ARX-NITROFURANTOIN CAPSULES

MIMS Revision Date: 01 August 2026

1 Name of Medicine

ARX-Nitrofurantoin capsules 50 mg and 100 mg (nitrofurantoin macrocrystals).

2 Qualitative and Quantitative Composition

Each 50 mg and 100 mg of ARX-Nitrofurantoin capsule contains 50 mg and 100 mg of nitrofurantoin (macrocrystals) respectively.
Excipient with known effect. "Lactose monohydrate".
For the full list of excipients, see Section 6.1 List of Excipients.

3 Pharmaceutical Form

Nitrofurantoin capsules (macrocrystals) 50 mg. Size '3' opaque yellow cap and opaque white body hard gelatin capsule, imprinted with "EM28" with 360 degree thin band, in black ink on cap filled with yellow powder.
Nitrofurantoin capsules (macrocrystals) 100 mg. Size '2' opaque yellow cap and opaque yellow body hard gelatin capsule, imprinted with "EM29" with 360 degree thin band, in black ink on cap filled with yellow powder.

4 Clinical Particulars

4.1 Therapeutic Indications

Treatment of urinary tract infections such as cystitis and pyelitis when due to susceptible pathogens. Nitrofurantoin does not reach effective levels in plasma and consequently is not indicated for cortical or perinephric abscesses and in cases of prostatitis.

4.2 Dose and Method of Administration

To be taken with food or milk.
Adults. 50-100 mg four times a day. Do not exceed 400 mg daily.
Prophylactic therapy: 50 mg or 100 mg night.
Children. Should be calculated on the basis of 5-7 mg/kg body weight per 24 hours to be given in divided doses four times a day.
ARX-Nitrofurantoin should not be administered to infants under three months of age.
Therapy should be continued for at least one week and for at least 3 days after sterility of the urine is obtained. Continued infection indicates the need for re-evaluation. If the drug is to be used for prophylactic or for long-term suppressive therapy, consideration should be given to finding the lowest effective dose.

4.3 Contraindications

Anuria and oliguria or extensive impairment of renal function (creatinine clearance under 60 mL/min or clinically significant elevated serum creatinine);
Patients suffering from renal disfunction with an eGFR below 45 mL/min;
G6PD deficiency (also see Section 4.6 Fertility, Pregnancy and Lactation);
Hypersensitivity to the active substance, or other nitrofurans or any of the excipients listed in Section 6.1 List of Excipients;
Acute porphyria;
Nitrofurantoin should not be administered to pregnant women during labour and delivery, or when the onset of labour is imminent;
Neonates and infants under three months of age because of the possibility of producing a haemolytic anaemia due to immature enzyme systems (glutathione instability) in the early neonatal period.

