Lithostat acetohydroxamic acid 250 mg Tablet, 100-count
🆔 Identity & classification
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🏷️ RxNorm drug class
This medicine belongs to the Urease Inhibitor class.
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🏭 Manufacturer & labeler
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🩺 Clinical
Patient education
Supplement & herbal interactions
Some supplements/herbs that may interact with Acetohydroxamic Acid — tap one for details:
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💊 What it looks like
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🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
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240 mg
UNII OP1R32D61U
Microcrystalline cellulose is a purified form of cellulose, a natural fiber from plant sources. It acts as a binder and filler in tablets and capsules, helping hold ingredients together and give the medicine its shape and size.
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3 mg
UNII 70097M6I30
Magnesium stearate is a salt made from magnesium and stearic acid, a fatty substance. It's used in tablets and capsules as a lubricant and glidant to help ingredients flow smoothly during manufacturing and prevent sticking.
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0.2 mg
UNII AV092KU4JH
A natural oil extracted from peppermint plants. It's used as a flavoring agent to mask bitter tastes and add a refreshing mint flavor to medicines, making them easier to take.
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5 mg
UNII ETJ7Z6XBU4
Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
4 inactive ingredients listed in the exact product block matched to this NDC.
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ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.Inactive ingredient FAQ
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💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per ea | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | $6.663 | $666.32 / 100 tablets |
| Medicaid paysCMS SDUD · 12 mo | $7.01 | $701.05 / 100 tablets |
| Medicare drug plans payPart D · Q2 2026 | $7.44 | $744.37 / 100 tablets |
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🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Lithostat 250 mgthis 00178-0500-01 | Mission | 100 tablets | $6.663 | — | Availability likely | — |
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⏳ Availability & generic status
We did not find an FDA-approved generic match for this exact strength, form and route.
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🗺️ Medicaid utilization & spend
📊 Medicare Part D spend CMS · PART D · 2026 (Q1)
🔬 Reported adverse events (FAERS)
Top reported reactions
Age at onset
Reporter sex
Serious outcomes
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📦 Packaging — all sizes for this product
| Package NDC | Description | Marketing start | Status |
|---|---|---|---|
| 00178-0500-01 You're viewing this | 100 TABLET in 1 BOTTLE (0178-0500-01) | 1983-05-31 | Active |
📄 Full prescribing information FDA SPL
🎯 Indications and Usage ▾
INDICATIONS AND USAGE Acetohydroxamic acid is indicated as adjunctive therapy in patients with chronic urea-splitting urinary infection. AHA is intended to decrease urinary ammonia and alkalinity, but it should not be used in lieu of curative surgical treatment (for patients with stones) or antimicrobial treatment. Long-term treatment with AHA may be warranted to maintain urease inhibition as long as urea-splitting infection is present.
Experience with AHA does not go beyond 7 years. A patient package insert should be distributed to each patient who receives AHA.
⏱️ Dosage and Administration ▾
DOSAGE AND ADMINISTRATION AHA should be administered orally, one tablet 3-4 times a day in a total daily dose of 10-15 mg/kg/day. The recommended starting dose is 12 mg/kg/day, administered at 6-8 hour intervals at a time when the stomach is empty. The maximum daily dose should be no more than 1.5 grams, regardless of body weight.
The dosage should be reduced in patients with reduced renal function. Patients whose serum creatinine is greater than 1.8 mg/dl should take no more than 1.0 gm/day; such patients should be dosed at q-12-h intervals. Further reductions in dosage to prevent the accumulation of toxic concentrations in the blood may also be desirable.
Insufficient data exists to accurately characterize the optimum dose and/or dose interval in patients with moderate degrees of renal insufficiency. Patients with advanced renal insufficiency (i.e., serum creatinine more than 2.5 mg/dl) should not be treated with AHA. The risk of accumulation of toxic blood levels of AHA seems to be greater than the chances for a beneficial effect in such patients.
In children an initial dose of 10 mg/kg/day is recommended. Close monitoring of the patient’s clinical condition and hematologic status is recommended. Titration of the dose to higher or lower levels may be required to obtain an optimum therapeutic effect and/or to reduce the risk of side effects.
⛔ Contraindications ▾
Acetohydroxamic acid should not be used in: a. patients whose physical state and disease are amenable to definitive surgery and appropriate antimicrobial agents b. patients whose urine is infected by non-urease producing organisms c. patients whose urinary infections can be controlled by culture-specific oral antimicrobial agents d. patients whose renal function is poor (i.e., serum creatinine more than 2.5 mg/dl and/or creatinine clearance less than 20 ml/min) e. female patients who do not evidence a satisfactory method of contraception f. patients who are pregnant Acetohydroxamic acid may cause fetal harm when administered to a pregnant woman.
AHA was teratogenic (retarded and/or clubbed rear leg at 750 mg/kg and above and exencephaly and encephalocele at 1,500 mg/kg) when given intraperitoneally to rats. AHA is contraindicated in women who are or may become pregnant. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be informed of the potential hazard to the fetus.
