DRUGS & SUPPLEMENTS

Azamun

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Published: 2021-11-11T10:10:10+00:00

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INDICATIONS AND USAGE:

Azamun is indicated as an adjunct for the prevention of rejection in renal homotransplantation. It is also indicated for the management of active rheumatoid arthritis to reduce signs and symptoms.

Renal Homotransplantation: Azamun is indicated as an adjunct for the prevention of rejection in renal homotransplantation. Experience with over 16,000 transplants shows a 5-year patient survival of 35% to 55%, but this is dependent on donor, match for HLA antigens, anti-donor or anti-B-cell alloantigen antibody, and other variables. The effect of Azamun on these variables has not been tested in controlled trials.

Rheumatoid Arthritis: Azamun is indicated for the treatment of active rheumatoid arthritis (RA) to reduce signs and symptoms. Aspirin, non-steroidal anti-inflammatory drugs and/or low dose glucocorticoids may be continued during treatment with Azamun. The combined use of Azamun with disease modifying anti-rheumatic drugs (DMARDs) has not been studied for either added benefit or unexpected adverse effects. The use of Azamun with these agents cannot be recommended.

CONTRAINDICATIONS:

Azamun should not be given to patients who have shown hypersensitivity to the drug. Azamun should not be used for treating rheumatoid arthritis in pregnant women. Patients with rheumatoid arthritis previously treated with alkylating agents (cyclophosphamide, chlorambucil, melphalan, or others) may have a prohibitive risk of malignancy if treated with Azamun.

WARNINGS:

Malignancy

Patients receiving immunosuppressants, including Azamun, are at increased risk of developing lymphoma and other malignancies, particularly of the skin. Physicians should inform patients of the risk of malignancy with Azamun. As usual for patients with increased risk for skin cancer, exposure to sunlight and ultraviolet light should be limited by wearing protective clothing and using a sunscreen with a high protection factor.

Post-transplant

Renal transplant patients are known to have an increased risk of malignancy, predominantly skin cancer and reticulum cell or lymphomatous tumors. The risk of post-transplant lymphomas may be increased in patients who receive aggressive treatment with immunosuppressive drugs, including Azamun. Therefore, immunosuppressive drug therapy should be maintained at the lowest effective levels.

Rheumatoid Arthritis

Information is available on the risk of malignancy with the use of Azamun in rheumatoid arthritis. It has not been possible to define the precise risk of malignancy due to Azamun. The data suggest the risk may be elevated in patients with rheumatoid arthritis, though lower than for renal transplant patients. However, acute myelogenous leukemia as well as solid tumors have been reported in patients with rheumatoid arthritis who have received Azamun.

Inflammatory Bowel Disease

Postmarketing cases of hepatosplenic T-cell lymphoma (HSTCL), a rare type of T-cell lymphoma, have been reported in patients treated with Azamun. These cases have had a very aggressive disease course and have been fatal. The majority of reported cases have occurred in patients with Crohn's disease or ulcerative colitis and the majority were in adolescent and young adult males. Some of the patients were treated with Azamun as monotherapy and some had received concomitant treatment with a TNFα blocker at or prior to diagnosis. The safety and efficacy of Azamun for the treatment of Crohn's disease and ulcerative colitis have not been established.

Cytopenias

Severe leukopenia, thrombocytopenia, anemias including macrocytic anemia, and/or pancytopenia may occur in patients being treated with Azamun. Severe bone marrow suppression may also occur. Patients with intermediate thiopurine S-methyl transferase (TPMT) activity may be at an increased risk of myelotoxicity if receiving conventional doses of Azamun. Patients with low or absent TPMT activity are at an increased risk of developing severe, life-threatening myelotoxicity if receiving conventional doses of Azamun. TPMT genotyping or phenotyping can help identify patients who are at an increased risk for developing Azamun toxicity.^2-9. Hematologic toxicities are dose-related and may be more severe in renal transplant patients whose homograft is undergoing rejection. It is suggested that patients on Azamun have complete blood counts, including platelet counts, weekly during the first month, twice monthly for the second and third months of treatment, then monthly or more frequently if dosage alterations or other therapy changes are necessary. Delayed hematologic suppression may occur. Prompt reduction in dosage or temporary withdrawal of the drug may be necessary if there is a rapid fall in or persistently low leukocyte count, or other evidence of bone marrow depression. Leukopenia does not correlate with therapeutic effect; therefore the dose should not be increased intentionally to lower the white blood cell count.

