Ibuprofen CAS 15687-27-1
Introduction：Basic information about Ibuprofen CAS 15687-27-1, including its chemical name, molecular formula, synonyms, physicochemical properties, and safety information, etc.
Ibuprofen Basic informationdescription Indications Used in Particular Diseases Increase stroke risk Precautions Drug Interactions Side Effects
| Product Name: | Ibuprofen |
| Synonyms: | (+/-)-2-(4-ISOBUTYLPHENYL)-PROPIONIC ACID;2-(4-ISOBUTYLPHENYL)PROPIONIC ACID;4-ISOBUTYL-ALPHA-METHYLPHENYLACETIC ACID;AKOS NCG1-0060;(+/-)-ALPHA-METHYL-4-(2-METHYLPROPYL)-BENZENEACETIC ACID;ALPHA-METHYL-4-[2-METHYLPROPYL]BENZENEACETIC ACID;ALPHA-METHYL-4-(ISOBUTYL)PHENYLACETIC ACID;[A-METHYL-4-ISOBUTYL]PHENYLACETIC ACID |
| CAS: | 15687-27-1 |
| MF: | C13H18O2 |
| MW: | 206.28 |
| EINECS: | 239-784-6 |
| Product Categories: | pharmacetucial intermediate;Pharmaceutical ingredients;API's;APIs;Inhibitors;Intermediates & Fine Chemicals;Pharmaceuticals;Active Pharmaceutical Ingredients;API;Other APIs;Isotopically Labeled Pharmaceutical Reference Standard;ADVIL;Lipid signaling;15687-27-1 |
| Mol File: | 15687-27-1.mol |
Ibuprofen Chemical Properties
| Melting point | 77-78 °C |
| alpha | [α]D20 -1～+1°(c=1,C2H5OH) |
| Boiling point | 157 °C (4 mmHg) |
| density | 1.0364 (rough estimate) |
| refractive index | 1.5500 (estimate) |
| Fp | 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. |
| pka | pKa 4.45± 0.04(H2O,t = 25±0.5,I=0.15(KCl))(Approximate) |
| form | Crystalline Powder |
| color | white to off-white |
| biological source | synthetic (organic) |
| Water Solubility | insoluble |
| Merck | 14,4881 |
| BCS Class | 2 |
| Stability: | Stable. Combustible. Incompatible with strong oxidizing agents. |
| Cosmetics Ingredients Functions | SKIN CONDITIONING |
| InChI | 1S/C13H18O2/c1-9(2)8-11-4-6-12(7-5-11)10(3)13(14)15/h4-7,9-10H,8H2,1-3H3,(H,14,15) |
| InChIKey | HEFNNWSXXWATRW-UHFFFAOYSA-N |
| SMILES | CC(C)Cc1ccc(cc1)C(C)C(O)=O |
| LogP | 3.970 |
| 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
| Hazard Codes | Xn |
| Risk Statements | 22-63-51/53-39/23/24/25-23/24/25-11 |
| Safety Statements | 36-61-36/37-45-16-7 |
| WGK Germany | WGK 1 |
| TSCA | TSCA listed |
| HS Code | 29163920 |
| Storage Class | 11 - Combustible Solids |
| Hazard Classifications | Acute Tox. 4 Oral Eye Irrit. 2 STOT SE 3 |
| Hazardous Substances Data | 15687-27-1(Hazardous Substances Data) |
| Toxicity | LD50 in male mice, rats (mg/kg): 495, 626 i.p.; 1255, 1050 orally (Orzalesi) |
| description | Ibuprofen belongs to a non-steroidal anti-inflammatory analgesic. It has excellent anti-inflammatory, analgesic and antipyretic effect with less adverse reactions. It has been widely used in the world, as the world's best-selling non-prescription drugs. It, together with aspirin and paracetamol are listed as the three key antipyretic analgesics products. In our country, it is mainly used in pain alleviation and anti-rheumatism, etc. It has much less applications in the treatment of cold and fever compared with paracetamol and aspirin. There are a dozens of pharmaceutical companies qualified for production of ibuprofen in China. But the bulk of the domestic market sales of ibuprofen have been occupied by Tianjin Sino-US Company. The Ibuprofen was co-discovered by Dr. Stewart Adams (later he becomes a professor and won the Medal of the British Empire) and his team including CoLinBurrows and Dr. John Nicholson. The aim of the initial study was to develop a "super aspirin" to obtain an alternative for the treatment of rheumatoid arthritis that is comparable to that of aspirin but with less serious adverse reactions. For other drugs such as phenylbutazone, it has a high risk of causing adrenal suppression and other adverse events such as gastrointestinal ulcers. Adams decided to look for a drug with good gastrointestinal resistance, which is particularly important for all non-steroidal anti-inflammatory drugs. Phenyl acetate drugs have aroused people's interest. Although some of these drugs have been found to be at risk of causing ulcers based on the dog's test, Adams is aware of that this phenomenon may be due to a relatively long half-life of the drug clearance. In this class of drugs there is a compound – ibuprofen, which has a relatively short half-life, sustaining only 2 hours. Among the screened alternative drugs, although it is not the most effective, it is the most secure. In 1964, ibuprofen had become the most promising alternative to aspirin. |
| Indications |
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| 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. |
