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Allopurinol V.1.svg
ChemSpider 2D Image | Allopurinol | C5H4N4O


  • Molecular FormulaC5H4N4O
  • Average mass136.111 Da
  • аллопуринол [Russian]ألوبيرينول [Arabic]别嘌醇 [Chinese]

4H-Pyrazolo[3,4-d]pyrimidin-4-one, 1,5-dihydro-, radical ion(1+)
4H-Pyrazolo[3,4-d]pyrimidin-4-one, 1,7-dihydro-

Allopurinol is a medication used to decrease high blood uric acid levels.[2] It is specifically used to prevent gout, prevent specific types of kidney stones and for the high uric acid levels that can occur with chemotherapy.[3][4] It is taken by mouth or injected into a vein.[4]

Common side effects when used by mouth include itchiness and rash.[4] Common side effects when used by injection include vomiting and kidney problems.[4] While not recommended historically, starting allopurinol during an attack of gout appears to be safe.[5][6] In those already on the medication, it should be continued even during an acute gout attack.[5][3] While use during pregnancy does not appear to result in harm, this use has not been well studied.[1] Allopurinol is in the xanthine oxidase inhibitor family of medications.[4]

Allopurinol was approved for medical use in the United States in 1966.[4] It is on the World Health Organization’s List of Essential Medicines, the safest and most effective medicines needed in a health system.[7] Allopurinol is available as a generic medication.[4] In 2019, it was the 43rd most commonly prescribed medication in the United States, with more than 15 million prescriptions.[8][9]

ALLUPRINOLCAS Registry Number: 315-30-0 
CAS Name: 1,5-Dihydro-4H-pyrazolo[3,4-d]pyrimidin-4-one 
Additional Names: 1H-pyrazolo[3,4-d]pyrimidin-4-ol; 4-hydroxypyrazolo[3,4-d]pyrimidine; HPP 
Manufacturers’ Codes: BW-56158 
Trademarks: Adenock (Mitsubishi); Allurit (Aventis); Aloral (Lagap); Alositol (Tanabe); Allo-Puren (Isis); Allozym (Sawai); Allural (Rovi); Anoprolin (Azwell); Anzief (Nippon Chemiphar); Apulonga (Dorsch); Apurol (Siegfried); Apurin (GEA); Bleminol (Gepepharm); Caplenal (Teva); Cellidrin (Hennig); Cosuric (DDSA); Dabroson (Hoyer); Embarin (Merckle); Epidropal (Teofarma); Foligan (DESMA); Gichtex (Gerot); Hamarin (Roche); Hexanurat (Durascan); Ketanrift (Ohta); Lopurin (Abbott); Lysuron (Roche); Miniplanor (Galen); Monarch (SS Pharm.); Remid (TAD); Riball (Schering AG); Sigapurol (Siegfried); Suspendol (Merckle); Takanarumin (Takata); Uricemil (Molteni); Uripurinol (Azupharma); Urosin (Roche); Urtias (Novartis); Zyloprim (GSK); Zyloric (GSK) 
Molecular Formula: C5H4N4O, Molecular Weight: 136.11 
Percent Composition: C 44.12%, H 2.96%, N 41.16%, O 11.75% 
Literature References: Xanthine oxidase inhibitor; decreases uric acid production. Prepn: Robins, J. Am. Chem. Soc.78, 784 (1956); Schmidt, Druey, Helv. Chim. Acta39, 986 (1956); Druey, Schmidt, US2868803 (1959 to Ciba); GB798646 (1958 to Wellcome Found.); Hitchings, Falco, US3474098 (1969 to Burroughs Wellcome). Physiological and biochemical studies: Hitchings, in Biochem. Aspects Antimetab. Drug Hydroxylation, D. Shugar, Ed. (Academic Press, London, 1969) pp 11-22, C.A.75, 3531h (1971). Clinical trial in treatment of renal calculi: M. J. V. Smith, J. Urol.117, 690 (1977); B. Ettinger et al.,N. Engl. J. Med.315, 1386 (1986). Use in hyperuricemia and gout: G. R. Boss, J. E. Seegmiller, ibid.300, 1459 (1977). Effect on renal function in treatment of gout: T. Gibson, Ann. Rheum. Dis.41, 59 (1982). Comprehensive description: S. A. Benezra, T. R. Bennett, Anal. Profiles Drug Subs.7, 1-17 (1978). 
Properties: Crystals, mp above 350°. uv max (0.1N NaOH): 257 nm (e 7200); (0.1N HCl): 250 nm (e 7600); (methanol): 252 nm (e 7600). Soly in mg/ml at 25°: water 0.48; n-octanol <0.01; chloroform 0.60; ethanol 0.30; DMSO 4.6. pKa 10.2. 
Melting point: mp above 350° 
pKa: pKa 10.2 
Absorption maximum: uv max (0.1N NaOH): 257 nm (e 7200); (0.1N HCl): 250 nm (e 7600); (methanol): 252 nm (e 7600) 
Derivative Type: Sodium salt 
CAS Registry Number: 17795-21-0 
Trademarks: Aloprim (Nabi) 
Molecular Formula: C5H3N4NaO, Molecular Weight: 158.09Percent Composition: C 37.99%, H 1.91%, N 35.44%, Na 14.54%, O 10.12% 
Properties: White amorphous mass. pKa 9.31. 
pKa: pKa 9.31 
Therap-Cat: Treatment of hyperuricemia and chronic gout. Antiurolithic. 
Keywords: Antigout; Antiurolithic; Xanthine Oxidase Inhibitor.