Serious infections

Patients receiving immunosuppressants, including Azamun, are at increased risk for bacterial, viral, fungal, protozoal, and opportunistic infections, including reactivation of latent infections. These infections may lead to serious, including fatal outcomes.

Progressive Multifocal Leukoencephalopathy

Cases of JC virus-associated infection resulting in progressive multifocal leukoencephalopathy, sometimes fatal, have been reported in patients treated with immunosuppressants, including Azamun. Risk factors for PML include treatment with immunosuppressant therapies and impairment of immune function. Consider the diagnosis of PML in any patient presenting with new-onset neurological manifestations and consider consultation with a neurologist as clinically indicated. Consider reducing the amount of immunosuppression in patients who develop PML. In transplant patients, consider the risk that the reduced immunosuppression represents to the graft.

Effect on Sperm in Animals

Azamun has been reported to cause temporary depression in spermatogenesis and reduction in sperm viability and sperm count in mice at doses 10 times the human therapeutic dose;¹⁰ a reduced percentage of fertile matings occurred when animals received 5 mg/kg. ¹¹

Pregnancy: Pregnancy Category D. Azamun can cause fetal harm when administered to a pregnant woman. Azamun should not be given during pregnancy without careful weighing of risk versus benefit. Whenever possible, use of Azamun in pregnant patients should be avoided. This drug should not be used for treating rheumatoid arthritis in pregnant women. ¹²

Azamun is teratogenic in rabbits and mice when given in doses equivalent to the human dose (5 mg/kg daily). Abnormalities included skeletal malformations and visceral anomalies. ¹¹

Limited immunologic and other abnormalities have occurred in a few infants born of renal allograft recipients on Azamun. In a detailed case report, ¹³ documented lymphopenia, diminished IgG and IgM levels, CMV infection, and a decreased thymic shadow were noted in an infant born to a mother receiving 150 mg Azamun and 30 mg prednisone daily throughout pregnancy. At 10 weeks most features were normalized. DeWitte et al reported pancytopenia and severe immune deficiency in a preterm infant whose mother received 125 mg Azamun and 12.5 mg prednisone daily. ¹⁴ There have been two published reports of abnormal physical findings. Williamson and Karp described an infant born with preaxial polydactyly whose mother received Azamun 200 mg daily and prednisone 20 mg every other day during pregnancy. ¹⁵ Tallent et al described an infant with a large myelomeningocele in the upper lumbar region, bilateral dislocated hips, and bilateral talipes equinovarus. The father was on long-term Azamun therapy. ¹⁶

Benefit versus risk must be weighed carefully before use of Azamun in patients of reproductive potential. There are no adequate and well-controlled studies in pregnant women. If this drug is used during pregnancy or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus. Women of childbearing age should be advised to avoid becoming pregnant.

PRECAUTIONS:

General: A gastrointestinal hypersensitivity reaction characterized by severe nausea and vomiting has been reported. These symptoms may also be accompanied by diarrhea, rash, fever, malaise, myalgias, elevations in liver enzymes, and occasionally, hypotension. Symptoms of gastrointestinal toxicity most often develop within the first several weeks of therapy with Azamun and are reversible upon discontinuation of the drug. The reaction can recur within hours after re-challenge with a single dose of Azamun.

