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HomeProduct name listIbuprofen

Ibuprofen

Synonym(s):α-Methyl-4-(isobutyl)phenylacetic acid;(±)-2-(4-Isobutylphenyl)propanoic acid;[(±)-2-(4-Isobutylphenyl)-propionic Acid;IB;IBU

  • CAS NO.:15687-27-1
  • Empirical Formula: C13H18O2
  • Molecular Weight: 206.28
  • MDL number: MFCD00010393
  • EINECS: 239-784-6
  • SAFETY DATA SHEET (SDS)
  • Update Date: 2024-11-08 21:13:59
Ibuprofen Structural

What is Ibuprofen?

Absorption

It is very well absorbed orally and the peak serum concentration can be attained in 1 to 2 hours after extravascular administration. When ibuprofen is administered immediately after a meal there is a slight reduction in the absorption rate but there is no change in the extent of the absorption.
When orally administered, the absorption of ibuprofen in adults is very rapidly done in the upper GI tract. The average Cmax, Tmax and AUC ranges around 20 mcg/ml, 2 h and 70 mcg.h/ml. These parameters can vary depending on the enantiomer form, route, and dose of administration.

Toxicity

The symptoms of overdose are presented in individuals that consumed more than 99 mg/kg. Most common symptoms of overdose are abdominal pain, nausea, vomiting, lethargy, vertigo, drowsiness (somnolence), dizziness and insomnia. Other symptoms of overdose include headache, loss of consciousness, tinnitus, CNS depression, convulsions and seizures. May rarely cause metabolic acidosis, abnormal hepatic function, hyperkalemia, renal failure, dyspnea, respiratory depression, coma, acute renal failure, and apnea (primarily in very young pediatric patients).
The reported LD50 of ibuprofen is of 636 mg/kg in rat, 740 mg/kg in mouse and 495 mg/kg in guinea pig.

Description

Ibuprofen is a frequently used over-the-counter drug for treating pain, inflammation, and fever. It is a relatively simple molecule that was discovered and developed in the 1950s and 1960s at Boots Pure Drug in Nottingham, UK (now Boots UK in Beeston). The initial British patent on ibuprofen and a long list of similar compounds was awarded to John Nicholson and Stewart Adams of Boots in 1964.
The trivial name ibuprofen comes from fragments of its chemical name, (±)-2-(p-isobutylphenyl)propionic acid. As the (±) implies, the article of commerce is racemic. The images show the more biologically active (S)-enantiomer. Ibuprofen is sold under a large number of trade names; Advil and Motrin are the most common in the United States.
In addition to its common uses, ibuprofen has been used to treat inflammatory diseases such as rheumatoid and juvenile idiopathic arthritis. But it is not without its risks: patients with cardiovascular disease, hypertension, and gastrointestinal disorders are cautioned against taking it. Ibuprofen also is contraindicated when individuals consume alcohol or low-dose aspirin.

Description

Ibuprofen is a white, crystalline anti-infl ammatory drug used in numerous medications. It is the active ingredient marketed under various trade names including Advil, Motrin, and Nurofen. Ibuprofen is a nonsteroidal anti-infl ammatory drug (NSAID) used as a pain reliever (analgesic), fever reducer (antipyretic), and inflammation reducer. Infl ammation is a general physiological response to tissue damage characterized by swelling, pain, and heat.
Ibuprofen works by inhibiting the enzyme cyclooxygenase (COX), which in turn interferes with the synthesis of prostaglandins. COX exists as several coenzyme forms that are similar in structure: COX-1, COX-2, COX-3; ibuprofen is a nonselective inhibitor of both COX-1 and COX-2. COX-1 is continually produced in mammalian cells throughout the body in response to physiological stimuli. It is responsible for the production of prostaglandins, which get their name because it was originally believed they were synthesized in the prostate gland. In fact, prostaglandins are synthesized throughout the body and act like hormones by stimulating action in target cells. Prostaglandins, which are fatty acid compounds consisting of a 20-carbon chain including a 5 carbon ring, are involved in numerous physiological processes including renal function, blood clotting, and stomach mucus production. COX-2 is synthesized only in specifi c parts of the body (kidneys, brain, trachea) as needed and is therefore called an induced enzyme. COX-2 produces prostaglandins in response to tissue damage and infl ammation. Infl ammatory prostaglandins produce swelling, pain, and fever.