4.4 Special Warnings and Precautions for Use

Nitrofurantoin is not effective for the treatment of parenchymal infections in a unilaterally non-functioning kidney. A surgical cause for infection should be excluded in recurrent or severe cases.
Nitrofurantoin may be used with caution as short-course therapy only for the treatment of uncomplicated lower urinary tract infection in individual cases with an eGFR between 30-44 mL/min to treat resistant pathogens, when the benefits are expected to outweigh the risks.
Since pre-existing conditions may mask adverse reactions, nitrofurantoin should be used with caution in patients with pulmonary disease, hepatic dysfunction, neurological disorders, and allergic diathesis.
Peripheral neuropathy. Peripheral neuropathy (including optic neuritis) and susceptibility to peripheral neuropathy, which may become severe or irreversible, has occurred. Fatalities have been reported. Therefore treatment should be stopped at the first signs of neural involvement (paraesthesia). Conditions such as renal impairment (creatinine clearance under 60 mL/min or clinically significant elevated serum creatinine), anaemia, diabetes mellitus, electrolyte imbalance, vitamin B deficiency, and debilitating disease may enhance the occurrence of peripheral neuropathy. Patients receiving long-term therapy should be monitored periodically for changes in renal function. If numbness or tingling occurs in any area, administration of the drug should be discontinued (see Section 4.8 Adverse Effects (Undesirable Effects), Neurological).
Use in hepatic impairment. Hepatic reactions, including hepatitis, cholestatic jaundice, chronic active hepatitis and hepatic necrosis occur rarely. Fatalities have been reported. The onset of chronic active hepatitis may be insidious, and patients should be monitored periodically for changes in liver function. If hepatitis occurs, the drug should be withdrawn immediately and appropriate measures should be taken (see Section 4.8 Adverse Effects (Undesirable Effects), Hepatic).
Use in renal impairment or acidosis. In the presence of impairment of renal function or acidosis, administer nitrofurantoin with caution. If employed under such circumstances the blood pH, CO₂-content or combining power and urea nitrogen or non-protein nitrogen should be followed closely. This is particularly important if treatment is continued beyond fourteen days.
Renal function should be monitored, especially those who are at risk of renal impairment (such as the elderly) or where renal function may acutely change (such as use of nephrotoxic medicines) (see Section 4.2 Dose and Method of Administration).
Pulmonary reactions. Acute, subacute or chronic pulmonary reactions have been observed in patients treated with nitrofurantoin in acute and prophylactic treatment. These reactions can be life threatening; therefore, if they occur treatment should be stopped immediately. Signs of pulmonary damage include difficulty and or pain when breathing, shortness of breath and coughing up blood or mucus.
Acute pulmonary reactions usually occur within the first week of treatment and are reversible with cessation of therapy. Increased vigilance for respiratory symptoms in patients who have just started therapy is warranted (especially in the elderly). Acute pulmonary reactions are commonly manifested by fever, chills, cough, chest pain, dyspnoea, pulmonary infiltration with consolidation or pleural effusion on chest x-ray, and eosinophilia. In subacute pulmonary reactions, fever and eosinophilia occur less often than in the acute form (see Section 4.8 Adverse Effects (Undesirable Effects)).
Chronic pulmonary reactions (diffuse interstitial pneumonitis or pulmonary fibrosis, or both) can develop insidiously and can often occur in elderly patients. These reactions occur rarely and generally in patients receiving therapy for six months or longer. Malaise, dyspnoea on exertion, difficulty breathing, cough, coughing up blood or mucus, and altered pulmonary function are common manifestations which can occur insidiously. Close monitoring of the pulmonary condition of patients receiving long-term therapy is warranted and requires that the benefits of therapy be weighed against potential risks (see Section 4.8 Adverse Effects (Undesirable Effects), Pulmonary hypersensitivity).
Patient should be monitored closely for signs of hepatitis (particularly in long term use). Urine may be coloured yellow or brown after taking nitrofurantoin. Patients on nitrofurantoin are susceptible to false positive urinary glucose (if tested for reducing substances).
Nitrofurantoin should be discontinued at any sign of haemolysis in those with suspected glucose-6-phosphate dehydrogenase deficiency.
Discontinue treatment with nitrofurantoin if otherwise unexplained pulmonary, hepatic, haematological or neurological syndromes occur.
Upon cessation of therapy, recovery may require several months. If the symptoms are not recognised as being drug-related and nitrofurantoin therapy is not stopped, the symptoms may become more severe.
Changes in ECG may occur associated with pulmonary reactions.
Patients who have experienced pulmonary toxicity with nitrofurantoin must not be re-exposed (see Section 4.3 Contraindications).
Hepatotoxicity. Hepatic reactions, including hepatitis, autoimmune hepatitis, cholestatic jaundice, chronic active hepatitis, and hepatic necrosis, occur rarely. Fatalities have been reported. The onset of chronic active hepatitis may be insidious, and patients should be monitored periodically for changes in biochemical tests that would indicate liver injury. If hepatitis occurs, the drug should be withdrawn immediately, and appropriate measures should be taken. Patients who have experienced hepatic toxicity with nitrofurantoin must not be re-exposed (see Section 4.3 Contraindications).
Use caution when prescribing nitrofurantoin in patients with hepatic dysfunction, which may mask the signs and symptoms of adverse reactions.
The onset of hepatitis may be gradual and may not have obvious symptoms at first.
Cholestatic jaundice is generally associated with short-term therapy (usually up to 2 weeks). Chronic active hepatitis, occasionally leading to hepatic necrosis is generally associated with long-term therapy (usually after 6 months).
It is important to monitor patients periodically for changes in biochemical tests that could indicate hepatic dysfunction and for clinical signs or symptoms of liver abnormality, especially in patients taking long-term nitrofurantoin.