Information for Patients: Patients being started on Azamun should be informed of the necessity of periodic blood counts while they are receiving the drug and should be encouraged to report any unusual bleeding or bruising to their physician. They should be informed of the danger of infection while receiving Azamun and asked to report signs and symptoms of infection to their physician. Careful dosage instructions should be given to the patient, especially when Azamun is being administered in the presence of impaired renal function or concomitantly with allopurinol. Patients should be advised of the potential risks of the use of Azamun during pregnancy and during the nursing period. The increased risk of malignancy following therapy with Azamun should be explained to the patient.

Laboratory Tests: Complete Blood Count (CBC) Monitoring: Patients on Azamun should have complete blood counts, including platelet counts, weekly during the first month, twice monthly for the second and third months of treatment, then monthly or more frequently if dosage alterations or other therapy changes are necessary.

TPMT Testing: It is recommended that consideration be given to either genotype or phenotype patients for TPMT. Phenotyping and genotyping methods are commercially available. The most common non-functional alleles associated with reduced levels of TPMT activity are TPMT*2, TPMT*3A and TPMT*3C. Patients with two non-functional alleles (homozygous) have low or absent TPMT activity and those with one non-functional allele (heterozygous) have intermediate activity. Accurate phenotyping (red blood cell TPMT activity) results are not possible in patients who have received recent blood transfusions. TPMT testing may also be considered in patients with abnormal CBC results that do not respond to dose reduction. Early drug discontinuation in these patients is advisable. TPMT TESTING CANNOT SUBSTITUTE FOR COMPLETE BLOOD COUNT (CBC) MONITORING IN PATIENTS RECEIVING Azamun. See CLINICAL PHARMACOLOGY, WARNINGS, ADVERSE REACTIONS and DOSAGE AND ADMINISTRATION sections.

Drug Interactions: Use with Allopurinol: One of the pathways for inactivation of Azamun is inhibited by allopurinol. Patients receiving Azamun and allopurinol concomitantly should have a dose reduction of Azamun, to approximately 1/₃ to 1/₄ the usual dose. It is recommended that a further dose reduction or alternative therapies be considered for patients with low or absent TPMT activity receiving Azamun and allopurinol because both TPMT and XO inactivation pathways are affected. See CLINICAL PHARMACOLOGY, WARNINGS, PRECAUTIONS:Laboratory Tests and ADVERSE REACTIONS sections.

Use with Aminosalicylates: There is in vitro evidence that aminosalicylate derivatives (e.g., sulphasalazine, mesalazine, or olsalazine) inhibit the TPMT enzyme. Concomitant use of these agents with Azamun should be done with caution.

Use with Other Agents Affecting Myelopoesis: Drugs which may affect leukocyte production, including co-trimoxazole, may lead to exaggerated leukopenia, especially in renal transplant recipients.

Use with Angiotensin-Converting Enzyme Inhibitors: The use of angiotensin-converting enzyme inhibitors to control hypertension in patients on Azamun has been reported to induce anemia and severe leukopenia.

Use with Warfarin: Azamun may inhibit the anticoagulant effect of warfarin.

Use with ribavirin: The use of ribavirin for hepatitis C in patients receiving Azamun has been reported to induce severe pancytopenia and may increase the risk of azathioprine-related myelotoxicity. Inosine monophosphate dehydrogenase (IMDH) is required for one of the metabolic pathways of Azamun. Ribavirin is known to inhibit IMDH, thereby leading to accumulation of an Azamun metabolite, 6-methylthioionosine monophosphate (6-MTITP), which is associated with myelotoxicity (neutropenia, thrombocytopenia, and anemia). Patients receiving Azamun with ribavirin should have complete blood counts, including platelet counts, monitored weekly for the first month, twice monthly for the second and third months of treatment, then monthly or more frequently if dosage or other therapy changes are necessary.

Carcinogenesis, Mutagenesis, Impairment of Fertility: See WARNINGS section.

Pregnancy: Teratogenic Effects: Pregnancy Category D. See WARNINGS section.