Synthesis ReferenceDruey, J. and Schmidt, P.; US. Patent 2868,803; January 13,1959; assigned to Ciba Pharmaceutical Products Inc. Hitchings, G.H. and Falco, EA.; U.S. Patent 3,474,098; October 21,1969; assigned to Bur- roughs Wellcome & Co. Cresswell, R.M.and Mentha, J.W.; US.Patent4,146,713; March27,1979; assigned to Bur- roughs Wellcome & Co.

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File:Allopurinol synthesis.svg


  1. US 2 868 803 (Ciba; 13.1.1959; CH-prior. 10.2.1956).
  2. DAS 1 720 024 (Wellcome Found; appl. 12.7.1967; GB-prior. 14.7.1966).

Similar process:

  1. DAS 1 904 894 (Wellcome Found; appl. 31.1.1969; GB-prior. 2.2.1968).
  2. US 4 146 713 (Burroughs Wellcome; 27.3.1979; GB-prior. 2.2.1968).

Alternative syntheses:

  1. US 3 474 098 (Burroughs Wellcome; 21.10.1969; prior. 29.3.1956).
  2. DAS 2 224 382 (Henning Berlin; appl. 18.5.1972).
  3. DE 1 118 221 (Wellcome Found; appl. 4.8.1956; GB-prior. 10.8.1955).
  4. DAS 1 814 082 (Wellcome Found; appl. 11.12.1968).
  5. DAS 1 950 075 (Henning Berlin; appl. 3.10.1969).

SYNCondensation of hydrazine with ethoxymethylenemalononitrile (I) leads to 3-amino-4-cyanopyrazole (II), which, by hydrolysis with sulphuric acid, gives the corresponding amide (III); heating III with formamide in excess results in allopurinol (IV). The synthesis of allopurinol can be illustrated as below: 




Infrared Spectrum The infrared spectrum of allopurinol is shown in Figure 1 . in KBr with a Perkin Elmer model 457 infrared spectrophotometer. with the structure of allopurinol . It was taken as a 0.2% dispersion of allopurinol Table I gives the infrareg assignments consistent Table I Infrared Spectral Assignments for Allopurinol Frequency (cm-l) Assignment