Chemical properties

Colourless, Crystalline Solid

Originator

Brufen,Boots,UK,1969

History

Ibuprofen was developed while searching for an alternative pain reliever to aspirin in the 1950s. It and related compounds were synthesized in 1961 by Stewart Adams, John Nicholson, and Colin Burrows who were working for the Boots Pure Drug Company in Great Britain. Adams and Nicholson filed for a British patent on ibuprofen in 1962 and obtained the patent in 1964; subsequent patents were obtained in the United States. The patent of Adams and Nicholson was for the invention of phenylalkane derivatives of the form shown in Figure 49.1, where R1 could be various alkyl groups, R2 was hydrogen or methyl, and X was COOH or COOR, with R being alkyl or aminoalkyl groups. The first clinical trials for ibuprofen were started in 1966. Ibuprofen was introduced under the trade name Brufen in 1969 in Great Britain. It was introduced in the United States in 1974. Ibuprofen was initially off ered by prescription, but it became available in over-the-counter medications in the 1980s.

The Uses of Ibuprofen

A selective cyclooxygenase inhibitor (IC50=14.9uM). Inhibits PGH synthase-1 and PGH synthase-2 with comparable potency

The Uses of Ibuprofen

Cyclo-oxygenase inhibitor; analgesic; anti-inflammatory.

The Uses of Ibuprofen

Antibiotic

The Uses of Ibuprofen

A common goal in the development of pain and inflammation medicines has been the creation of compounds that have the ability to treat inflammation, fever, and pain without disrupting other physiological functions. General pain relievers, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. A medication's specificaction toward COX-1 versus COX-2 determines the potential for adverse side effects. Medications with greater specificity toward COX-1 will have greater potential for producing adverse side effects. By deactivating COX-1, nonselective pain relievers increase the chance of undesirable side effects, especially digestive problems such as stomach ulcers and gastrointestinal bleeding. COX-2 inhibitors, such as Vioxx and Celebrex, selectively deactivate COX-2 and do not aff ect COX-1 at prescribed dosages. COX-2 inhibitors are widely prescribed for arthritis and pain relief. In 2004, the Food and Drug Administration (FDA) announced that an increased risk of heart attack and stroke was associated with certain COX-2 inhibitors. This led to warning labels and voluntary removal of products from the market by drug producers; for example, Merck took Vioxx off the market in 2004. Although ibuprofen inhibits both COX-1 and COX-2, it has several times the specificity toward COX-2 compared to aspirin, producing fewer gastrointestinal side effects.

What are the applications of Application

Ibuprofen is a Cox-1 and Cox-2 inhibitor. The administration of ibuprofen in patients with rheumatic diseases has been shown to control joint symptoms. Ibuprofen is largely used in OTC products such as an agent for the management of dysmenorrhea, which has been proven to reduce the amount of menstrual prostanoids and produce a reduction in uterine hypercontractility. It has also been reported to significantly reduce the fever and the pain caused by migraines. This effect is thought to be related to the effect on platelet activation and thromboxane A2 production, which produces local vascular effects in the affected regions. This effect is viable as ibuprofen can enter the central nervous system. In the investigational uses of ibuprofen, it has been reported to reduce neurodegeneration when given in low doses over a long time. On the other hand, its use in Parkinson disease is related to the importance of inflammation and oxidative stress in the pathology of this condition. The use of ibuprofen for breast cancer is related to a study that shows a decrease of 50% in the rate of breast cancer.