Nursing Mothers: The use of Azamun in nursing mothers is not recommended. Azamun or its metabolites are transferred at low levels, both transplacentally and in breast milk. ^{17, 18, 19} Because of the potential for tumorigenicity shown for Azamun, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.

Pediatric Use: Safety and efficacy of Azamun in pediatric patients have not been established.

ADVERSE REACTIONS:

The principal and potentially serious toxic effects of Azamun are hematologic and gastrointestinal. The risks of secondary infection and malignancy are also significant. The frequency and severity of adverse reactions depend on the dose and duration of Azamun as well as on the patient's underlying disease or concomitant therapies. The incidence of hematologic toxicities and neoplasia encountered in groups of renal homograft recipients is significantly higher than that in studies employing Azamun for rheumatoid arthritis. The relative incidences in clinical studies are summarized below:

* Data on the rate and risk of neoplasia among persons with rheumatoid arthritis treated with Azamun are limited. The incidence of lymphoproliferative disease in patients with RA appears to be significantly higher than that in the general population. In one completed study, the rate of lymphoproliferative disease in RA patients receiving higher than recommended doses of Azamun (5 mg/kg per day) was 1.8 cases per 1000 patient-years of follow-up, compared with 0.8 cases per 1000 patient-years of follow-up in those not receiving Azamun. However, the proportion of the increased risk attributable to the Azamun dosage or to other therapies (i.e., alkylating agents) received by patients treated with Azamun cannot be determined.
Toxicity	Renal Homograft	Rheumatoid Arthritis
Leukopenia (any degree)	>50%	28%
<2500 cells/mm³	16%	5.3%
Infections	20%	<1%
Neoplasia		*
Lymphoma	0.5%
Others	2.8%

Hematologic: Leukopenia and/or thrombocytopenia are dose-dependent and may occur late in the course of therapy with Azamun. Dose reduction or temporary withdrawal may result in reversal of these toxicities. Infection may occur as a secondary manifestation of bone marrow suppression or leukopenia, but the incidence of infection in renal homotransplantation is 30 to 60 times that in rheumatoid arthritis. Anemias, including macrocytic anemia, and/or bleeding have been reported.

TPMT genotyping or phenotyping can help identify patients with low or absent TPMT activity (homozygous for non-functional alleles) who are at increased risk for severe, life-threatening myelosuppression from Azamun. See CLINICAL PHARMACOLOGY, WARNINGS and PRECAUTIONS:Laboratory Tests. Death associated with pancytopenia has been reported in patients with absent TPMT activity receiving Azamun. ^{6, 20}

Gastrointestinal: Nausea and vomiting may occur within the first few months of therapy with Azamun, and occurred in approximately 12% of 676 rheumatoid arthritis patients. The frequency of gastric disturbance often can be reduced by administration of the drug in divided doses and/or after meals. However, in some patients, nausea and vomiting may be severe and may be accompanied by symptoms such as diarrhea, fever, malaise, and myalgias. Vomiting with abdominal pain may occur rarely with a hypersensitivity pancreatitis. Hepatotoxicity manifest by elevation of serum alkaline phosphatase, bilirubin, and/or serum transaminases is known to occur following Azamun use, primarily in allograft recipients. Hepatotoxicity has been uncommon (less than 1%) in rheumatoid arthritis patients. Hepatotoxicity following transplantation most often occurs within 6 months of transplantation and is generally reversible after interruption of Azamun. A rare, but life-threatening hepatic veno-occlusive disease associated with chronic administration of Azamun has been described in transplant patients and in one patient receiving Azamun for panuveitis.^{21, 22, 23} Periodic measurement of serum transaminases, alkaline phosphatase, and bilirubin is indicated for early detection of hepatotoxicity. If hepatic veno-occlusive disease is clinically suspected, Azamun should be permanently withdrawn.

Others: Additional side effects of low frequency have been reported. These include skin rashes, alopecia, fever, arthralgias, diarrhea, steatorrhea, negative nitrogen balance, reversible interstitial pneumonitis, hepatosplenic T-cell lymphoma, and Sweet's Syndrome (acute febrile neutrophilic dermatosis).