3060 CH stretching vibrations of the pyrimidine ring

1700 CO stretching vibration of the keto form of the 4-hydroxy tautomer 1

590 ring vibrations

1245 CH in-plane deformation


1 H-NMR Spectra of Allopurinol standard
Clinical data
Trade namesZyloprim, Caplenal, Zyloric, others
License dataUS DailyMedAllopurinol
AU: B2[1]
Routes of
By mouth (tablet), intravenous
ATC codeM04AA01 (WHO)
Legal status
Legal statusAU: S4 (Prescription only)UK: POM (Prescription only)US: ℞-only
Pharmacokinetic data
Protein bindingNegligible
Metabolismliver (80% oxipurinol, 10% allopurinol ribosides)
Elimination half-life2 h (oxipurinol 18–30 h)
showIUPAC name
CAS Number315-30-0 
PubChem CID135401907
CompTox Dashboard (EPA)DTXSID4022573 
ECHA InfoCard100.005.684 
Chemical and physical data
Molar mass136.114 g·mol−1
3D model (JSmol)Interactive image

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Medical uses


Allopurinol is used to reduce urate formation in conditions where urate deposition has already occurred or is predictable. The specific diseases and conditions where it is used include gouty arthritis, skin tophi, kidney stones, idiopathic gout; uric acid lithiasis; acute uric acid nephropathy; neoplastic disease and myeloproliferative disease with high cell turnover rates, in which high urate levels occur either spontaneously, or after cytotoxic therapy; certain enzyme disorders which lead to overproduction of urate, for example: hypoxanthine-guanine phosphoribosyltransferase, including Lesch–Nyhan syndromeglucose 6-phosphatase including glycogen storage diseasephosphoribosyl pyrophosphate synthetasephosphoribosyl pyrophosphate amidotransferaseadenine phosphoribosyltransferase.

It is also used to treat kidney stones caused by deficient activity of adenine phosphoribosyltransferase.

Tumor lysis syndrome

Allopurinol was also commonly used to treat tumor lysis syndrome in chemotherapeutic treatments, as these regimens can rapidly produce severe acute hyperuricemia;[10] however, it has gradually been replaced by urate oxidase therapy.[11] Intravenous formulations are used in this indication when people cannot take medicine by mouth.[12]

Inflammatory bowel disease

Allopurinol cotherapy is used to improve outcomes for people with inflammatory bowel disease and Crohn’s disease who do not respond to thiopurine monotherapy.[13][14] Cotherapy has also been shown to greatly improve hepatoxicity side effects in treatment of IBD.[15] Cotherapy invariably requires dose reduction of the thiopurine, usually to one-third of the standard dose depending upon the patient’s genetic status for thiopurine methyltransferase.[16]

Psychiatric disorders

Allopurinol has been tested as an augmentation strategy for the treatment of mania in bipolar disorder. Meta-analytic evidence showed that adjunctive allopurinol was superior to placebo for acute mania (both with and without mixed features).[17] Its efficacy was not influenced by dosage, follow-up duration, or concurrent standard treatment.[17]

Side effects

Because allopurinol is not a uricosuric, it can be used in people with poor kidney function. However, for people with impaired kidney function, allopurinol has two disadvantages. First, its dosing is complex.[18] Second, some people are hypersensitive to the drug; therefore, its use requires careful monitoring.[19][20]

Allopurinol has rare but potentially fatal adverse effects involving the skin. The most serious adverse effect is a hypersensitivity syndrome consisting of fever, skin rash, eosinophiliahepatitis, and worsened renal function, collectively referred to as DRESS syndrome.[19] Allopurinol is one of the drugs commonly known to cause Stevens–Johnson syndrome and toxic epidermal necrolysis, two life-threatening dermatological conditions.[19] More common is a less-serious rash that leads to discontinuing this drug.[19]

More rarely, allopurinol can also result in the depression of bone marrow elements, leading to cytopenias, as well as aplastic anemia. Moreover, allopurinol can also cause peripheral neuritis in some patients, although this is a rare side effect. Another side effect of allopurinol is interstitial nephritis.[21]

Allopurinol should not be given to people who are allergic to it.[10]

Drug interactions

Drug interactions are extensive, and are as follows:[10]

  • Azathioprine and 6-mercaptopurine: Azathioprine is metabolised to 6-mercaptopurine which in turn is inactivated by the action of xanthine oxidase – the target of allopurinol. Giving allopurinol with either of these drugs at their normal dose will lead to overdose of either drug; only one-quarter of the usual dose of 6-mercaptopurine or azathioprine should be given;
  • Didanosine: plasma didanosine Cmax and AUC values were approximately doubled with concomitant allopurinol treatment; it should not be co-administered with allopuroinol and if it must be, the dose of should be reduced and the person should be closely monitored.