⚠️ Warnings ▾
WARNINGS A Coombs negative hemolytic anemia has occurred in patients receiving AHA. Gastrointestinal upset characterized by nausea, vomiting, anorexia and generalized malaise have accompanied the most severe forms of hemolytic anemia. Approximately 15% of patients receiving AHA have had only laboratory findings of an anemia.
However, most patients developed a mild reticulocytosis. The untoward reactions have reverted to normal following cessation of treatment. A complete blood count, including a reticulocyte count, is recommended after two weeks of treatment.
If the reticulocyte count exceeds 6%, a reduced dosage should be entertained. A CBC and reticulocyte count are recommended at 3-month intervals for the duration of treatment.
🤒 Adverse Reactions ▾
ADVERSE REACTIONS Experience with AHA is limited. About 150 patients have been treated, most for periods of more than a year. Adverse reactions have occurred in up to thirty percent (30%) of the patients receiving AHA.
In some instances the reactions were symptomatic; in others only changes in laboratory parameters were noted. Adverse reactions seem to be more prevalent in patients with preexisting thrombophlebitis or phlebothrombosis and/or in patients with advanced degrees of renal insufficiency. The risk of adverse reactions is highest during the first year of treatment.
Chronic treatment does not seem to increase the risk nor the severity of adverse reactions. The following reactions have been reported: NEUROLOGICAL: Mild headaches are commonly reported (about 30%) during the first 48 hours of treatment. These headaches are mild, responsive to oral salicylate-type analgesics, and usually disappear spontaneously.
The headaches have not been associated with vertigo, tinnitus, or visual or auditory abnormalities. Tremulousness and nervousness have also been reported. GASTROINTESTINAL: Gastrointestinal symptoms, nausea, vomiting, anorexia, and malaise have occurred in 20-25% of patients.
In most patients the symptoms were mild, transitory, and did not result in interruption of treatment. Approximately 3% of patients developed a hemolytic anemia of sufficient magnitude to warrant interruption in treatment; several of these patients also had symptoms of gastrointestinal upset. HEMATOLOGICAL: Approximately 15% of patients have had laboratory findings characteristic of a hemolytic anemia.
A mild reticulocytosis (5- 6%) without anemia, is even more prevalent. The laboratory findings are occasionally accompanied by systemic symptoms such as malaise, lethargy and fatigue, and gastrointestinal symptoms. Symptoms and laboratory findings have invariably improved following cessation of treatment with AHA.
The hematological abnormalities are more prevalent in patients with advanced renal failure. DERMATOLOGICAL: A nonpruritic, macular skin rash has occurred in the upper extremities and on the face of several patients taking AHA on a long-term basis, usually when AHA has been taken concomitantly with alcoholic beverages, but in a few patients in the absence of alcohol consumption. The rash commonly appears 30-45 minutes after ingestion of alcoholic beverages; it characteristically disappears spontaneously in 30-60 minutes.
The rash may be associated with a general sensation of warmth. In some patients the rash is sufficiently severe to warrant discontinuation of treatment, but most patients have continued treatment, avoiding alcohol or using smaller quantities of it. Alopecia has also been reported in patients taking AHA.
CARDIOVASCULAR: Superficial phlebitis involving the lower extremities has occurred in several patients on AHA during the early (Phase II) clinical trials. Several of the affected patients had had phlebitic episodes prior to treatment. One patient developed deep vein thrombosis of the lower extremities.
The patient with phlebothrombosis had an associated traumatic injury to the groin. It is unclear whether the phlebitis was related to or exacerbated by treatment with AHA. No patient in the three (3) year controlled (Phase III) clinical trial developed phlebitis.
In all instances these vascular abnormalities returned to normal following appropriate medical therapy. Embolic phenomena have been reported in three patients taking AHA in the Phase II trial. The phlebitis and emboli resolved following discontinuation of AHA and implementation of appropriate medical therapy.
Several patients have resumed treatment with AHA without ill effect. Palpitations have also been reported in patients taking AHA. RESPIRATORY: No symptoms have been reported.
Radiographic evidence of small pulmonary emboli has been seen in three patients with phlebitis in their lower legs. PSYCHIATRIC: Depression, anxiety, nervousness, and tremulousness have b…
🔄 Drug Interactions ▾
DRUG INTERACTIONS AHA has been used concomitantly with insulin, oral and parenteral antibiotics, and progestational agents. No clinically significant interactions have been noted, but until wider clinical experience is obtained, AHA should be used with caution in patients receiving other therapeutic agents. AHA taken in association with alcoholic beverages has resulted in a rash.
(See Adverse Reactions.) AHA chelates heavy metals-notably iron. The absorption of iron and AHA from the intestinal lumen may be reduced when both drugs are taken concomitantly. When iron administration is indicated, intramuscular iron is probably the product of choice.
🤰 Pregnancy ▾
(See Contraindications.)