Advise parents and caregivers of the symptoms of hepatic dysfunction: yellowing of the skin or eyes, upper right abdominal pain, dark urine and pale or grey-coloured stools, itching or joint pain and swelling to seek immediate medical advice if these occur.
Haemolytic anaemia. Haemolytic anaemia of the primaquine-sensitivity type has been induced by nitrofurantoin. The haemolysis appears to be linked to a glucose-6-phosphate dehydrogenase deficiency in the affected patients' red blood cells. This deficiency is found in 10% of African descent individuals and in a small percentage of ethnic groups of Mediterranean and Near Eastern origin. G6PD deficiency has also been reported occasionally amongst Caucasian groups. Any sign of haemolysis is an indication to discontinue the drug. Haemolysis ceases when the drug is withdrawn.
Colitis. Antibiotic associated Pseudomembranous colitis has been reported with many antibacterials including sporadic reports with nitrofurantoin. A toxin produced with Clostridium difficile appears to be the primary cause. The severity of the colitis may range from mild to life threatening. It is important to consider this diagnosis in patients who develop diarrhoea or colitis in association with antibiotic use (this may occur up to several weeks after cessation of antibiotic therapy). Mild cases usually respond to drug discontinuation alone. However, in moderate to severe cases appropriate therapy with a suitable oral antibacterial agent effective against Clostridium difficile should be considered. Fluids, electrolytes and protein replacement should be provided when indicated. Drugs which delay peristalsis, e.g. opiates and diphenoxylate with atropine may prolong and/or worsen the condition and should not be used.
Patients should be advised that nitrofurantoin may cause brownish discolouration of the urine.
Clostridium difficile-associated diarrhoea. Clostridium difficile-associated diarrhoea (CDAD) has been reported with use of nearly all antibacterial agents, including nitrofurantoin, and may range in severity from mild diarrhoea to fatal colitis. Treatment with antibacterial agents alters the normal flora of the colon leading to overgrowth of C. difficile.
C. difficile produces toxins A and B which contribute to the development of CDAD. Hypertoxin producing strains of C. difficile cause increased morbidity and mortality, as these infections can be refractory to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhoea following antibiotic use. Careful medical history is necessary since CDAD has been reported to occur over two months after the administration of antibacterial agents.
If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difficile may need to be discontinued. Appropriate fluid and electrolyte management, protein supplementation, antibiotic treatment of C. difficile, and surgical evaluation should be instituted as clinically indicated.
Excipients. Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine. See Section 2 Qualitative and Quantitative Composition; Section 6.1 List of Excipients.
Information for patients. Patients should be advised to take nitrofurantoin capsules with food (ideally breakfast and dinner) to further enhance tolerance and improve drug absorption. Patients should be instructed to complete the full course of therapy; however, they should be advised to contact their physician if any unusual symptoms occur during therapy. Patients should be advised not to use antacid preparations containing magnesium trisilicate while taking nitrofurantoin capsules.
Patients should be counselled that antibacterial drugs including nitrofurantoin should only be used to treat bacterial infections. They do not treat viral infections (e.g. the common cold). When nitrofurantoin capsules are prescribed to treat a bacterial infection, patients should be told that although it is common to feel better early in the course of therapy, the medication should be taken exactly as directed. Skipping doses or not completing the full course of therapy may decrease the effectiveness of the immediate treatment and increase the likelihood that bacteria will develop resistance and will not be treatable by nitrofurantoin or other antibacterial drugs in the future.
Diarrhoea is a common problem caused by antibiotics which usually ends when the antibiotic is discontinued. Sometimes after starting treatment with antibiotics, patients can develop watery and bloody stools (with or without stomach cramps and fever) even as late as two or more months after having taken the last dose of the antibiotic. If this occurs, patients should contact their physician as soon as possible.
Use in the elderly. Clinical studies of nitrofurantoin did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. Spontaneous reports suggest a higher proportion of pulmonary reactions, including fatalities, in elderly patients; these differences appear to be related to the higher proportion of elderly patients receiving long-term nitrofurantoin therapy.
As in younger patients, chronic pulmonary reactions generally are observed in patients receiving therapy for six months or longer (see Section 4.4 Special Warnings and Precautions for Use). Spontaneous reports also suggest an increased proportion of severe hepatic reactions, including fatalities, in elderly patients (see Section 4.4 Special Warnings and Precautions for Use).
In general, the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy in elderly patients should be considered when prescribing nitrofurantoin. This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Anuria, oliguria, or significant impairment of renal function (creatinine clearance under 60 mL per minute or clinically significant elevated serum creatinine) are contraindications (see Section 4.3 Contraindications). Because elderly patients are more likely to have decreased renal function, it may be useful to monitor renal function.
Paediatric use. Nitrofurantoin should not be administered to infants under three months of age. For information regarding dosage in children see Section 4.2 Dose and Method of Administration.
Safety and effectiveness in paediatric patients below the age of twelve years have not been established.
Effects on laboratory tests. Nitrofurantoin can interfere with certain laboratory tests e.g. serum bilirubin (false positive or spuriously high reading), urine creatinine (false positive, or accurate readings cannot be made, due to interference), serum urea (no accurate reading due to interference), urine glucose (false positive or spuriously high readings have been observed with Benedict's and Fehling's solutions). Urine glucose tests dependent on glucose oxidase are not affected e.g. Clinistix and Testape.