Allopurinol may also increase the activity or half-life of the following drugs, in order of seriousness and certainty of the interaction:[10]

Co-administration of the following drugs may make allopurinol less active or decrease its half-life:[10]

Co-administration of the following drugs may cause hypersensitivity or skin rash:[10]


A common misconception is that allopurinol is metabolized by its target, xanthine oxidase, but this action is principally carried out by aldehyde oxidase.[22] The active metabolite of allopurinol is oxipurinol, which is also an inhibitor of xanthine oxidase. Allopurinol is almost completely metabolized to oxipurinol within two hours of oral administration, whereas oxipurinol is slowly excreted by the kidneys over 18–30 hours. For this reason, oxipurinol is believed responsible for the majority of allopurinol’s effect.[23]

Mechanism of action

Allopurinol is a purine analog; it is a structural isomer of hypoxanthine (a naturally occurring purine in the body) and is an inhibitor of the enzyme xanthine oxidase.[2] Xanthine oxidase is responsible for the successive oxidation of hypoxanthine and xanthine, resulting in the production of uric acid, the product of human purine metabolism.[2] In addition to blocking uric acid production, inhibition of xanthine oxidase causes an increase in hypoxanthine and xanthine. While xanthine cannot be converted to purine ribotides, hypoxanthine can be salvaged to the purine ribotides adenosine and guanosine monophosphates. Increased levels of these ribotides may cause feedback inhibition of amidophosphoribosyl transferase, the first and rate-limiting enzyme of purine biosynthesis. Allopurinol, therefore, decreases uric acid formation and may also inhibit purine synthesis.[24]


The HLA-B*5801 allele is a genetic marker for allopurinol-induced severe cutaneous adverse reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).[25][26] The frequency of the HLA-B*5801 allele varies between ethnicities: Han Chinese and Thai populations have HLA-B*5801 allele frequencies of around 8%, as compared to European and Japanese populations, who have allele frequencies of around 1.0% and 0.5%, respectively.[27] The increase in risk for developing allopurinol-induced SJS or TEN in individuals with the HLA-B*5801 allele (as compared to those who do not have this allele) is very high, ranging from a 40-fold to a 580-fold increase in risk, depending on ethnicity.[25][26] As of 2011 the FDA-approved drug label for allopurinol did not contain any information regarding the HLA-B*5801 allele, though FDA scientists did publish a study in 2011 which reported a strong, reproducible and consistent association between the allele and allopurinol-induced SJS and TEN.[28] However, the American College of Rheumatology recommends screening for HLA-B*5801 in high-risk populations (e.g. Koreans with stage 3 or worse chronic kidney disease and those of Han Chinese and Thai descent), and prescribing patients who are positive for the allele an alternative drug.[29] The Clinical Pharmacogenetics Implementation Consortium guidelines state that allopurinol is contraindicated in known carriers of the HLA-B*5801 allele.[30][31]


Allopurinol was first synthesized and reported in 1956 by Roland K. Robins (1926-1992), in a search for antineoplastic agents.[2][32] Because allopurinol inhibits the breakdown (catabolism) of the thiopurine drug mercaptopurine, and it was later tested by Wayne Rundles, in collaboration with Gertrude Elion‘s lab at Wellcome Research Laboratories to see if it could improve treatment of acute lymphoblastic leukemia by enhancing the action of mercaptopurine.[2][33] However, no improvement in leukemia response was noted with mercaptopurine-allopurinol co-therapy, so that work turned to other compounds and the team then started testing allopurinol as a potential for gout.[34] Allopurinol was first marketed as a treatment for gout in 1966.[33]

Society and culture

Pure allopurinol is a white powder.