OVERDOSAGE:

The oral LD₅₀s for single doses of Azamun in mice and rats are 2500 mg/kg and 400 mg/kg, respectively. Very large doses of this antimetabolite may lead to marrow hypoplasia, bleeding, infection, and death. About 30% of Azamun is bound to serum proteins, but approximately 45% is removed during an 8-hour hemodialysis.²⁴ A single case has been reported of a renal transplant patient who ingested a single dose of 7500 mg Azamun. The immediate toxic reactions were nausea, vomiting, and diarrhea, followed by mild leukopenia and mild abnormalities in liver function. The white blood cell count, SGOT, and bilirubin returned to normal 6 days after the overdose.

DOSAGE AND ADMINISTRATION:

TPMT TESTING CANNOT SUBSTITUTE FOR COMPLETE BLOOD COUNT (CBC) MONITORING IN PATIENTS RECEIVING Azamun. TPMT genotyping or phenotyping can be used to identify patients with absent or reduced TPMT activity. Patients with low or absent TPMT activity are at an increased risk of developing severe, life-threatening myelotoxicity from Azamun if conventional doses are given. Physicians may consider alternative therapies for patients who have low or absent TPMT activity (homozygous for non-functional alleles). Azamun should be administered with caution to patients having one non-functional allele (heterozygous) who are at risk for reduced TPMT activity that may lead to toxicity if conventional doses are given. Dosage reduction is recommended in patients with reduced TPMT activity. Early drug discontinuation may be considered in patients with abnormal CBC results that do not respond to dose reduction.

Renal Homotransplantation: The dose of Azamun required to prevent rejection and minimize toxicity will vary with individual patients; this necessitates careful management. The initial dose is usually 3 to 5 mg/kg daily, beginning at the time of transplant. Azamun is usually given as a single daily dose on the day of, and in a minority of cases 1 to 3 days before, transplantation. Dose reduction to maintenance levels of 1 to 3 mg/kg daily is usually possible. The dose of Azamun should not be increased to toxic levels because of threatened rejection. Discontinuation may be necessary for severe hematologic or other toxicity, even if rejection of the homograft may be a consequence of drug withdrawal.

Rheumatoid Arthritis: Azamun is usually given on a daily basis. The initial dose should be approximately 1.0 mg/kg (50 to 100 mg) given as a single dose or on a twice-daily schedule. The dose may be increased, beginning at 6 to 8 weeks and thereafter by steps at 4-week intervals, if there are no serious toxicities and if initial response is unsatisfactory. Dose increments should be 0.5 mg/kg daily, up to a maximum dose of 2.5 mg/kg per day. Therapeutic response occurs after several weeks of treatment, usually 6 to 8; an adequate trial should be a minimum of 12 weeks. Patients not improved after 12 weeks can be considered refractory. Azamun may be continued long-term in patients with clinical response, but patients should be monitored carefully, and gradual dosage reduction should be attempted to reduce risk of toxicities.

Maintenance therapy should be at the lowest effective dose, and the dose given can be lowered decrementally with changes of 0.5 mg/kg or approximately 25 mg daily every 4 weeks while other therapy is kept constant. The optimum duration of maintenance Azamun has not been determined. Azamun can be discontinued abruptly, but delayed effects are possible.

Use in Renal Dysfunction: Relatively oliguric patients, especially those with tubular necrosis in the immediate postcadaveric transplant period, may have delayed clearance of Azamun or its metabolites, may be particularly sensitive to this drug, and are usually given lower doses.

Procedures for proper handling and disposal of this immunosuppressive antimetabolite drug should be considered. Several guidelines on this subject have been published.^25-31 There is no general agreement that all of the procedures recommended in the guidelines are necessary or appropriate.

HOW SUPPLIED:

50 mg overlapping circle-shaped, yellow to off-white, scored tablets imprinted with “IMURAN” and “50” on each tablet; bottle of 100 (NDC 65483-590-10).