Background

Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics. The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin. Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.
On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer in vivo by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.

Indications

Ibuprofen is the most commonly used and prescribed NSAID. It is a very common over-the-counter medication widely used as an analgesic, anti-inflammatory and antipyretic.
The use of ibuprofen and its enantiomer Dexibuprofen in a racemic mix is common for the management of mild to moderate pain related to dysmenorrhea, headache, migraine, postoperative dental pain, spondylitis, osteoarthritis, rheumatoid arthritis, and soft tissue disorder.
Due to its activity against prostaglandin and thromboxane synthesis, ibuprofen has been attributed to alteration of platelet function and prolongation of gestation and labour.

Definition

ChEBI: A monocarboxylic acid that is propionic acid in which one of the hydrogens at position 2 is substituted by a 4-(2-methylpropyl)phenyl group.

Indications

Ibuprofen (Advil, Motrin) is used as an analgesic and antipyretic as well as a treatment for rheumatoid arthritis and degenerative joint disease. The most frequently observed side effects are nausea, heartburn, epigastric pain, rash, and dizziness. Incidence of GI side effects is lower than with indomethacin.Visual changes and cross-sensitivity to aspirin have been reported. Ibuprofen inhibits COX-1 and COX-2 about equally. It decreases platelet aggregation, but the duration is shorter and the effect quantitatively lower than with aspirin. Ibuprofen prolongs bleeding times toward high normal value and should be used with caution in patients who have coagulation deficits or are receiving anticoagulant therapy.

Manufacturing Process

Isobutylbenzene is first acetylated to give isobutylacetophenone. 4-ibutylacetophenone (40 g), sulfur (11 g) and morpholine (30 ml) were refluxed for 16 hours, cooled, acetic acid (170 ml) and concentrated hydrochloric acid (280 ml) were added and the mixture was refluxed for a further 7 hours. The mixture was concentrated in vacuo to remove acetic acid and the concentrate was diluted with water.
The oil which separated was isolated with ether, the ethereal solution was extracted with aqueous sodium carbonate and this extract was acidified with hydrochloric acid. The oil was isolated with ether, evaporated to dryness and the residue was esterified by refluxing with ethanol (100 ml) and concentrated sulfuric acid (3 ml) for 5 hours. The excess alcohol was distilled off, the residue was diluted with water, and the oil which separated was isolated with ether. The ethereal solution was washed with sodium carbonate solution; then with water and was dried. The ether was evaporated off and the oil was distilled to give ethyl 4-i-butylphenylacetate.
Sodium ethoxide from sodium (3.67 g) in absolute alcohol (64 ml) was added over 20 minutes with stirring to a mixture of ethyl 4-i-butylphenylacetate (28.14 g) and ethyl carbonate (102 ml) at 100°C. The reaction flask was fitted with a Fenske column through which alcohol and then ethyl carbonate distilled. After 1 hour when the still head reached 124°C heating was discontinued. Glacial acetic acid (12 ml) and water (50 ml) was added to the stirred ice-cooled mixture and the ester isolated in ether, washed with sodium carbonate solution, water and distilled to give ethyl 4-i-butylphenylmalonate.
Ethyl 4-i-butylphenylmalonate (27.53 g) in absolute alcohol (25 ml) was added with stirring to a solution of sodium ethoxide From sodium (2.17 g) in absolute alcohol (75 ml). Ethyl iodide (15 ml) was added and the mixture refluxed for 2% hours, the alcohol distilled and the residue diluted with water, extracted with ether, washed with sodium bisulfite, water, and evaporated to dryness.
The residual oil was stirred and refluxed with sodium hydroxide (75 ml of 5 N), water (45 ml) and 95% ethanol (120 ml). Within a few minutes a sodium salt separated and after 1 hour the solid was collected, washed with ethanol, dissolved in hot water and acidified with dilute hydrochloric acid to give the methyl malonic acid which was collected and dried in vacuo MP 177° to 180°C (dec.).
The malonic acid (9 g) was heated to 210° to 220°C in an oil bath for 20 minutes until decarboxylation had ceased. The propionic acid was cooled and recrystallized from light petroleum (BP 60° to 80°C). Two further recrystallizations from the same solvent gave colorless prisms of 2-(4- isobutylphenyl)propionicacid MP 75° to 77.5°C. (The procedure was reported in US Patent 3,228,831.)