Allopurinol is sold as an injection for intravenous use[12] and as a tablet.[10]


Allopurinol has been marketed in the United States since 19 August 1966, when it was first approved by FDA under the trade name Zyloprim.[35] Allopurinol was marketed at the time by Burroughs-Wellcome. Allopurinol is a generic drug sold under a variety of brand names, including Allohexal, Allosig, Milurit, Alloril, Progout, Ürikoliz, Zyloprim, Zyloric, Zyrik, and Aluron.[36]

See also


  1. Jump up to:a b “Allopurinol Use During Pregnancy”Drugs.comArchived from the original on 20 August 2016. Retrieved 20 December 2016.
  2. Jump up to:a b c d e Pacher P, Nivorozhkin A, Szabó C (March 2006). “Therapeutic effects of xanthine oxidase inhibitors: renaissance half a century after the discovery of allopurinol”Pharmacological Reviews58 (1): 87–114. doi:10.1124/pr.58.1.6PMC 2233605PMID 16507884.
  3. Jump up to:a b World Health Organization (2009). Stuart MC, Kouimtzi M, Hill SR (eds.). WHO Model Formulary 2008. World Health Organization. p. 39. hdl:10665/44053ISBN 9789241547659.
  4. Jump up to:a b c d e f g “Allopurinol”. The American Society of Health-System Pharmacists. Archived from the original on 29 April 2016. Retrieved 8 December 2016.
  5. Jump up to:a b Robinson PC, Stamp LK (May 2016). “The management of gout: Much has changed”. Australian Family Physician45 (5): 299–302. PMID 27166465.
  6. ^ Satpanich, P; Pongsittisak, W; Manavathongchai, S (18 August 2021). “Early versus Late Allopurinol Initiation in Acute Gout Flare (ELAG): a randomized controlled trial”. Clinical Rheumatologydoi:10.1007/s10067-021-05872-8PMID 34406530S2CID 237156638.
  7. ^ World Health Organization (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. hdl:10665/325771. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
  8. ^ “The Top 300 of 2019”ClinCalc. Retrieved 16 October 2021.
  9. ^ “Allopurinol – Drug Usage Statistics”ClinCalc. Retrieved 16 October 2021.
  10. Jump up to:a b c d e f g “300 mg Allopurinol tables”UK Electronic Medicines Compendium. 7 April 2016. Archived from the original on 11 September 2016.
  11. ^ Jeha S (October 2001). “Tumor lysis syndrome”. Seminars in Hematology38 (4 Suppl 10): 4–8. doi:10.1016/S0037-1963(01)90037-XPMID 11694945.
  12. Jump up to:a b “Label for injectable Allopurinol”DailyMed. June 2014. Archived from the original on 13 September 2016.
  13. ^ Bradford K, Shih DQ (October 2011). “Optimizing 6-mercaptopurine and azathioprine therapy in the management of inflammatory bowel disease”World Journal of Gastroenterology17 (37): 4166–73. doi:10.3748/wjg.v17.i37.4166PMC 3208360PMID 22072847.
  14. ^ Sparrow MP, Hande SA, Friedman S, Cao D, Hanauer SB (February 2007). “Effect of allopurinol on clinical outcomes in inflammatory bowel disease nonresponders to azathioprine or 6-mercaptopurine”. Clinical Gastroenterology and Hepatology5 (2): 209–14. doi:10.1016/j.cgh.2006.11.020PMID 17296529.
  15. ^ Ansari A, Patel N, Sanderson J, O’Donohue J, Duley JA, Florin TH (March 2010). “Low-dose azathioprine or mercaptopurine in combination with allopurinol can bypass many adverse drug reactions in patients with inflammatory bowel disease”Alimentary Pharmacology & Therapeutics31 (6): 640–7. doi:10.1111/j.1365-2036.2009.04221.xPMID 20015102S2CID 6000856.
  16. ^ Ansari AR, Duley JA (March 2012). “Azathioprine co-therapy with allopurinol for inflammatory bowel disease: trials and tribulations” (PDF). Rev Assoc Med Bras58 (Suppl.1): S28–33.
  17. Jump up to:a b Bartoli F, Cavaleri D, Bachi B, Moretti F, Riboldi I, Crocamo C, Carrà G (September 2021). “Repurposed drugs as adjunctive treatments for mania and bipolar depression: A meta-review and critical appraisal of meta-analyses of randomized placebo-controlled trials”. Journal of Psychiatric Research143: 230–238. doi:10.1016/j.jpsychires.2021.09.018PMID 34509090S2CID 237485915.
