NSAIDs, the primary mechanism responsible for its anti-inflammatory, antipyretic, and analgesic action is thought to be inhibition of prostaglandin synthesis through COX-inhibition.<unk>  inhibits COX-1 and COX-2 with relative equipotency. The main target in inhibition of prostaglandin synthesis appears to be the transiently expressed prostaglandin-endoperoxide synthase-2 (PGES-2) also known as cycloxygenase-2 (COX-2). It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis.<unk>  has a relatively high lipid solubility, making it one of the few NSAIDs that are able to enter the brain by crossing the blood-brain barrier. In the brain, too, it is thought to exert its effect through inhibition of COX-2. In addition, it may have effects inside the spinal cord.<unk>  may be a unique member of the NSAIDs in other aspects. Some evidence indicates it inhibits the lipoxygenase pathways, thus reducing formation of the leukotrienes (also pro-inflammatory autacoids). It also may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain its high potency – it is the most potent NSAID on a broad basis. Marked differences exist among NSAIDs in their selective inhibition of the two subtypes of cyclooxygenase, COX-1 and COX-2. Much pharmaceutical drug design has attempted to focus on selective COX-2 inhibition as a way to minimize the gastrointestinal side effects of NSAIDs such as aspirin. In practice, use of some COX-2 inhibitors with their adverse effects has led to massive numbers of patient family lawsuits alleging wrongful death by heart attack, yet other significantly COX-selective NSAIDs, such as<unk> , have been well tolerated by most of the population. Besides the COX-inhibition, a number of other molecular targets of<unk>  possibly contributing to its pain-relieving actions have recently been identified. These include: * Blockage of voltage-dependent sodium channels (after activation of the channel,<unk>  inhibits its reactivation also known as phase inhibition) * Blockage of acid-sensing ion channels (ASICs) * Positive allosteric modulation of KCNQ- and BK-potassium channels<unk>  opens these channels, leading to hyperpolarization of the cell membrane) The action of one single dose is much longer (6 to 8 h) than the very short 1.2–2 h half-life of the drug would indicate. This could be partly because it persists for over 11 hours in synovial fluids.
Diclofenac
Aceclofenac
Ketoprofen
Indoprofen
Loxoprofen
Fenoprofen
Celecoxib
Ibuprofen