brand name

Abbifen;Abuprohm;Abu-tab;Aches-n-pain;Acril;Actifen;Actiprofen;Actren;Addaprin;Advil 200 mg;Advil cold & sinus;Agisan;Aktren;Aldospray;Algiasdin;Algifor;Algisan;Algofer;Altior;Amersol;Anadin ibuprofen;Analgesico;Analgil;Analgyl;Anco;Antalgil;Antiflam;Antiruggen;Apsifen;Artofen;Artren;Artril;Artrofen;Bayer select ibuprofen pain reliever;Benflogin;Betagesic;Betaprofen;Brofen 200 mg;Brofen 400 mg;Brufert;Brufort;Buborone;Bufedon;Bufigen;Burana;Cesra;Children's advil;Children's motrin;Codafen continus;Contraneural;Contrneural;Cuisialigil;Cunil;Cuprofen;Dansida;Dentigoa forte;Dignoflex;Dimetap sinus;Dimidon;Dismenodl n;Dolgirit;Dolocyl;Dolo-dolgit;Dologesic;Dolo-neos;Dolo-puren;Doltibil;Dolven;Donjust-b;Dorival;Dristan sinus;Duradyne;Dura-ibu;Duralbuprofen;Dysdolen;Ecoprofen;Ediluna;Esprenit;Excedrin ib;Exidol;Exneural;Femafen;Femapirin;Femidol;Fenalgic;Fenlong;Genpril;Guildprofen;Halprin;Ibenon;Ibol;Ibosure;Ibruthalal;Ibu-attritin;Ibucasen;Ibu-cream;Ibufac;Ibufen tablets;Ibufen-l;Ibufug;Ibugel;Ibugesic;Ibuhexal;Ibular;Ibulav;Ibuleve;Ibulgan;Ibumetin;Ibuphlogont;Ibupirac;Ibuprin;Ibuprofen 200;Ibuprohm;Ibu-slow;Ibusure;Ibu-tab;Ibutad;Ibutid;Ibutop;Ibuvivimed;Ibux;Imben;Inabrin;Incefal;Inflam;Inoven;Inza;Iproben;Irfen;Isdol;Isisfen;Junifen;Kalma;Kos;Lacondan;Librofem;Librofen;Lidifen;Lisi-budol;Mediprofen;Melfen;Menado ibuprofen usp;Midol 200 advanced pain formula;Midol ib;Migrafen;Minadol;Moment;Motrin ib;Narfen;Neobrofen;Neobrufen;Nerofen;Niapren;Novaprin;Novogent;Novoprofen;Nu-ibuprofen;Optifen;Opturem;Pacifene;Padudent;Paxofen;Pfeil;Phor pain;Posodolor;Prontalgin;Recudik;Relcofen;Rheufen;Rimafen;Saleto-600;Seclodin;Sedaspray;Serviprofen;Sine-aid ib;Solufen;Spedifen;Stadasan;Superior pain medicine;Supreme pain medicine;Supren;Suspren;Tabalon;Tempil;Tendar;Trauma-dolgit;Ultraprin;Valprin.

Therapeutic Function

Antiinflammatory

World Health Organization (WHO)

Ibuprofen, a non-steroidal anti-inflammatory agent, was introduced in 1969. It was approved for sale without prescription in packages containing no more than 400 mg, in the United Kingdom in 1983. This action was followed by the USA, Canada and several European countries. Since this time reports of suspected adverse effects have increased. Most of these relate to gastrointestinal disturbances, hypersensitivity reactions but aseptic meningitis, skin rashes and renal damage have been recorded.