4.5 Interactions with Other Medicines and Other Forms of Interactions

The excretion of nitrofurantoin is decreased by acidifying drugs, whereby potentiation of nitrofurantoin may occur. Conversely, alkalinising drugs increase the rate of excretion and may diminish the effect of nitrofurantoin. Phenobarbitone has an inhibitory action on nitrofurantoin. Uricosuric drugs, such as probenecid and sulfinpyrazone, can inhibit renal tubular secretion of nitrofurantoin. The resulting increase in nitrofurantoin serum levels may increase toxicity and the decreased urinary levels could lessen its efficacy as a urinary tract antibacterial.
Antacids reduce the potency of the drug. Patients should be advised not to use antacid preparations at the same time as nitrofurantoin. Antacids containing magnesium trisilicate, when administered concomitantly with nitrofurantoin, reduce both the rate and extent of absorption. The mechanism for this interaction probably is adsorption of nitrofurantoin onto the surface of magnesium trisilicate.
There may be decreased antibacterial activity for nitrofurantoin in the presence of carbonic anhydrase inhibitors and urine alkalinising agents.
Antagonism has been demonstrated in vitro between nitrofurantoin and quinolone antimicrobials. The clinical significance of this finding is unknown.
Use with other medicines that are known to cause pulmonary or hepatic toxicity, such as methotrexate, may increase the risk of adverse effects.
As nitrofurantoin is an antibacterial, it will inactivate oral typhoid vaccines.

4.6 Fertility, Pregnancy and Lactation

Effects on fertility. Rats given large doses of nitrofurantoin have developed lesions in seminiferous tubules which vary from atrophy to arrest of spermatogenesis. The arrest of spermatogenesis was reversible and treated male rats sired normal litters after recovery. In man, nitrofurantoin can decrease sperm counts and produce abnormal testicular histology suggestive of arrested spermatogenesis.
Use in pregnancy. (Category A)
Short term therapy. Nitrofurantoin has had widespread clinical use for many years. Studies, to date, have not shown a potential for nitrofurantoin to cause birth defects. Nitrofurantoin crosses the placenta, and caution should be exercised when administering nitrofurantoin at term or to infants under three months of age because of the possibility of producing a haemolytic anaemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency due to immature enzyme systems in the early neonatal period.
As with all other drugs, the maternal side effects may adversely affect the course of pregnancy. The drug should be used at the lowest dose as appropriate for the specific indication and only after careful assessment of benefits and risks.
Use in lactation. Although studies have shown that the amount of nitrofurantoin excreted in breast milk after normal therapeutic doses is negligible, the possibility of producing a haemolytic anaemia due to immature enzyme systems in the early neonatal period should be considered when administering the drug to nursing mothers.
Breast feeding an infant known or suspected to have an erythrocyte enzyme deficiency (including G6PD deficiency), must be temporarily avoided, since nitrofurantoin is detected in trace amounts in breast milk.