  18. ^ Dalbeth N, Stamp L (2007). “Allopurinol dosing in renal impairment: walking the tightrope between adequate urate lowering and adverse events”. Seminars in Dialysis20 (5): 391–5. doi:10.1111/j.1525-139X.2007.00270.xPMID 17897242S2CID 1150852.
  19. Jump up to:a b c d Chung WH, Wang CW, Dao RL (July 2016). “Severe cutaneous adverse drug reactions”. The Journal of Dermatology43 (7): 758–66. doi:10.1111/1346-8138.13430PMID 27154258S2CID 45524211.
  20. ^ Tsai TF, Yeh TY (2010). “Allopurinol in dermatology”. American Journal of Clinical Dermatology11 (4): 225–32. doi:10.2165/11533190-000000000-00000PMID 20509717S2CID 36847530.
  21. ^ De Broe ME, Bennett WM, Porter GA (2003). Clinical Nephrotoxins: Renal Injury from Drugs and ChemicalsSpringer Science+Business MediaISBN 9781402012778Acute interstitial nephritis has also been reported associated with by the administration of allopurinol.
  22. ^ Reiter S, Simmonds HA, Zöllner N, Braun SL, Knedel M (March 1990). “Demonstration of a combined deficiency of xanthine oxidase and aldehyde oxidase in xanthinuric patients not forming oxipurinol”. Clinica Chimica Acta; International Journal of Clinical Chemistry187 (3): 221–34. doi:10.1016/0009-8981(90)90107-4PMID 2323062.
  23. ^ Day RO, Graham GG, Hicks M, McLachlan AJ, Stocker SL, Williams KM (2007). “Clinical pharmacokinetics and pharmacodynamics of allopurinol and oxypurinol”. Clinical Pharmacokinetics46 (8): 623–44. doi:10.2165/00003088-200746080-00001PMID 17655371S2CID 20369375.
  24. ^ Cameron JS, Moro F, Simmonds HA (February 1993). “Gout, uric acid and purine metabolism in paediatric nephrology”. Pediatric Nephrology7 (1): 105–18. doi:10.1007/BF00861588PMID 8439471S2CID 34815040.
  25. Jump up to:a b “Uric Acid-Lowering Drugs Pathway, Pharmacodynamics”PharmGKB. Archived from the original on 8 August 2014.
  26. Jump up to:a b “PharmGKB”Archived from the original on 8 August 2014. Retrieved 1 August 2014.
  27. ^ “Allele Frequency Net Database”. Archived from the original on 28 August 2009.
  28. ^ Zineh I, Mummaneni P, Lyndly J, Amur S, La Grenade LA, Chang SH, et al. (December 2011). “Allopurinol pharmacogenetics: assessment of potential clinical usefulness”Pharmacogenomics12 (12): 1741–9. doi:10.2217/pgs.11.131PMID 22118056.
  29. ^ Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, et al. (October 2012). “2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia”Arthritis Care & Research64 (10): 1431–46. doi:10.1002/acr.21772PMC 3683400PMID 23024028.
  30. ^ “Annotation of CPIC Guideline for allopurinol and HLA-B”PharmGKBArchived from the original on 8 August 2014. Retrieved 1 August 2014.
  31. ^ Hershfield MS, Callaghan JT, Tassaneeyakul W, Mushiroda T, Thorn CF, Klein TE, Lee MT (February 2013). “Clinical Pharmacogenetics Implementation Consortium guidelines for human leukocyte antigen-B genotype and allopurinol dosing”Clinical Pharmacology and Therapeutics93 (2): 153–8. doi:10.1038/clpt.2012.209PMC 3564416PMID 23232549.
  32. ^ Robins RK (1956). “Potential Purine Antagonists. I. Synthesis of Some 4,6-Substituted Pyrazolo \3,4-d] pyrimidines1”. J. Am. Chem. Soc78 (4): 784–790. doi:10.1021/ja01585a023.
  33. Jump up to:a b Sneader W (2005). Drug Discovery: A History. John Wiley & Sons. p. 254. ISBN 9780471899792.
  34. ^ Elion GB (April 1989). “The purine path to chemotherapy”. Science244 (4900): 41–7. Bibcode:1989Sci…244…41Edoi:10.1126/science.2649979PMID 2649979.
  35. ^ “FDA Approved Drug Products”Drugs@FDAArchived from the original on 14 August 2012. Retrieved 8 November 2013.
  36. ^ “Search Results for Allopurinol”DailyMedArchived from the original on 25 March 2012. Retrieved 27 July 2011.