Synthesis Reference(s)

Chemical and Pharmaceutical Bulletin, 31, p. 3139, 1983 DOI: 10.1248/cpb.31.3139
The Journal of Organic Chemistry, 52, p. 287, 1987 DOI: 10.1021/jo00378a027

General Description

Ibuprofen, 2-(4-isobutylphenyl)propionic acid (Motrin,Advil, Nuprin), was introduced into clinical practice followingextensive clinical trials. It appears to have comparableefficacy to aspirin in the treatment of RA, but with a lowerincidence of side effects. It has also been approved for usein the treatment of primary dysmenorrhea, which is thoughtto be caused by an excessive concentration of PGs and endoperoxides. However, a recent study indicates that concurrentuse of ibuprofen and aspirin may actually interferewith the cardioprotective effects of aspirin, at least in patientswith established cardiovascular disease. This is becauseibuprofen can reversibly bind to the platelet COX-1isozymes, thereby blocking aspirin’s ability to inhibit TXA2synthesis in platelets.

Flammability and Explosibility

Non flammable

Biochem/physiol Actions

Primary TargetCOX-1

Pharmacokinetics

Ibuprofen is rapidly absorbed on oral administration, with peak plasma levels being generally attained within 2 hours and a duration of action of less than 6 hours. As with most of these acidic NSAIDs, ibuprofen (pKa = 4.4) is extensively bound to plasma proteins (99%) and will interact with other acidic drugs that are protein bound.

Clinical Use

Ibuprofen is indicated for the relief of the signs and symptoms of rheumatoid arthritis and osteoarthritis, the relief of mild to moderate pain, the reduction of fever, and the treatment of dysmenorrhea.

Synthesis

Ibuprofen, 2-(4-iso-butylphenyl)propionic acid (3.2.23), can be synthesized by various methods [88–98]. The simplest way to synthesize ibuprofen is by the acylation of iso-butylbenzol by acetyl chloride. The resulting iso-butylbenzophenone (3.2.21) is reacted with sodium cyanide, giving oxynitrile (3.2.22), which upon reaction with hydroiodic acid in the presence of phosphorus is converted into 2-(4-iso-butylphenyl)propionic acid (3.2.23), which subsequently undergoes phases of dehydration, reduction, and hydrolysis.
CB4336930-1.jpg
Another way to synthesize ibuprofen consists of the chloromethylation of iso-butylbenzene, giving 4-iso-butylbenzylchloride (3.2.24). This product is reacted with sodium cyanide, making 4-iso-butylbenzyl cyanide (3.2.25), which is alkylated in the presence of sodium amide by methyl iodide into 2-(4-iso-butylbenzyl)propionitrile (3.2.26). Hydrolysis of the resulting product in the presence of a base produces ibuprofen (3.2.23).
CB4336930-2.jpg

Drug interactions

Potentially hazardous interactions with other drugs
ACE inhibitors and angiotensin-II antagonists: antagonism of hypotensive effect; increased risk of nephrotoxicity and hyperkalaemia.
Analgesics: avoid concomitant use of 2 or more NSAIDs, including aspirin (increased side effects); avoid with ketorolac (increased risk of side effects and haemorrhage); possibly reduced antiplatelet effect with aspirin.
Antibacterials: possibly increased risk of convulsions with quinolones.
Anticoagulants: effects of coumarins and phenindione enhanced; possibly increased risk of bleeding with heparins, dabigatran and edoxaban - avoid long term use with edoxaban.
Antidepressants: increased risk of bleeding with SSRIs and venlaflaxine.
Antidiabetic agents: effects of sulphonylureas enhanced.
Antiepileptics: possibly increased phenytoin concentration.
Antivirals: increased risk of haematological toxicity with zidovudine; concentration possibly increased by ritonavir.
Ciclosporin: may potentiate nephrotoxicity.
Cytotoxics: reduced excretion of methotrexate; increased risk of bleeding with erlotinib.
Diuretics: increased risk of nephrotoxicity; antagonism of diuretic effect; hyperkalaemia with potassium-sparing diuretics.
Lithium: excretion decreased.
Pentoxifylline: increased risk of bleeding.
Tacrolimus: increased risk of nephrotoxicity.

