-ibuprofen-

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*MAYO CLINIC LINK*

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-ADVIL JOURNALS-

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-as of [2 MARCH 2024]

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pharmacology

NSAIDs such as ibuprofen work by inhibiting the cyclo-oxygenase (COX) enzymes, which convert arachidonic acid to prostaglandin H2 (PGH2). PGH2,

in turn, is converted by other enzymes to several other prostaglandins

(which are mediators of pain, inflammation, and fever)

and to thromboxane A2

(which stimulates platelet aggregation, leading to the formation of blood clots)

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Like aspirin and indomethacin, ibuprofen is a nonselective COX inhibitor, in that it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2.

The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to operate mainly through inhibition of COX-2, which decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling

Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation

Inhibition of COX-1 instead would be responsible for unwanted effects on the gastrointestinal tract.[53] However, the role of the individual COX isoforms in the analgesic, anti-inflammatory, and gastric damage effects of NSAIDs is uncertain, and different compounds cause different degrees of analgesia and gastric damage.[54]

Ibuprofen is administered as a racemic mixture. The R-enantiomer undergoes extensive interconversion to the S-enantiomer in vivo. The S-enantiomer is believed to be the more pharmacologically active enantiomer.[55] The R-enantiomer is converted through a series of three main enzymes. These enzymes include acyl-CoA-synthetase, which converts the R-enantiomer to (โˆ’)-R-ibuprofen I-CoA; 2-arylpropionyl-CoA epimerase, which converts (โˆ’)-R-ibuprofen I-CoA to (+)-S-ibuprofen I-CoA; and hydrolase, which converts (+)-S-ibuprofen I-CoA to the S-enantiomer.[41] In addition to the conversion of ibuprofen to the S-enantiomer, the body can metabolize ibuprofen to several other compounds, including numerous hydroxyl, carboxyl and glucuronyl metabolites. Virtually all of these have no pharmacological effects.[41]

Unlike most other NSAIDs, ibuprofen also acts as an inhibitor of Rho kinase and may be useful in recovery from spinal-cord injury.[56][57]

Pharmacokinetics
After oral administration, peak serum concentration is reached after 1โ€“2 hours, and up to 99% of the drug is bound to plasma proteins.[58] The majority of ibuprofen is metabolized and eliminated within 24 hours in the urine; however, 1% of the unchanged drug is removed through biliary excretion.[55]

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*official name* –>

“Iso-BUtyl-phenyl-PROanoic acid”
(*groan*)

(“where did the “FEN” come from?”)

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*aka ‘advil’*

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*’ibuprofen’ is a ‘non-steroidal anti-inflammatory drug’ (NSAID) used for treating [‘pain’ / ‘fever’ / ‘inflammation’]*

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(this includes painful menstrual periods, migraines, and rheumatoid arthritis)

About 60% of people improve with any given NSAID, and it is recommended that if one does not work then another should be tried.

It may also be used to close a patent ductus arteriosus in a premature baby. It can be used by mouth or intravenously. It typically begins working within an hour.

Common side effects includes heartburn and a rash.

Compared to other NSAIDs it may have fewer side effects such as gastrointestinal bleeding.

At high doses and long term use it increases the risk of heart failure, kidney failure, and liver failure.

At low doses it does not appear to increase the risk of myocardial infarction;

however, at higher doses it may. It may result in worsened asthma

While it is unclear if it is safe in early pregnancy, it appears to be harmful in later pregnancy.

Like other NSAIDs, it works by inhibiting the making of prostaglandins by decreasing the activity of the enzyme cyclooxygenase.[4]

Ibuprofen might be a weaker anti-inflammatory than other NSAIDs.[5]

Ibuprofen was discovered in 1961 by Stewart Adams and marketed as Brufen.[6]

It is available under a number of trade names, including Advil, Motrin, andNurofen.[4][7]

It was first marketed in 1969 in the United Kingdom and in the United States in 1974.[4][6]

It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system.[8]

It is available as a generic medication.[4]

(the wholesale cost is between 0.01 and 0.04 USD per dose

(in the United States it costs about 0.05 USD per dose)

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*9 CATEGORIES*
(*get to 12*)

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*POTENTIAL BENEFITS*

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*POTENTIAL SIDE EFFECTS*

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*MECHANISM OF ACTION*

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*LEGAL STATUS*

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*DOSES*

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*COST*

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*POPULARITY*

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*HISTORY*

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*ROOTS*

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(‘synthetic’? or ‘natural’?)

(OR IS EVERYTHING “NATURAL”)

(EVEN THE “MAN-MADE”)

(for ‘men’ naturally ‘make’)

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*๐Ÿ‘จโ€๐Ÿ”ฌ๐Ÿ•ต๏ธโ€โ™€๏ธ๐Ÿ™‡โ€โ™€๏ธ*SKETCHES*๐Ÿ™‡โ€โ™‚๏ธ๐Ÿ‘ฉโ€๐Ÿ”ฌ๐Ÿ•ต๏ธโ€โ™‚๏ธ*

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๐Ÿ“š๐Ÿ“–|/\-*WIKI-LINK*-/\|๐Ÿ“–๐Ÿ“š

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๐Ÿ‘ˆ๐Ÿ‘ˆ๐Ÿ‘ˆโ˜œ*โ€œNSAIDโ€* โ˜ž ๐Ÿ‘‰๐Ÿ‘‰๐Ÿ‘‰

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๐Ÿ’•๐Ÿ’๐Ÿ’–๐Ÿ’“๐Ÿ–ค๐Ÿ’™๐Ÿ–ค๐Ÿ’™๐Ÿ–ค๐Ÿ’™๐Ÿ–คโค๏ธ๐Ÿ’š๐Ÿ’›๐Ÿงกโฃ๏ธ๐Ÿ’ž๐Ÿ’”๐Ÿ’˜โฃ๏ธ๐Ÿงก๐Ÿ’›๐Ÿ’šโค๏ธ๐Ÿ–ค๐Ÿ’œ๐Ÿ–ค๐Ÿ’™๐Ÿ–ค๐Ÿ’™๐Ÿ–ค๐Ÿ’—๐Ÿ’–๐Ÿ’๐Ÿ’˜

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*๐ŸŒˆโœจ *TABLE OF CONTENTS* โœจ๐ŸŒท*

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๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ*we won the war* ๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ๐Ÿ”ฅ