Mebendazole

295.29

295.29

250-635-4

81G6I5V05I

757838|184849

DTXSID4040682

C47595

Off-white amorphous powder|Crystals from acetic acid and methanol

P02CA01|P - Antiparasitic products, insecticides and repellents

29339900

84.1

2.8

Mebendazole is a white to slightly yellow powder. Pleasant taste. Practically water insoluble. (NTP, 1992)

1.38 g/cm³

288.5 °C

1.702

35.4mg/L(25 ºC)

0-6°C

5.3X10-11 mm Hg at 25 deg C (est)

LD50 orally: >80 mg/kg in sheep; >40 mg/kg in mice, rats and chickens (Van Gelder)

NOT UNPLEASANT

Henry's Law constant = 5.4X10-16 atm-cu m/mol at 25 °C (est)

pKa = 6.6 (double-bonded nitrogen) (est)

171.2 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|174.4 Ų [M+H]+ [CCS Type: TW, Method: calibrated with Waters Major Mix]|187.8 Ų [M+Na]+ [CCS Type: TW, Method: calibrated with Waters Major Mix]

Hydroxyl radical reaction rate constant = 1.4X10-10 cu cm/molecule-sec at 25 °C (est)

Insoluble in water.

Carbamates

MEBENDAZOLE is a carbamate ester-amine. Amines behave as chemical bases. Carbamates are chemically similar to, but more reactive than amides. Like amides they form polymers such as polyurethane resins. Carbamates are incompatible with strong acids and bases, and especially incompatible with strong reducing agents such as hydrides. Flammable gaseous hydrogen is produced by the combination of active metals or nitrides with carbamates. Strongly oxidizing acids, peroxides, and hydroperoxides are incompatible with carbamates.

UN 2811

3

22

36

EY8600000

Xn

TABLETS HAVE EXPIRATION DATE OF 3 YR FOLLOWING DATE OF MFR

P264, P270, P273, P301+P312, P330, P391, P501

H302

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl mebendazole, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.|Oral dosage form new animal drugs. Mebendazole oral. (1) Horses: Indications for use: It is used in horses for treatment of infections caused by large roundworms (Parascaris equorum); large strongyles (Strongylus edentatus, S. equinus, S. vulgaris); small strongyles; and mature and immature (4th larval stage pinworms (Oxyuris equi)). ... (2) Dogs. Indications for use: The drug is used for treatment of infections of roundworms (Toxocara canis), hookworms (Ancylostoma caninum, Uncinaria stenocephala), whipworms (Trichuris vulpis), and tapeworms (Taenia pisiformis).|Oral dosage form new animal drugs. Mebendazole and trichlorfon powder. Each gram contains 83.3 mg of mebendazole and 375.0 mg of trichlorofon. ... (1) Horses... Indications for use: It is used in horses for the treatment of infections of bots (Gastrophilus intestinalis and G. nasalis), large roundworms (Parascaris equorum), large strongyles (Strongylus edentatus, S. equinus, S. vulgaris), small strongyles, and pinworms (Oxyuris equi.)|Oral dosage form new animal drugs. Mebendazole and trichlorfon paste. Each gram of paste contains 100 mg of mebendazole and 454 mg of trichlorfon. ... It is used in horses for treatment of infections of bots (Gastrophilus intestinalis and G. nasalis), large roundworms (Parascaris equorum), large strongyles (Strongylus edentatus, S. equinus, S. vulgaris), small strongyles, and pinworms (Oxyuris equi).|The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Mebendazole is included on this list.

Dayan AD; Preparing to control Schistosomiasis and Soil-transmitted Helminthiasis in the Twenty-First Century; Acta Tropica 86 (2-3): 141-159 (2003)

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)

|Warning|H302 (98.63%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P273, P301+P312, P330, P391, and P501|Aggregated GHS information provided by 73 companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

STORAGE PRECAUTIONS: You should store this material under ambient temperatures. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

The concentration of mebendazole measured in a water basin of a fish nursery was 5 mg/L(1).