| Precautions | 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:
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| 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 | Ibuprofenwas developed while searching for an alternative pain reliever to aspirin in the 1950s. It andrelated compounds were synthesized in 1961 by Stewart Adams, John Nicholson, and ColinBurrows who were working for the Boots Pure Drug Company in Great Britain. Adams andNicholson filed for a British patent on ibuprofen in 1962 and obtained the patent in 1964;subsequent patents were obtained in the United States. The first clinical trials for ibuprofen were started in1966. Ibuprofen was introduced under the trade name Brufen in 1969 in Great Britain. It wasintroduced in the United States in 1974. Ibuprofen was initially off ered by prescription, butit became available in over-the-counter medications in the 1980s. |
| Uses | A selective cyclooxygenase inhibitor (IC50=14.9uM). Inhibits PGH synthase-1 and PGH synthase-2 with comparable potency |
| Uses | Cyclo-oxygenase inhibitor; analgesic; anti-inflammatory. |
| Uses | Antibiotic |
| Uses | 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. |
| Indications | Ibuprofen (Advil, Motrin) is used as an analgesicand antipyretic as well as a treatment for rheumatoidarthritis and degenerative joint disease. The most frequentlyobserved side effects are nausea, heartburn,epigastric pain, rash, and dizziness. Incidence of GI sideeffects is lower than with indomethacin.Visual changesand cross-sensitivity to aspirin have been reported.Ibuprofen inhibits COX-1 and COX-2 about equally. Itdecreases platelet aggregation, but the duration isshorter and the effect quantitatively lower than with aspirin.Ibuprofen prolongs bleeding times toward highnormal value and should be used with caution in patientswho have coagulation deficits or are receiving anticoagulanttherapy. |
| 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. |
| Manufacturing Process | Isobutylbenzene is first acetylated to give isobutylacetophenone. 4-ibutylacetophenone (40 g), sulfur (11 g) and morpholine (30 ml) were refluxedfor 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 concentratewas diluted with water. The oil which separated was isolated with ether, the ethereal solution wasextracted with aqueous sodium carbonate and this extract was acidified withhydrochloric acid. The oil was isolated with ether, evaporated to dryness andthe residue was esterified by refluxing with ethanol (100 ml) and concentratedsulfuric acid (3 ml) for 5 hours. The excess alcohol was distilled off, theresidue was diluted with water, and the oil which separated was isolated withether. The ethereal solution was washed with sodium carbonate solution; thenwith water and was dried. The ether was evaporated off and the oil wasdistilled to give ethyl 4-i-butylphenylacetate. Sodium ethoxide from sodium (3.67 g) in absolute alcohol (64 ml) was addedover 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 wasfitted with a Fenske column through which alcohol and then ethyl carbonatedistilled. After 1 hour when the still head reached 124°C heating wasdiscontinued. Glacial acetic acid (12 ml) and water (50 ml) was added to thestirred ice-cooled mixture and the ester isolated in ether, washed with sodiumcarbonate solution, water and distilled to give ethyl 4-i-butylphenylmalonate. Ethyl 4-i-butylphenylmalonate (27.53 g) in absolute alcohol (25 ml) wasadded with stirring to a solution of sodium ethoxide From sodium (2.17 g) inabsolute alcohol (75 ml). Ethyl iodide (15 ml) was added and the mixturerefluxed for 2% hours, the alcohol distilled and the residue diluted with water,extracted with ether, washed with sodium bisulfite, water, and evaporated todryness. The residual oil was stirred and refluxed with sodium hydroxide (75 ml of 5N), water (45 ml) and 95% ethanol (120 ml). Within a few minutes a sodiumsalt separated and after 1 hour the solid was collected, washed with ethanol,dissolved in hot water and acidified with dilute hydrochloric acid to give themethyl 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 20minutes until decarboxylation had ceased. The propionic acid was cooled andrecrystallized from light petroleum (BP 60° to 80°C). Two furtherrecrystallizations from the same solvent gave colorless prisms of 2-(4-isobutylphenyl)propionicacid MP 75° to 77.5°C. (The procedure was reportedin 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, wasintroduced in 1969. It was approved for sale without prescription in packagescontaining no more than 400 