• Ibuprofen


  • CasNo:15687-27-1
  • Purity:99%

Product Details;

CasNo: 15687-27-1

Molecular Formula: C13H18O2

Appearance: Colourless, crystalline solid

Factory Supply Ibuprofen, Factory Sells 15687-27-1 Cheap Price

  • Molecular Formula:C13H18O2
  • Molecular Weight:206.285
  • Appearance/Colour:Colourless, crystalline solid 
  • Vapor Pressure:0.000139mmHg at 25°C 
  • Melting Point:77-78 °C(lit.) 
  • Refractive Index:1.5500 (estimate) 
  • Boiling Point:319.6 °C at 760 mmHg 
  • PKA:pKa 4.45± 0.04(H2O,t = 25±0.5,I=0.15(KCl))(Approximate) 
  • Flash Point:216.7 °C 
  • PSA:37.30000 
  • Density:1.029 g/cm3 
  • LogP:3.07320 

Ibuprofen(Cas 15687-27-1) Usage


Ibuprofen is a non-steroidal anti-inflammatory analgesic (NSAID) that is widely used for its anti-inflammatory, analgesic, and antipyretic (fever-reducing) effects. It is one of the world's best-selling non-prescription drugs and is known under various trade names, including Advil, Motrin, and Nurofen. Ibuprofen belongs to the NSAID class of medications. NSAIDs work by inhibiting the enzyme cyclooxygenase (COX), which interferes with the synthesis of prostaglandins. Prostaglandins are compounds that play a role in inflammation, pain, and fever.


Alleviate the acute phase of various kinds of chronic arthritis such as rheumatoid arthritis, osteoarthritis, spondyloarthropathies, gouty arthritis and rheumatoid arthritis as well as persistent symptoms of joint swelling and pain. It can be used for the non-cause treatment and control of disease. For the treatment of various kinds of non-joint soft tissue rheumatic pain, such as shoulder pain, tenosynovitis, bursitis, myalgia and post-exercise pain. For the treatment of acute mild to moderate pain such as: post-surgery, post-trauma, post-strain, primary dysmenorrhea, toothache, headache and so on. It has an antipyretic effect against the fever of adults and children.

Used in Particular Diseases

Acute Gouty Arthritis: Dosage and Frequency:?800 mg four times a day

Increase stroke risk

Ibuprofen is one of the most commonly used non-prescription painkillers, commonly used in the treatment of arthritis, muscle pain, neuralgia, headache, migraine, toothache, dysmenorrhea or low back pain. A recent study published in the British Medical Journal found that people who have taken a large number of antipyretic drugs, ibuprofen, have a 3-fold increase in the risk of getting stroke or heart disease. Researchers from the University of Berne in Switzerland reviewed 31 clinical trials involving more than 11.6 million patients. Patients were treated with one of seven common analgesics. The results showed that patients subjecting to long-term administration of large doses of ibuprofen not only have a risk of getting stroke increased by 3 times, but also have significantly increased risk of suffering heart attack and heart disease death. However, the study also showed that occasionally taking ibuprofen for the treatment of headache will not be dangerous. The study also found that commonly used analgesic diclofenac sodium also has a similar problem. The study found a health risk associated with long-term use of ibuprofen, being similar to the anti-arthritis drug rofecoxib (Velcro), which was halted in 2004 due to safety concerns.


1.For late pregnancy women, it can prolong the pregnancy, causing dystocia and prolonged pregnancy course. Pregnant women and lactating women should not administrate it. 2. Inhibition of platelet aggregation; it can extent the bleeding time. This effect will disappear at 24 hours after withdrawal of the drug. 3. It can increase the blood urea nitrogen and serum creatinine content, further reducing the creatinine clearance rate. The following circumstances should be used with caution: Bronchial asthma can be aggravated after treatment. Heart failure, high blood pressure; medication can cause water retention, edema. Hemophilia or other hemorrhagic diseases (including coagulation disorders and platelet dysfunction); medication can cause prolonged bleeding time, increase the bleeding tendency. Patients with a history of gastrointestinal ulcers are prone to get gastrointestinal side effects, including generating new ulcers. Patients of renal dysfunction, after administration, can get increased renal adverse reactions, and even get renal failure. During long-term medication, it should be regularly checked of blood phase and liver, kidney function.

