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Two main categories of antiplatelets are COX-1 inhibitors and ADP receptor inhibitors, while anticoagulants include vitamin K antagonists, direct oral anticoagulants (DOACs) and indirect thrombin inhibitors. Since cardiovascular agents have narrow therapeutic windows, a slight rise in dose may result in severe toxicity. Hence, monitoring at ...
Prostaglandin inhibitors are drugs that inhibit the synthesis of prostaglandin in human body. [1] There are various types of prostaglandins responsible for different physiological reactions such as maintaining the blood flow in stomach and kidney, regulating the contraction of involuntary muscles and blood vessels, and act as a mediator of inflammation and pain.
Targeting selectivity for COX-2 reduces the risk of peptic ulceration and is the main feature of celecoxib, rofecoxib, and other members of this drug class. [1] After several COX-2–inhibiting drugs were approved for marketing, data from clinical trials revealed that COX-2 inhibitors caused a significant increase in heart attacks and strokes ...
Ketorolac is a non-selective COX inhibitor. [26] It is considered a first-generation NSAID, [15]: 279 a group of drugs that non-selectively inhibit both COX-1 and COX-2 enzymes, which can lead to gastrointestinal side effects. [27]
Newer NSAID drugs called COX-2 selective inhibitors have been developed that inhibit only COX-2, with the hope for reduction of gastrointestinal side-effects. [8] However, several COX-2 selective inhibitors have subsequently been withdrawn after evidence emerged that COX-2 inhibitors increase the risk of heart attack. [9]
Piroxicam, the most popular drug of the oxicam class. [1] Oxicam is a class of non-steroidal anti-inflammatory drugs (NSAIDs), [2] meaning that they have anti-inflammatory, analgesic, and antipyretic therapeutic effects. Oxicams bind closely to plasma proteins. [1] Most oxicams are unselective inhibitors of the cyclooxygenase (COX) enzymes.
They induce the lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect.
[13] [14] The bulky sulfonamide group in COX-2 inhibitors such as celecoxib and rofecoxib prevent the molecule from entering the COX-1 channel. For optimal activity and selectivity of the coxibs, a 4-methylsulfonylphenyl attached to an unsaturated (usually) five-membered ring with a vicinal lipophilic group is required (rofecoxib).