4.7 Effects on Ability to Drive and Use Machines

Nitrofurantoin may cause dizziness and drowsiness and the patient should not drive or operate machinery if affected this way.

4.8 Adverse Effects (Undesirable Effects)

A tabulated list of undesirable effects is outlined, see Table 1.
The undesirable effects are listed according to organ systems and following frequencies: rare (≥ 1/10,000 to < 1/1,000); not known (cannot be estimated from the available data).

Description of selected adverse reactions. Gastrointestinal reactions. Nausea with associated anorexia and emesis is the most common adverse effect of nitrofurantoin therapy. This can be reduced by taking the drug with food or milk. Less frequent are abdominal pain and diarrhoea and, rarely, hepatitis - these latter dose-related toxic effects can be minimised by reduction of the dose especially in females on long term treatment. Dyspepsia, flatulence and constipation have also been reported. There have been sporadic reports of pseudomembranous colitis with the use of nitrofurantoin. The onset of pseudomembranous colitis symptoms may occur during or after antimicrobial treatment.
Neurological reactions. Polyneuropathy, (including optic neuritis) which starts peripherally with initial sensory loss and paraesthesia but progresses to motor loss often with severe muscle atrophy, has occurred during nitrofurantoin therapy. A predisposing condition in most of these patients was renal failure which often was accompanied by anaemia, diabetes, electrolyte imbalance, vitamin B deficiency and debilitating disease. After stopping nitrofurantoin therapy, further deterioration is generally halted and total or partial regression occurs in almost 80% of those affected. These reactions may be severe or irreversible, but are rarely fatal. Polyneuropathy occurs in adults and children.
If numbness or tingling occurs in any area, administration of the drug should be discontinued. Headache, dizziness, nystagmus, drowsiness, asthenia, vertigo, amblyopia, depression, euphoria, confusion, psychotic reactions and benign intracranial hypertension have also been reported.
Peripheral neuropathy, which may become severe or irreversible, has occurred. Fatalities have been reported. Conditions such as renal impairment (creatinine clearance under 60 mL per minute or clinically significant elevated serum creatinine), anemia, diabetes mellitus, electrolyte imbalance, vitamin B deficiency, and debilitating diseases may increase the possibility of peripheral neuropathy.
Respiratory reactions. Chronic, subacute, or acute pulmonary hypersensitivity reactions may occur with the use of nitrofurantoin.
Chronic pulmonary reactions generally occur in patients who have received continuous treatment for six months or longer. Malaise, dyspnoea on exertion, cough, and altered pulmonary function are common manifestations which can occur insidiously. Radiologic and histologic findings of diffuse interstitial pneumonitis or fibrosis, or both, are also common manifestations of the chronic pulmonary reaction. Fever is rarely prominent. The severity of chronic pulmonary reactions and their degree of resolution appear to be related to the duration of therapy after the first clinical signs appear. Pulmonary function may be impaired permanently, even after cessation of therapy. The risk is greater when chronic pulmonary reactions are not recognized early.
Acute pulmonary reactions are commonly manifested by fever, chills, cough, chest pain, dyspnoea, pulmonary infiltration with consolidation or pleural effusion on x-ray, and eosinophilia. Acute reactions usually occur within the first week of treatment and are reversible with cessation of therapy. Resolution often is dramatic. (See Section 4.4 Special Warnings and Precautions for Use.)
In subacute pulmonary reactions, fever and eosinophilia occur less often than in the acute form.
Upon cessation of therapy, recovery may require several months. If the symptoms are not recognized as being drug-related and nitrofurantoin therapy is not stopped, the symptoms may become more severe.
Changes in ECG (e.g. non-specific ST/T wave changes, bundle branch block) have been reported in association with pulmonary reactions.
Cyanosis has been reported rarely.
Hepatic reactions. Hepatic reactions can occur, including hepatitis, cholestatic jaundice, chronic active hepatitis and hepatic necrosis. These reactions can be life threatening, therefore, if they occur treatment should be stopped immediately. Chronic hepatic reactions can develop insidiously, but usually occur in patients on therapy for 5 months or longer. Patients on prolonged therapy should be re-examined at intervals not exceeding 6 months.
Dermatological reactions. Exfoliative dermatitis, erythema multiforme, (including Stevens-Johnson syndrome) maculopapular, erythematous or eczematous eruptions and transient alopecia may occur.
Haematological reactions. Glucose-6-phosphate dehydrogenase deficiency anaemia, haemolytic anaemia, leucopenia, granulocytopenia, eosinophilia, thrombocytopenia, agranulocytosis, aplastic anaemia and megaloblastic anaemia. Return of the blood picture to normal has followed cessation of therapy. Cyanosis secondary to methemoglobinemia has been reported rarely.
Allergic reactions. Vasculitis (sometimes associated with pulmonary reactions) have been reported. Hypersensitivity reactions represent the most frequent spontaneously-reported adverse events in worldwide post-marketing experience with nitrofurantoin formulations.
Miscellaneous reactions. As with other microbial agents, urinary tract superinfections by resistant organisms (e.g. Pseudomonas or Candida) can occur. There are sporadic reports of Clostridium difficile superinfections, or pseudomembranous colitis, with the use of nitrofurantoin.
The most frequent laboratory test abnormalities reported with use of nitrofurantoin are as follows: eosinophilia, increased AST (SGOT), increased ALT (SGPT), decreased haemoglobin, increased serum phosphate.
The following laboratory adverse events also have been reported with the use of nitrofurantoin: glucose-6-phosphate dehydrogenase deficiency anaemia (see Section 4.4 Special Warnings and Precautions for Use), agranulocytosis, leukopenia, granulocytopenia, haemolytic anaemia, thrombocytopenia, megaloblastic anaemia. In most cases, these hematologic abnormalities resolved following cessation of therapy. Aplastic anaemia has been reported rarely.
Reporting suspected adverse effects. Reporting suspected adverse reactions after registration of the medicinal product is important. It allows continued monitoring of the benefit-risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions at www.tga.gov.au/reporting-problems.