Further reading

/////////////////////ALLUPURINOL, BW-56158, аллопуринол , ألوبيرينول , 别嘌醇 , 




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DR ANTHONY MELVIN CRASTO, Born in Mumbai in 1964 and graduated from Mumbai University, Completed his Ph.D from ICT, 1991,Matunga, Mumbai, India, in Organic Chemistry, The thesis topic was Synthesis of Novel Pyrethroid Analogues, Currently he is working with AFRICURE PHARMA, ROW2TECH, CLEANCHEM LABS as ADVISOR, earlier assignment was with GLENMARK LIFE SCIENCES LTD, as CONSUlTANT, Retired from GLENMARK in Jan2022 Research Centre as Principal Scientist, Process Research (bulk actives) at Mahape, Navi Mumbai, India. Total Industry exp 32 plus yrs, Prior to joining Glenmark, he has worked with major multinationals like Hoechst Marion Roussel, now Sanofi, Searle India Ltd, now RPG lifesciences, etc. He has worked with notable scientists like Dr K Nagarajan, Dr Ralph Stapel, Prof S Seshadri, etc, He did custom synthesis for major multinationals in his career like BASF, Novartis, Sanofi, etc., He has worked in Discovery, Natural products, Bulk drugs, Generics, Intermediates, Fine chemicals, Neutraceuticals, GMP, Scaleups, etc, he is now helping millions, has 9 million plus hits on Google on all Organic chemistry websites. His friends call him Open superstar worlddrugtracker. His New Drug Approvals, Green Chemistry International, All about drugs, Eurekamoments, Organic spectroscopy international, etc in organic chemistry are some most read blogs He has hands on experience in initiation and developing novel routes for drug molecules and implementation them on commercial scale over a 32 PLUS year tenure till date Feb 2023, Around 35 plus products in his career. He has good knowledge of IPM, GMP, Regulatory aspects, he has several International patents published worldwide . He has good proficiency in Technology transfer, Spectroscopy, Stereochemistry, Synthesis, Polymorphism etc., He suffered a paralytic stroke/ Acute Transverse mylitis in Dec 2007 and is 90 %Paralysed, He is bound to a wheelchair, this seems to have injected feul in him to help chemists all around the world, he is more active than before and is pushing boundaries, He has 100 million plus hits on Google, 2.5 lakh plus connections on all networking sites, 100 Lakh plus views on dozen plus blogs, 227 countries, 7 continents, He makes himself available to all, contact him on +91 9323115463, email, Twitter, @amcrasto , He lives and will die for his family, 90% paralysis cannot kill his soul., Notably he has 38 lakh plus views on New Drug Approvals Blog in 227 countries...... , He appreciates the help he gets from one and all, Friends, Family, Glenmark, Readers, Wellwishers, Doctors, Drug authorities, His Contacts, Physiotherapist, etc He has total of 32 International and Indian awards

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