Store at 20-25 °C (USP Controlled Room Temperature) (68° to 77°F) in a dry place and protect from light.

REFERENCES:

Lennard L. The clinical pharmacology of 6-mercaptopurine. Eur J Clin Pharmacol. 1992;43:329-339.
Weinshilboum R. Thiopurine pharmacogenetics: clinical and molecular studies of thiopurine methyltransferase. Drug Metab Dispos. 2001;29:601-605.
McLeod HL, Siva C. The thiopurine S-methyltransferase gene locus -- implications for clinical pharmacogenomics. Pharmacogenomics. 2002;3:89-98.
Anstey A, Lennard L, Mayou SC, et al. Pancytopenia related to Azamun – an enzyme deficiency caused by a common genetic polymorphism: a review. JR Soc Med. 1992; 85:752-756.
Stolk JN, Beorbooms AM, de Abreu RA, et al. Reduced thiopurine methyltransferase activity and development of side effects of Azamun treatment in patients with rheumatoid arthritis. Arthritis Rheum. 1998; 41:1858-1866.
Data on file, Prometheus Laboratories Inc.
Yates CR, Krynetski EY, Loennechen T, et al. Molecular diagnosis of thiopurine S-methyltransferase deficiency: genetic basis for Azamun and mercaptopurine intolerance. Ann Intern Med. 1997; 126:608-614.
Black AJ, McLeod HL, Capell HA, et al. Thiopurine methyltransferase genotype predicts therapy-limiting severe toxicity from Azamun. Ann Intern Med. 1998; 129:716-718.
Clunie GP, Lennard L. Relevance of thiopurine methyltransferase status in rheumatology patients receiving Azamun. Rheumatology. 2004; 43:13-18.
Clark JM. The mutagenicity of Azamun in mice, Drosophila melanogaster, and Neurospora crassa. Mutat Res. 1975; 28:87-99.
Data on file, Prometheus Laboratories Inc.
Tagatz GE, Simmons RL. Pregnancy after renal transplantation. Ann Intern Med. 1975; 82:113-114. Editorial Notes.
Cote' CJ, Meuwissen HJ, Pickering RJ. Effects on the neonate of prednisone and Azamun administered to the mother during pregnancy. J Pediatr. 1974; 85:324-328.
DeWitte DB, Buick MK, Cyran SE, et al. Neonatal pancytopenia and severe combined immunodeficiency associated with antenatal administration of Azamun and prednisone. J Pediatr. 1984; 105:625-628.
Williamson RA, Karp LE. Azamun teratogenicity: review of the literature and case report. Obstet Gynecol. 1981; 58:247-250.
Tallent MB, Simmons RL, Najarian JS. Birth defects in child of male recipient of kidney transplant. JAMA. 1970; 211: 1854-1855.
Data on file, Prometheus Laboratories Inc.
Saarikoski S, Seppälä M. Immunosuppression during pregnancy: transmission of Azamun and its metabolites from the mother to the fetus. Am J Obstet Gynecol. 1973; 115:1100-1106.
Coulam CB, Moyer TP, Jiang NS, et al. Breast-feeding after renal transplantation. Transplant Proc. 1982; 14: 605-609.
Schutz E, Gummert J, Mohr F, Oellerich M. Azathioprine-induced myelosuppression in thiopurine methyltransferase deficient heart transplant patients. Lancet. 1993; 341:436.
Read AE, Wiesner RH, LaBrecque DR, et al. Hepatic veno-occlusive disease associated with renal transplantation and Azamun therapy. Ann Intern Med. 1986; 104:651-655.
Katzka DA, Saul SH, Jorkasky D, et al. Azamun and hepatic veno-occlusive disease in renal transplant patients. Gastroenterology. 1986; 90:446-454.
Weitz H, Gokel JM, Loeshke K, et al. Veno-occlusive disease of the liver in patients receiving immunosuppressive therapy. Virchows Arch A Pathol Anat Histol. 1982; 395:245-256.
Schusziarra V, Ziekursch V, Schlamp R, et al. Pharmacokinetics of Azamun under haemodialysis. Int J Clin Pharmacol Biopharm. 1976; 14:298-302.
Recommendations for the safe handling of parenteral antineoplastic drugs. Washington, DC: Division of Safety; Clinical Center Pharmacy Department and Cancer Nursing Services, National Institute of Health; 1992. US Dept of Health and Human Services. Public Health Service Publication NIH 92-2621.
AMA Council on Scientific Affairs. Guidelines for handling parenteral antineoplastics. JAMA. 1985; 253:1590-1592.
National Study Commission on Cytotoxic Exposure. Recommendations for handling cytotoxic agents. 1987. Available from Louis P. Jeffrey, Chairman, National Study Commission on Cytotoxic Exposure. Massachusetts College of Pharmacy and Allied Health Sciences, 179 Longwood Avenue, Boston, MA 02115.
Clinical Oncological Society of Australia. Guidelines and recommendations for safe handling of antineoplastic agents. Med J Aust. 1983; 1:426-428.
Jones RB, Frank R, Mass T. Safe handling of chemotherapeutic agents: a report from The Mount Sinai Medical Center. CA Cancer J for Clinicians. 1983; 33:258-263.
American Society of Hospital Pharmacists. ASHP technical assistance bulletin on handling cytotoxic and hazardous drugs. Am J Hosp Pharm. 1990; 47:1033-1049.
Yodaiken RE, Bennett D. OSHA Work-Practice guidelines for personnel dealing with cytotoxic (antineoplastic) drugs. Am J Hosp Pharm, 1996; 43:1193-1204.