Drug Interactions

Drinking or combination with other non-steroidal anti-inflammatory drugs can increase the gastrointestinal side effects, and have the risk of ulcers. Long-term combination with acetaminophen can increase the toxic side effects on the kidney. Combination with aspirin or other salicylic acid drugs causes no increase in the efficacy, but cam cause gastrointestinal adverse reactions and increase of the bleeding tendency. Combination with heparin, dicoumarol and other anticoagulants as well as platelet aggregation inhibitors has the risk for increasing bleeding. Combination with furosemide can weaken the sodium excretion effect and antihypertensive effect. Combination with verapamil and nifedipine can increase the plasma concentration of the product. Ibuprofen can increase the plasma concentration of digoxin; pay attention to adjusting the dose of digoxin upon co-administration. Ibuprofen can enhance the role of anti-diabetic drugs (including oral hypoglycemic agents). The goods, when used in combination with antihypertensive drugs can affect the antihypertensive effect of the latter one. Probenecid can reduce the excretion of the goods, increase the concentration of blood, thereby increasing the toxicity, so it is proper to reduce the dosage upon co-administration. The goods can reduce the excretion of methotrexate, increase the blood concentration which can reach up to the level of poisoning, so the goods should not be used with medium or large doses of methotrexate.

Side Effects

Gastrointestinal symptoms include indigestion, stomach burning sensation, stomach pain and nausea as well as vomiting. This usually appears in 16% long-term administrators. These symptoms will disappear upon drug withdraw. In most cases, the patients can tolerate even without withdrawal. A small number (<1%) of patients can get gastric ulcer and gastrointestinal bleeding. This are also cases of perforation due to ulcer. Neurological symptoms such as headache, lethargy and dizziness; Tinnitus (rare) appears in 1% to 3% of patients. Renal insufficiency is rare, mostly occur in patients of potential kidney disease; but a small number of patients may obtain lower extremity edema. Other rare symptoms also include rash, bronchial asthma attack, elevated liver enzymes and leukopenia. During medication, there might be emergence of gastrointestinal bleeding, liver and kidney dysfunction, visual impairment, abnormal blood and allergic reactions, etc., that should be discontinued.

Chemical Properties

Colourless, Crystalline Solid




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.


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.

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


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.31.3139The 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


Biochem/physiol Actions

Primary TargetCOX-1


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.


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.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).

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.


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.


15687-27-1 Relevant articles


Harusawa, Shinya,Yoneda, Ryuji,Kurihara, Takushi,Hamada, Yasumasa,Shioiri, Takayuki

, p. 427 - 428 (1984)

Reaction of aromatic ketones with diethy...

Synthesis, pharmacological activity and hydrolytic behavior of glyceride prodrugs of ibuprofen

Khan,Akhter, Mymoona

, p. 371 - 376 (2005)

For reducing the gastrointestinal toxici...

The continuous-flow synthesis of ibuprofen

Bogdan, Andrew R.,Poe, Sarah L.,Kubis, Daniel C.,Broadwater, Steven J.,McQuade, D. Tyler

, p. 8547 - 8550 (2009)

Let relief flow forth I A three-step, co...

Nickel-Catalyzed Markovnikov Addition of Hydrogen Cyanide to Olefins. Application to Nonsteroidal Antiinflammatories

Nugent, William A.,McKinney, Ronald J.

, p. 5370 - 5372 (1985)


The digital code driven autonomous synthesis of ibuprofen automated in a 3D-printer-based robot

Kitson, Philip J.,Glatzel, Stefan,Cronin, Leroy

, p. 2776 - 2783 (2016)

An automated synthesis robot was constru...

