Brands, Medical Use, Clinical Data
- Free Radical Scavengers
- Enzyme Inhibitors Antimetabolites
- Gout Suppressants
- Tablet for oral administration (100mg, 200mg and 300mg)
Brands / Synonyms
7HP; Adenock; Ailural; Allo-Puren; Allopur; Allopurinol Sodium; Allopurinolum [Inn-Latin]; Allozym; Allural; Aloprim; Alopurinol [Inn-Spanish]; Aloral; Alositol; Aluline; Anoprolin; Anzief; Apo-Allopurinol; Apulonga; Apurin; Apurol; Atisuril; Bleminol; Bloxanth; Caplenal; Cellidrin; Cosuric; Dabrosin; Dabroson; Dura Al; Embarin; Epidropal; Epuric; Foligan; Geapur; Gichtex; Gotax; Hamarin; Hexanuret; HPP; Ketanrift; Ketobun-A; Ledopur; Lopurin; Lysuron; Milurit; Miniplanor; Monarch; Nektrohan; Progout; Purinol; Remid; Riball; Sigapurol; Suspendol; Takanarumin; Urbol; Uricemil; Uriprim; Uripurinol; Uritas; Urobenyl; Urolit; Urosin; Urtias; Urtias 100; Xanturat; Zyloprim; Zyloric
For the treatment of hyperuricemia associated with primary or secondary gout.
Allopurinol, a structural analog of the natural purine base hypoxanthine, is used to prevent gout and renal calculi due to either uric acid or calcium oxalate and to treat uric acid nephropathy, hyperuricemia, and some solid tumors.
Mechanism of Action
Allopurinol inhibits the enzyme xanthine oxidase, blocking the conversion of the oxypurines hypoxanthine and xanthine to uric acid. Elevated concentrations of oxypurine and oxypurine inhibition of xanthine oxidase through negative feedback results in a decrease in the concentrations of uric acid in the blood and urine. Allopurinol also facilitates the incorporation of hypoxanthine and xanthine into DNA and RNA, resulting in further reductions of serum uric acid concentrations.
Approximately 90% absorbed from the gastrointestinal tract.
LD50=214 mg/kg (in mice)
Biotrnasformation / Drug Metabolism
Patients who have developed a severe reaction to allopurinol should not be restarted on the drug.
The following drug interactions were observed in some patients undergoing treatment with oral allopurinol.
Although the pattern of use for oral allopurinol includes longer term therapy, particularly for gout and renal
calculi, the experience gained may be relevant.
Mercaptopurine/Azathioprine: Allopurinol inhibits the enzymatic oxidation of mercaptopurine and
azathioprine to 6-thiouric acid. This oxidation, which is catalyzed by xanthine oxidase, inactivates mercaptopurine.
In patients receiving mercaptopurine (Purinethol) or azathioprine (Imuran), the concomitant administration of 300-600
mg of allopurinol per day will require a reduction in dose to approximately one-third to one-fourth of the usual dose
of mercaptopurine or azathioprine. Subsequent adjustment of doses of mercaptopurine or azathioprine should be made on
the basis of therapeutic response and the appearance of toxic effects.
Dicumarol: It has been reported that allopurinol prolongs the half-life of the anticoagulant,
dicumarol. The clinical basis of this drug interaction has not been established but should be noted when allopurinol
is given to patients already on dicumarol therapy. Consequently, prothrombin time should be reassessed periodically
in patients receiving both drugs.
Uricosuric Agents: Since the excretion of oxipurinol is similar to that of urate, uricosuric
agents, which increase the excretion of urate, are also likely to increase the excretion of oxipurinol and thus lower
the degree of inhibition of xanthine oxidase. The concomitant administration of uricosuric agents and allopurinol has
been associated with a decrease in the excretion of oxypurines (hypoxanthine and xanthine) and an increase in urinary
uric acid excretion compared with that observed with allopurinol alone. Although clinical evidence to date has not
demonstrated renal precipitation of oxypurines in patients either on allopurinol alone or in combination with
uricosuric agents, the possibility should be kept in mind.
Thiazide Diuretics: The reports that the concomitant use of allopurinol and thiazide diuretics
may contribute to the enhancement of allopurinol toxicity in some patients have been reviewed in an attempt to
establish a cause-and-effect relationship and a mechanism of causation. Review of these case reports indicates that
the patients were mainly receiving thiazide diuretics for hypertension and that tests to rule out decreased renal
function secondary to hypertensive nephropathy were not often performed. In those patients in whom renal
insufficiency was documented, however, the recommendation to lower the dose of allopurinol was not followed. Although
a causal mechanism and a cause-and-effect relationship have not been established, current evidence suggests that
renal function should be monitored in patients on thiazide diuretics and allopurinol even in the absence of renal
failure, and dosage levels should be even more conservatively adjusted in those patients on such combined therapy if
diminished renal function is detected..
Ampicillin/Amoxicillin: An increase in the frequency of skin rash has been reported among
patients receiving ampicillin or amoxicillin concurrently with allopurinol compared to patients who are not receiving
both drugs. The cause of the reported association has not been established.
Cytotoxic Agents: Enhanced bone marrow suppression by cyclophosphamide and other cytotoxic
agents has been reported among patients with neoplastic disease, except leukemia, in the presence of allopurinol.
However, in a well-controlled study of patients with lymphoma on combination therapy, allopurinol did not increase
the marrow toxicity of patients treated with cyclophosphamide, doxorubicin, bleomycin, procarbazine and/or
Chlorpropamide: Chlorpropamide's plasma half-life may be prolonged by allopurinol, since
allopurinol and chlorpropamide may compete for excretion in the renal tubule. The risk of hypoglycemia secondary to
this mechanism may be increased if allopurinol and chlorpropamide are given concomitantly in the presence of renal
Cyclosporin: Reports indicate that cyclosporine levels may be increased during concomitant
treatment with allopurinol sodium for injection. Monitoring of cyclosporine levels and possible adjustment of
cyclosporine dosage should be considered when these drugs are co-administered.
Tolbutamide's conversion to inactive metabolites has been shown to be catalyzed by xanthine oxidase from rat
liver. The clinical significance, if any, of these observations is unknown.