mg, in the United Kingdom in 1983. This action wasfollowed by the USA, Canada and several European countries. Since this timereports of suspected adverse effects have increased. Most of these relate to gastrointestinaldisturbances, hypersensitivity reactions but aseptic meningitis, skinrashes 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 hoursand a duration of action of less than 6 hours. As with most of these acidic NSAIDs, ibuprofen (pKa = 4.4) isextensively 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 ofmild 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 synthesizedby various methods [88–98]. The simplest way to synthesize ibuprofen is by the acylationof iso-butylbenzol by acetyl chloride. The resulting iso-butylbenzophenone (3.2.21) isreacted with sodium cyanide, giving oxynitrile (3.2.22), which upon reaction withhydroiodic 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, andhydrolysis. Another way to synthesize ibuprofen consists of the chloromethylation of iso-butylbenzene, giving 4-iso-butylbenzylchloride (3.2.24). This product is reacted with sodiumcyanide, making 4-iso-butylbenzyl cyanide (3.2.25), which is alkylated in the presence ofsodium 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 ofnephrotoxicity and hyperkalaemia. Analgesics: avoid concomitant use of 2 or moreNSAIDs, including aspirin (increased side effects);avoid with ketorolac (increased risk of side effectsand haemorrhage); possibly reduced antiplateleteffect with aspirin. Antibacterials: possibly increased risk of convulsionswith quinolones. Anticoagulants: effects of coumarins andphenindione enhanced; possibly increased risk ofbleeding with heparins, dabigatran and edoxaban -avoid long term use with edoxaban. Antidepressants: increased risk of bleeding withSSRIs and venlaflaxine. Antidiabetic agents: effects of sulphonylureasenhanced. Antiepileptics: possibly increased phenytoinconcentration. Antivirals: increased risk of haematological toxicitywith zidovudine; concentration possibly increased byritonavir. 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 withpotassium-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, whichsuggest a high mobility in the aquatic environment. This makesit a commonly detected chemical of the pharmaceutical andpersonal care products (PPCPs) in the environment. It is not aspersistent, however, as many other chemicals. Ibuprofenundergoes photodegradation with exposure to direct andindirect sunlight, although degradation products can haveeffects on aquatic environments. |
| Metabolism | Metabolism occurs rapidly, and the drug is nearly completely excreted in the urine as unchanged drug and oxidativemetabolites 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. Whenibuprofen is administered as the individual enantiomers, the major metabolite isolated is the S-(+)-enantiomerwhatever the configuration of the starting enantiomer. Interestingly, the R-(–)-enantiomer is inverted to theS-(+)-enantiomer in vivo via an acetyl–coenzyme A intermediate, accounting for the observation that the twoenantiomers are bioequivalent in vivo. This is a metabolic phenomenon that also has been observed for otherarylpropionic acids, such as ketoprofen, benoxaprofen, fenoprofen, and naproxen. |
| Toxicity evaluation | The mechanisms of ibuprofen-induced toxicity have not beenclearly defined. Acute renal failure is postulated to result fromdecreased production of intrarenal prostaglandins via inhibitionof the cyclooxygenase pathway. In turn, this will decreasethe renal blood flow and glomerular filtration rate. Ibuprofenalso interferes with prostaglandin synthesis in the gastrointestinalsystem, which can contribute to its irritating effect on themucosa of the gastrointestinal tract. Anion gap metabolicacidosis is likely caused by elevated lactate due to hypotensionand hypoperfusion and also due to ibuprofen and its metabolites,which are all weak acids. Seizures have been reported inlarge ibuprofen overdoses, but the mechanism of toxicityremains unknown. In massive overdoses, ibuprofen is thoughtto have cellular toxicity disrupting mitochondrial energyprocesses 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. |
Ibuprofen Preparation Products And Raw materials
| Raw materials | Ethanol-->Aluminum chloride-->Acetyl chloride-->neopentyl glycol-->Isobutylbenzene-->2-Chloropropionic acid-->Iodoethane-->Diethyl carbonate-->Sodium hydroxide-->Sodium-->Sulfur |
| Preparation Products | Aminoprofen-->rac 2-Hydroxy Ibuprofen-->1-Hydroxyibuprofen-->4-Isobutylbenzaldehyde-->4'-(2-Methylpropyl)acetophenone |