Highly active supported palladium catalyst for the regioselective synthesis of 2-arylpropionic acids by carbonylation


, p. 1067 - 1068 (1999)

A catalyst system consisting of supporte...

One-step synthesis of methyl 2-arylpropanoates from 2-hydroxypropiophenone dimethylacetals using sulfuryl chloride and an amide or a weak base


, p. 1044 - 1045 (1986)


Synthesis of Methyl 2-Arylpropanoates by 1,2-Aryl Migration of Aryl Ethyl Ketones using Diacetoxyphenyliodine

Tamura, Yasumitsu,Shirouchi, Yoshiaki,Haruta, Jun-ichi

, p. 231 - 232 (1984)


Synthesis and hydrolytic behaviour of glycerol-1,2-diibuprofenate-3-nitrate, a putative pro-drug of ibuprofen and glycerol-1-nitrate


, p. 345 - 350 (2001)

Nitroxylated derivatives of non-steroida...

Carbonylation of vinyl aromatics: Convenient regioselective synthesis of 2-arylpropanoic acids


, p. 459 - 461 (1999)

(equation presented) Various substituted...

Separate mechanisms of ion oligomerization tune the physicochemical properties of n-butylammonium acetate: Cation-base clusters vs. Anion-acid dimers

Berton, Paula,Kelley, Steven P.,Wang, Hui,Myerson, Allan S.,Rogers, Robin D.

, p. 25544 - 25554 (2017)

We investigated the ability of the ions ...

NMR spectroscopic studies on the in vitro acyl glucuronide migration kinetics of ibuprofen ((±)-(R,S)-2-(4-isobutylphenyl) propanoic acid), its metabolites, and analogues

Johnson, Caroline H.,Wilson, Ian D.,Harding, John R.,Stachulski, Andrew V.,Iddon, Lisa,Nicholson, Jeremy K.,Lindon, John C.

, p. 8720 - 8727 (2007)

Carboxylic acid-containing drugs are oft...

Expanding the substrate scope of enzymes: Combining mutations obtained by CASTing

Reetz, Manfred T.,Carballeira, Jose Daniel,Peyralans, Jerome,Hoebenreich, Horst,Maichele, Andrea,Vogel, Andreas

, p. 6031 - 6038 (2006)

In a previous paper, the combinatorial a...

Room-temperature Pd-catalyzed methoxycarbonylation of terminal alkynes with high branched selectivity enabled by bisphosphine-picolinamide ligand

Chen, Fen-Er,Ke, Miaolin,Liu, Ding,Ning, Yingtang,Ru, Tong

, p. 1041 - 1044 (2022/01/28)

We report the room-temperature Pd-cataly...

15687-27-1 Process route

ethyl 6-O-(2'-(4'-isobutylphenyl)propionyl)-D-glucopyranoside

ethyl 6-O-(2'-(4'-isobutylphenyl)propionyl)-D-glucopyranoside

ethyl D-glucopyranoside

ethyl D-glucopyranoside



Conditions Yield
With phosphate buffer; potassium chloride; at 37 ℃; pH=7.4; Further Variations:; pH-values; Reagents; Kinetics;




methyl N-methylcarbamate

methyl N-methylcarbamate



Conditions Yield
With aq. buffer; In acetonitrile; at 39 ℃; pH=7.1; Kinetics;

15687-27-1 Upstream products

  • 60561-56-0


  • 70101-35-8


  • 75-69-4


  • 38861-78-8


15687-27-1 Downstream products

  • 61566-34-5

    (+/-)-ibuprofen methyl ester

  • 104400-52-4

    2-(4-isobutylphenyl)propionic acid N-oxysuccinimide ester

  • 193149-67-6

    4-Nitrophenyl 2-(4-isobutylphenyl)propanoate

  • 124235-67-2