Acute oral toxicity (LD50): 620 mg/kg [Mouse]. Symptoms of overdose include elevated liver enzymes, headaches, hair loss, low levels of white blood cells (neutropenia), fever, and itching.

Mebendazole when given in typical doses has not been associated with serum enzyme elevations, although the duration of therapy is usually short and monitoring for enzyme elevations has rarely been reported. With high dose therapy (which is now rarely used with the availability of albendazole), elevations in serum aminotransferase levels (2 to 10 times normal) can occur, but are usually well tolerated. There have been rare reports of acute liver injury due to mebenazole, particularly when it is given repeatedly or in higher doses. The onset is usually with fever and malaise within days of starting or restarting therapy. The pattern of serum enzyme elevations is typically hepatocellular, and jaundice is uncommon. The abnormalities usually resolve rapidly with stopping therapy. Signs of hypersensitivity (rash, fever and eosinophilia) are typical and liver biopsy may show granulomas.

Preliminary evidence suggests that cimetidine inhibits mebendazole metabolism and may result in increased plasma concentrations of the drug.|Limited data suggest that both carbamazepine and phenytoin may enhance the metabolism of mebendazole, probably by inducing hepatic microsomal enzymes, resulting in decreased plasma mebendazole concentrations.This interaction is unlikely to be clinically important in patients receiving mebendazole for the management of intestinal helminth infections; however, use of carbamazepine or phenytoin may prevent an adequate therapeutic response in patients receiving the anthelmintic for the management of extraintestinal infections (e.g., hydatid disease). Pending further accumulation of data, use of alternative anticonvulsant agents (e.g., valproic acid) should be considered in patients receiving mebendazole for extraintestinal infections.

LD50 Sheep orally greater than 80 mg/kg

Mebendazole is a potent embryotoxin and teratogen in laboratory animals ... Despite a lack of evidence for teratogenicity in human beings, it is advised that mebendazole not be given to pregnant women or to children less than 2 yr of age.

90-95%

Mebendazole's production and use as an anthelmintic treatment in both humans and animals(1-3) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 830(SRC), determined from a log Kow of 2.83(2) and a regression-derived equation(3), indicates that mebendazole is expected to have low mobility in soil(SRC). Volatilization of mebendazole from moist soil surfaces is not expected to be an important fate process(SRC) based on an estimated Henry's Law constant of 5.4X10-16 atm-cu m/mole for the neutral species(SRC), calculated using a fragment constant estimation method(4). Mebendazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.3X10-11 mm Hg(SRC), determined from a fragment constant method(75. Biodegradation data were not available(SRC, 2006).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 830(SRC), determined from a log Kow of 2.83(2) and a regression-derived equation(3), indicates that mebendazole is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 5.4X10-16 atm-cu m/mole(SRC), developed using a fragment constant estimation method(5). According to a classification scheme(6), an estimated BCF of 83(SRC), from its log Kow(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). A base-catalyzed second-order hydrolysis rate constant of 2.6X10-4 L/mole-sec(SRC) was estimated using a structure estimation method(8); this corresponds to half-lives of 840 and 84 years at pH values of 7 and 8, respectively(8). Based on photolysis half-lives of less than 80 minutes in sun-lit waters determined for the structurally similar compound albendazole(9,10), mebendazole is expected to be susceptible to direct photolysis by sunlight. Biodegradation data were not available(SRC, 2006).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), mebendazole, which has an estimated vapor pressure of 5.3X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase mebendazole may be removed from the air by wet or dry deposition(SRC). Based on photolysis half-lives of less than 80 minutes in sun-lit waters determined for the structurally similar compound albendazole(3,4), mebendazole is expected to be susceptible to direct photolysis by sunlight.

A base-catalyzed second-order hydrolysis rate constant of 2.6X10-4 L/mole-sec(SRC) was estimated using a structure estimation method(1); this corresponds to half-lives of 840 and 84 years at pH values of 7 and 8, respectively(1). Based on photolysis half-lives of less than 80 minutes in sun-lit waters determined for the structurally similar compound albendazole(2,3), mebendazole is expected to be susceptible to direct photolysis by sunlight.