Environmental Fate

Ibuprofen has a high water solubility and low volatility, which suggest a high mobility in the aquatic environment. This makes it a commonly detected chemical of the pharmaceutical and personal care products (PPCPs) in the environment. It is not as persistent, however, as many other chemicals. Ibuprofen undergoes photodegradation with exposure to direct and indirect sunlight, although degradation products can have effects on aquatic environments.

Mode of action

Ibuprofen has multiple actions in different inflammatory pathways involved in acute and chronic inflammation. The main effects reported in ibuprofen are related to pain control, fever, and acute inflammation by inhibiting the synthesis of prostanoids by COX-1 and COX-2. Pain relief is attributed to peripheral affected regions and central nervous system effects in the pain transmission mediated by the dorsal horn and higher spinothalamic tract. Some reports have tried to link pain regulation with a possible enhancement in synthesizing endogenous cannabinoids and action on the NMDA receptors. The effect on pain is related to the cortically evoked potentials. The antipyretic effect is reported to be linked to the effect on prostanoid synthesis due to the fact that the prostanoids are the main signaling mediator of paresis in the hypothalamic-preoptic region. The use of ibuprofen in dental procedures is attributed to the local inhibition of prostanoid production, anti-oedemic activity, and an increase of plasma beta-endorphins. Some reports have suggested a rapid local reduction of the expression of COX-2 in dental pulp derived by the administration of ibuprofen.

Metabolism

Ibuprofen is rapidly metabolized and biotransformed in the liver to the formation of major metabolites which are the hydroxylated and carboxylated derivatives. As soon as it is absorbed, the R-enantiomer undergoes extensive enantiomeric conversion (53-65%) to the more active S-enantiomer in vivo by the activity of alpha-methylacyl-CoA racemase.
Ibuprofen metabolism can be divided in phase I which is represented by the hydroxylation of the isobutyl chains for the formation of 2 or 3-hydroxy derivatives followed by oxidation to 2-carboxy-ibuprofen and p-carboxy-2-propionate. These oxidative reactions are performed by the activity of the cytochrome P450 isoforms CYP 2C9, CYP 2C19 and CYP 2C8. Therefore, these enzymes participate in the oxidation of the alkyl side chain to hydroxyl and carboxyl derivatives. From this enzymes, the major catalyst in the formation of oxidative metabolites is the isoform CYP 2C9.
The metabolic phase I is followed by a phase II in which the oxidative metabolites may be conjugated to glucuronide prior to excretion. This activity forms phenolic and acyl glucuronides.

Metabolism

Metabolism occurs rapidly, and the drug is nearly completely excreted in the urine as unchanged drug and oxidative metabolites within 24 hours following administration. Metabolism by CYP2C9 (90%) and CYP2C19 (10%) involves primarily ω-, and ω1-, and ω2-oxidation of the p-isobutyl side chain, followed by alcohol oxidation of the primary alcohol resulting from ω–oxidation to the corresponding carboxylic acid. All metabolites are inactive. When ibuprofen is administered as the individual enantiomers, the major metabolite isolated is the S-(+)-enantiomer whatever the configuration of the starting enantiomer. Interestingly, the R-(–)-enantiomer is inverted to the S-(+)-enantiomer in vivo via an acetyl–coenzyme A intermediate, accounting for the observation that the two enantiomers are bioequivalent in vivo. This is a metabolic phenomenon that also has been observed for other arylpropionic acids, such as ketoprofen, benoxaprofen, fenoprofen, and naproxen.

