IndexTopic 1: Structure, Functional Groups, Effects Mechanism of ActionTopic 2: Side Effects and ToxicityTopic 3: Packaging and ManufacturingPain and chronic inflammatory diseases are major health problems worldwide, responsible for three out of five deaths and contributed to the global opioid epidemic (Pahwa & Jialal, 2018). Nonsteroidal anti-inflammatory drugs (NSAIDs), and in particular ibuprofen, are among the most frequently consumed available medications for the nonaddictive treatment of mild inflammatory pain (Grosser, Ricciotti, & FitzGerald, 2017). NSAIDs generally have both analgesic and anti-inflammatory effects, making them particularly useful for treating pain. Sometimes referred to as nonopioid analgesics, these drugs denote a divergent group of chemical compounds whose mechanism of action generally involves inhibition of components of the inflammatory response system (Hersh & Dionne, 1998). Before the discovery of ibuprofen, inadequate analgesic NSAID drugs were available. Aspirin was relied upon for treatment; however, gastric irritation at doses high enough to control symptoms has limited the drug's usefulness. As a result, ibuprofen was industrialized soon after complications associated with conventional NSAIDs of the time. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay Easily accepted, the therapeutic efficacy of the drug was believed to compensate for the severity of its side effects (Busson, 1986). Ibuprofen was the first FDA-permitted single-entity oral analgesic that showed potency greater than or similar to that of aspirin. Discovered in the UK in the 1960s from a derivative of propionic acid in an attempt to find a safer alternative to aspirin to relieve inflammatory pain symptoms, the medicine has several advantages over drugs designed to have similar effects in the body human like paracetamol, is original: aspirin and opioid codeine. Despite its similarities, ibuprofen is rightfully a drug of greater importance in everyday life thanks to the chemical structure of the drug known as RS-2-4-isobutylphenyl propanoic acid, its low toxicity and limited side effects in comparison , and to the environmentally friendly manufacturing process (National Center for Biotechnology Information, 2018).Topic 1: Structure, functional groups, mode of effect Mechanism of actionBelonging to the class of organic complexes known as phenylpropanoic acids and molecular ring attached to an acid propanoic, ibuprofen is composed of a carboxylic acid functional group and alkane substituents (Purdue University, 2018). Essential for the analgesic and anti-inflammatory qualities of the medicine, the central mechanism of action is the non-selective and reversible inhibition of cyclooxygenase I and II, which are enzymes involved in the synthesis of prostaglandins, similarly to other NSAIDs, aspirin and paracetamol (Bushra & Aslam, 2010). This subsequently blocks the pool of fatty acid molecules, or lipids, that are produced at the site of tissue damage or infection, processing and releasing inflammation, blood flow, and blood clot responses (Ophardt, 2003). Among its properties, the optical activity of ibuprofen is particularly interesting. With the ability to exist as a pair of optical isomers that are non-superimposable mirror images of each other, the two isomers are identified as the R-enantiomer and the S+Enantiomer. The medicine is administered as a racemic mixture, due to its unique stereocenter, which means that it is a compound that has equal amounts on the left enantiomer andright side of the chiral molecule. Through this, R-ibuprofen undergoes extensive conversion to S+ibuprofen in vivo in an attempt to minimize side effects (Chen, et al., 1991). The isomers are identical in solubility properties and melting and boiling points; however, the S-enantiomer is the most pharmacologically active enantiomer due to its behavior when interacting with prostaglandins. They are distinguished by the rotation of the plane of polarization of polarized light in different directions: the S-isomer rotates clockwise as the subject looks at the light, compared to the R-isomer counter-clockwise (Royal Society of Chemistry, 2007) . Before the development of ibuprofen and further development of the technology in the 1990s, the existence of a second or third COX enzyme was suspected, but there was no empirical evidence. Both ibuprofen and its original, aspirin, inhibit both COX I and COX II; but through different ties. Ibuprofen binds non-covalently to enzymes, thus competing with the enzyme's natural counterpart, otherwise known as reversible inhibition. In contrast, aspirin forms covalent bonds with the serine residue in the enzyme, a bond that cannot be broken, making the inhibition irreversible. This creates major problems in the context of side effects such as stomach ulcers and internal bleeding with aspirin, and thus the reasoning behind wider use of ibuprofen. However, the new selective targeting of COX enzymes has created a challenge for the development of drugs that interact pharmacologically with specific enzymes and bindings (Autret, et al., 1997). Topic 2: Side Effects and Toxicity The abuse and misuse associated with painkillers and medications of all types represents one of the major problems facing society today. Although there is no safe level of use of the drug due to the associated risks and unwanted side effects, ibuprofen is certainly the preferred NSAID and anti-inflammatory analgesic in general, based on its advantageous gastrointestinal and nephrotoxicity characteristics (Ungprasert, et al., 2012). Although the selection of the most appropriate type of medicine for each patient is tailored to his medical background and the choice of a doctor, ibuprofen is the least ulcerogenic NSAID. With multiple modes of action underlying the behavior of drug agents, pharmacokinetics are linked to toxicological and pharmacological effects. Rapid oral absorption of the two isomers leads to accumulation of the enantiomers in inflamed pathways and sites (Rainsford, 2015). Despite the minor gastrointestinal irritation due to aspirin, competition between R- and S+ isomers with active sites on the COX-1 enzyme may explain the still viable, but low ulcerogenicity. The significant inhibitory effect on leukocytes, or more commonly known on white blood cells, influences their accumulation and activation at inflamed sites. However, among the available drugs, the chronic gastrointestinal ulceration and leukocyte effect is significantly lower than some more potent ulcerogens such as aspirin and naproxen, as according to data from a human study conducted by Cardoe in 1975 (Rainsford, 2015). In terms of toxicity, in the first fourteen years of ibuprofen's availability as a prescription anti-inflammatory drug it was rarely reported to be taken in overdose. However, once the drug was released as an over-the-counter pain reliever, predictions that it would lead to more frequent overdoses. Not only has there been abundant evidence of this and that painkillers, including ibuprofen, have been found to occur more frequently in overdoses, but epidemiological evidence has emerged that in the UK 50-76%.