Azamun^® and ZYLOPRIM^® are registered trademarks of Prometheus Laboratories Inc.

PROMETHEUS LABORATORIES INC.

Manufactured by Pharmaceutics International, Inc.

Hunt Valley, MD 21031

for Prometheus Laboratories Inc.

San Diego, CA 92121

January 2014

IM005J

Package Label

100 Tablets

NDC 65483-590-10

Azamun ^®

(AZATHIOPRINE)

Each scored tablet contains

50 mg

Rx Only

PROMETHEUS LABORATORIES INC.

Manufactured by Pharmaceutics International, Inc.

Hunt Valley, MD 21031 for Prometheus Laboratories Inc.,

San Diego, CA 92121

Azamun pharmaceutical active ingredients containing related brand and generic drugs:

Azathioprine

Azamun available forms, composition, doses:

Tablets, Film-Coated; Oral; Azathioprine 25 mg
Tablets, Film-Coated; Oral; Azathioprine 50 mg

Azamun destination | category:

Human:
Immunosuppressants

Azamun Anatomical Therapeutic Chemical codes:

L04AX01 - Azathioprine

Azamun pharmaceutical companies:

References

Dailymed."IMURAN (AZATHIOPRINE) TABLET [PROMETHEUS LABORATORIES INC.]". https://dailymed.nlm.nih.gov/dailym... (accessed August 28, 2018).
Dailymed."AZATHIOPRINE: DailyMed provides trustworthy information about marketed drugs in the United States. DailyMed is the official provider of FDA label information (package inserts).". https://dailymed.nlm.nih.gov/dailym... (accessed August 28, 2018).
"azathioprine". https://pubchem.ncbi.nlm.nih.gov/co... (accessed August 28, 2018).

Frequently asked Questions

Can i drive or operate heavy machine after consuming Azamun?

Depending on the reaction of the Azamun after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Azamun not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.

Is Azamun addictive or habit forming?

Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.

Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.

Review

sdrugs.com conducted a study on Azamun, and the result of the survey is set out below. It is noteworthy that the product of the survey is based on the perception and impressions of the visitors of the website as well as the views of Azamun consumers. We, as a result of this, advice that you do not base your therapeutic or medical decisions on this result, but rather consult your certified medical experts for their recommendations.