Toxicity evaluation

The mechanisms of ibuprofen-induced toxicity have not been clearly defined. Acute renal failure is postulated to result from decreased production of intrarenal prostaglandins via inhibition of the cyclooxygenase pathway. In turn, this will decrease the renal blood flow and glomerular filtration rate. Ibuprofen also interferes with prostaglandin synthesis in the gastrointestinal system, which can contribute to its irritating effect on the mucosa of the gastrointestinal tract. Anion gap metabolic acidosis is likely caused by elevated lactate due to hypotension and hypoperfusion and also due to ibuprofen and its metabolites, which are all weak acids. Seizures have been reported in large ibuprofen overdoses, but the mechanism of toxicity remains unknown. In massive overdoses, ibuprofen is thought to have cellular toxicity disrupting mitochondrial energy processes causing the formation of lactic acid.

References

[1]. kato m, nishida s, kitasato h, et al. cyclooxygenase-1 and cyclooxygenase-2 selectivity of non-steroidal anti-inflammatory drugs: investigation using human peripheral monocytes. j pharm pharmacol, 2001, 53(12): 1679-1685.
[2]. janssen a, schiffmann s, birod k, et al. p53 is important for the anti-proliferative effect of ibuprofen in colon carcinoma cells. biochem biophys res commun, 2008, 365(4): 698-703.
[3]. dabhi jk, solanki jk, mehta a. antiatherosclerotic activity of ibuprofen, a non-selective cox inhibitor--an animal study. indian j exp biol, 2008, 46(6): 476-481.
[4]. redondo-castro e, navarro x. chronic ibuprofen administration reduces neuropathic pain but does not exert neuroprotection after spinal cord injury in adult rats. exp neurol, 2014, 252: 95-103.

Properties of Ibuprofen

Melting point: 77-78 °C
Boiling point: 157 °C (4 mmHg)
alpha  [α]D20 -1~+1°(c=1,C2H5OH)
Density  1.0364 (rough estimate)
refractive index  1.5500 (estimate)
Flash point: 9℃
storage temp.  2-8°C
solubility  Practically insoluble in water, freely soluble in acetone, in methanol and in methylene chloride. It dissolves in dilute solutions of alkali hydroxides and carbonates.
appearance colorless crystals
pka pKa 4.45± 0.04(H2O,t = 25±0.5,I=0.15(KCl))(Approximate)
form  Crystalline Powder
color  white to off-white
Water Solubility  insoluble
Merck  14,4881
Stability: Stable. Combustible. Incompatible with strong oxidizing agents.
CAS DataBase Reference 15687-27-1(CAS DataBase Reference)
NIST Chemistry Reference Ibuprofen(15687-27-1)
EPA Substance Registry System Benzeneacetic acid, .alpha.-methyl-4-(2-methylpropyl)- (15687-27-1)

Safety information for Ibuprofen

Signal word Warning
Pictogram(s)
ghs
Exclamation Mark
Irritant
GHS07
GHS Hazard Statements H302:Acute toxicity,oral
H319:Serious eye damage/eye irritation
H335:Specific target organ toxicity, single exposure;Respiratory tract irritation
Precautionary Statement Codes P261:Avoid breathing dust/fume/gas/mist/vapours/spray.
P264:Wash hands thoroughly after handling.
P264:Wash skin thouroughly after handling.
P270:Do not eat, drink or smoke when using this product.
P271:Use only outdoors or in a well-ventilated area.
P301+P312:IF SWALLOWED: call a POISON CENTER or doctor/physician IF you feel unwell.
P305+P351+P338:IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continuerinsing.

Computed Descriptors for Ibuprofen

InChIKey HEFNNWSXXWATRW-UHFFFAOYSA-N

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