4.9 Overdose

There are very little data available on toxicity of nitrofurantoin after overdose. No toxic serum levels have been established.
Symptoms. Symptoms expected would be mainly extensions of side effects. Occasional incidents of acute overdosage have not resulted in any specific symptoms other than vomiting.
Treatment. There is no specific treatment of overdosage and no antidotes are recommended. Treatment is essentially symptomatic and supportive.
As nitrofurantoin is excreted rapidly in the urine administration of adequate amounts of fluid will hasten excretion of the absorbed drug. In a patient with normal renal function 50 to 250 mg/L are considered normal urine levels after taking a therapeutic dose.
For information on the management of overdose, contact the Poisons Information Centre on 13 11 26 (Australia).

5 Pharmacological Properties

5.1 Pharmacodynamic Properties

Mechanism of action. Nitrofurantoin is bacteriostatic at low concentrations (1:100,000 to 1:200,000) and in vitro is considered to be bactericidal in higher concentrations. Its presumed mode of action is based upon its interference with several bacterial enzyme systems.
Nitrofurantoin is active against Gram-positive and Gram-negative urinary tract pathogens, particularly E. coli, but Ps. aeruginosa and some Klebsiella, Aerobacter and Proteus strains are insensitive. See Table 2.

Urine levels reached with normal therapeutic doses are usually in the range of 15-46 microgram/mL and levels above the MIC for the most sensitive organisms are detectable for about 6 hours.
Bacteria develop only a limited resistance to furan derivatives.
Clinical trials. No data available.