🧒 Pediatric Use ▾
PEDIATRIC USE Children with chronic, recalcitrant, urea-splitting urinary infection may benefit from treatment with AHA. However, detailed studies involving dosage and dose intervals in children have not been established. Children have tolerated a dose of 10 mg/kg/day, taken in two or three divided doses, satisfactorily for periods up to one year. Close monitoring of such patients is mandatory.
🆘 Overdosage ▾
OVERDOSAGE Acute deliberate overdosage in man has not occurred, but would be expected to induce the following symptoms: anorexia, malaise, lethargy, diminished sense of well being, tremulousness, anxiety, nausea and vomiting. Laboratory findings are likely to include an elevated reticulocyte count and a severe hemolytic reaction requiring hospitalization, symptomatic treatment, and possibly blood transfusions. Concomitant reduction in platelets and/or white blood cells should be anticipated.
Milder overdosages resulting in hemolysis have occurred in an occasional patient with reduced renal function after several weeks or months of continuous treatment. The acute LD 50 of AHA in animals (rats) is 4.8 gm/kg. Recommended treatment for an overdosage reaction consists of (1) cessation of treatment, (2) close monitoring of hematologic status, (3) symptomatic treatment, and (4) blood transfusions as required by the clinical circumstances.
The drug is probably dialyzable, but this property has not been tested clinically.
🧬 Clinical Pharmacology ▾
CLINICAL PHARMACOLOGY AHA reversibly inhibits the bacterial enzyme urease, thereby inhibiting the hydrolysis of urea and production of ammonia in urine infected with urea-splitting organisms. The reduced ammonia levels and decreased pH enhance the effectiveness of antimicrobial agents and allow an increased cure rate of these infections. AHA is well absorbed from the gastrointestinal tract after oral administration; peak blood levels occur from 0.25 to 1 hour after dosing.
The compound is distributed throughout body water, and there is no known binding to any tissue. AHA chelates with dietary iron within the gut. This reaction may interfere with absorption of AHA and with iron.
Concomitant hypochromic anemia should be treated with intramuscular iron. In rodents, the metabolic fate of AHA is well known; 55% is excreted unchanged in urine, 25% is excreted as acetamide or acetate and 7% is excreted by the lungs as carbon dioxide. Less than 1% is excreted in the feces.
Approximately 5% of the administered dose is unaccounted for. In rodents, AHA shows a dose-related change in pharmacokinetics; with increasing dose, there is an increase in the half-life and an increase in the percent of the administered dose recovered in urine as unchanged AHA. Pharmacokinetics in man are generally similar to rodents including the dose-related increase in half-life, but they are not as well characterized as in the rodent.
Thirty-six to sixty-five percent (36-65%) of the oral dosage is excreted unchanged in the urine. It is unaltered AHA in the urine that provides the therapeutic effect, but the precise concentration of AHA in urine that is necessary to inhibit urease is incompletely delineated. Therapeutic benefit may be obtained from concentrations as low as 8 mcg/ml; higher concentrations (i.e., 30 mcg/ml) are expected to provide more complete inhibition of urease.
The plasma half-life of AHA is approximately 5-10 hours in subjects with normal renal function and is prolonged in patients with reduced renal function. Acetohydroxamic acid has been evaluated clinically in patients with urea-splitting urinary infections, often accompanied by struvite stone disease, that were recalcitrant to other forms of medical and surgical management. In these clinical trials, AHA reduced the pathologically elevated urinary ammonia and pH levels that result from the hydrolysis of urea by the enzyme, urease.
AHA does not acidify urine directly nor does it have a direct antibacterial effect. The usefulness of reducing ammonia levels and decreasing urinary pH is suggested by single (not yet replicated) clinical trials in which urease inhibition 1) allowed successful antibiotic treatment of urea-splitting Proteus infections after surgical removal of struvite stones in patients not cured by 3 months of antibacterial treatment alone, and 2) reduced the rate of stone growth in patients who were not candidates for surgical removal of stones.
📦 How Supplied / Storage and Handling ▾
HOW SUPPLIED LITHOSTAT ® , NDC 0178-0500-01, is available for oral administration as 250 mg white, round tablets, in unit of use packages of 100 tablets. Each LITHOSTAT ® tablet is debossed MPC 500 on one side and blank on the other side. LITHOSTAT ® should be stored in a dry place at room temperature, 15° - 30°C (59° - 86°F). Container should be closed tightly. Rx only L050001R0824
📋 Description ▾
DESCRIPTION Acetohydroxamic acid (AHA) is a stable, synthetic compound derived from hydroxylamine and ethyl acetate. Its molecular structure is similar to urea: AHA is weakly acidic, highly soluble in water, and chelates metals - notably iron. The molecular weight is 75.068. AHA has a pKa of 9.32 and a melting point of 89-91° C. AHA is a urease inhibitor. Available as 250 mg tablets. Acetohydroxamic acid struct