5.2 Pharmacokinetic Properties

Absorption. Nitrofurantoin is well absorbed orally. The peak plasma level appears 1-2 hours after an oral dose and has been found not to exceed 2.5 microgram/mL. The presence of food or agents which delay gastric emptying can increase the bioavailability of nitrofurantoin.
Distribution. 25-60% of nitrofurantoin is bound to serum proteins. The plasma half life of the drug is 20 min. The average urinary drug recoveries following a therapeutic dose regimen (100 mg four times daily for 7 days) were reported to be 37.9% (day 1) and 35% (day 7) for the macrocrystalline dosage form.
Metabolism and excretion. Nitrofurantoin is excreted rapidly in the urine, mainly in the unchanged form, the only metabolic pathway of importance involving reduction of the nitro group. Excretion is via the kidney both in the glomerular filtrate and by tubular secretion.

5.3 Preclinical Safety Data

Genotoxicity. It may be concluded that although nitrofurantoin has genotoxic properties in vitro, it is of low genotoxic potential in whole animals. Thus, it is unlikely that the increased tumour incidences seen in male rats are due to genotoxic action.
Carcinogenicity. Nitrofurantoin has caused increases in the incidence of renal tubular cell adenomas when administered to male rats at 65-125 mg/kg/day for 2 years. The biological significance of this remains to be established. When administered to female mice at 375 mg/kg/day for 2 years, nitrofurantoin induced an increase in the incidence of benign ovarian tumours. It would appear that this effect may be secondary to its primary toxic activity of inducing ovarian atrophy and sterility.
Mutagenicity. Nitrofurantoin is mutagenic in certain bacterial systems and although it is not known how far this relates to the clinical situation the possibility of a permanent mutagenic effect on spermatozoa-producing cells requires that careful consideration be given to its use in young males.

6 Pharmaceutical Particulars

6.1 List of Excipients

Lactose monohydrate, pregelatinized starch and purified talc.
The capsule shells contain gelatin, titanium dioxide, quinoline yellow, iron oxide yellow, sodium lauryl sulfate and black ink TEK SW 9008.

6.2 Incompatibilities

See Section 4.5 Interactions with Other Medicines and Other Forms of Interactions.

6.3 Shelf Life

In Australia, information on the shelf life can be found on the public summary of the Australian Register of Therapeutic Goods (ARTG). The expiry date can be found on the packaging.

6.4 Special Precautions for Storage

Store below 25°C.

6.5 Nature and Contents of Container

PVC/Aluminium blisters of 3 x 10 capsules per carton (30s).

6.6 Special Precautions for Disposal

In Australia, any unused medicine or waste material should be disposed of in accordance with local requirements.

6.7 Physicochemical Properties

Nitrofurantoin is a synthetic antibacterial nitrofuran derivative. It occurs as lemon yellow crystals, or fine powder, and is very slightly soluble in water or alcohol. However, solubility of the drug in water and urine increases with rises in pH. Nitrofurantoin darkens on exposure to light or to alkali and is decomposed upon contact with metals other than stainless steel or aluminium. In view of this, the drug should not be exposed to light.
Note. Nitrofurantoin (macrocrystals) is a larger crystal form of nitrofurantoin. The absorption of nitrofurantoin is slower and the excretion of nitrofurantoin is somewhat less, when the two are compared. The reduced incidence of gastrointestinal intolerance with nitrofurantoin is probably due to delayed and decreased absorption; this however does not significantly reduce clinical effectiveness. A number of patients who cannot tolerate nitrofurantoin tablets can take nitrofurantoin capsules without nausea.
Chemical structure. Nitrofurantoin has the following chemical structure:

Chemical name: 1-(5-nitrofurfurylideneamino) hydantoin.
Molecular formula: C₈H₆N₄O₅.
Molecular weight: 238.2.
CAS number. 67-20-9.

7 Medicine Schedule (Poisons Standard)

S4, Prescription Only Medicine.

Date of First Approval

17 December 2021

Date of Revision

19 June 2026

Summary Table of Changes