An estimated BCF of 83 was calculated for mebendazole(SRC), using a log Kow of 2.83(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate(SRC), provided the compound is not metabolized by the organism(SRC).

The Koc of mebendazole is estimated as 830(SRC), using a log Kow of 2.83(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that mebendazole is expected to have low mobility in soil.

The Henry's Law constant for mebendazole is estimated as 5.4X10-16 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that mebendazole is expected to be essentially nonvolatile from moist soil or water surfaces(2). Mebendazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.3X10-11 mm Hg(SRC), determined from a fragment constant method(3).

Occupational exposure to mebendazole may occur through dermal contact with this compound at workplaces where mebendazole is produced or used. Exposure to mebendazole among the general population may be limited to those administered this substance as a drug and to those who administer mebendazole to animals. (SRC)

For the treatment of Enterobius vermicularis (pinworm), Trichuris trichiura (whipworm), Ascaris lumbricoides (common roundworm), Ancylostoma duodenale (common hookworm), Necator americanus (American hookworm) in single or mixed infections.

Mebendazole is an anthelmintic agent used commonly for roundworm (pinworm and hookworm) infections, trichinosis, capillariasis and toxocariasis and other parasitic worm infections. Mebendazole when given for prolonged periods in high doses has been associated with elevations in serum enzyme levels, and rare instances of acute, clinically apparent liver injury have been linked to its use.

Anthelmintic Agents

Mesh Heading: Antinematodal agents|Mebendazole is indicated as a primary agent for tichuriasis caused by Trichuris trichiura (whipworm). /Included in US product labeling/|Mebendazole is indicated in the treatment of multiple intestinal roundworm infections. /Included in US product labeling/|Mebendazole is indicated a a primary agent for enterobiasis caused by Enterobius vermicularis (pinworm). /Included in US product labeling/|For more Therapeutic Uses (Complete) data for MEBENDAZOLE (19 total), please visit the HSDB record page.

Organ system function (including hematopoietic and hepatic) should be assessed periodically during prolonged mebendazole therapy.|Other adverse effects reported rarely in patients receiving mebendazole include alopecia, rash, pruritus, urticaria, angioedema, flushing, hiccups, cough, weakness,drowsiness, chills, hypotension, seizures, transient abnormalities in liver function tests (e.g., increased serum concentrations of aminotransferases, alkaline phosphatase, and/or bilirubin), hepatitis, increased BUN, decreased hemoglobin concentration and/or hematocrit, leukopenia, thrombocytopenia, eosinophilia, hematuria, and cylindruria.Migration of roundworms through the mouth and nose also has been reported.|Myelosuppression manifested as neutropenia (including agranulocytosis) and/or thrombocytopenia also has been reported in patients receiving high-dose (e.g., 30-50 mg/kg daily) mebendazole therapy for extraintestinal infections; while the myelosuppression usually was reversible following discontinuance of the drug, death has occurred rarely.|At usual recommended dosages (i.e., 100-200 mg daily), mebendazole appears to cause minimal adverse effects. Adverse effects appear to occur more frequently when higher dosages (e.g., those used in the treatment of extraintestinal infections such as hydatid disease) are used, and may be related to effects resulting from drug-induced killing of the parasites in some cases. Transient diarrhea and abdominal pain have occurred occasionally during mebendazole treatment, but usually have been associated with massive infections and expulsion of the helminths. Nausea, vomiting, headache, tinnitus, numbness, and dizziness also have been reported occasionally during mebendazole therapy. Fever has occurred in some patients, particularly in those receiving high-dose therapy for extraintestinal infections.|For more Drug Warnings (Complete) data for MEBENDAZOLE (9 total), please visit the HSDB record page.

Mebendazole is a (synthetic) broad-spectrum anthelmintic. The principal mode of action for Mebendazole is by its inhibitory effect on tubulin polymerization which results in the loss of cytoplasmic microtubules.

Agents that interact with TUBULIN to inhibit or promote polymerization of MICROTUBULES. (See all compounds classified as Tubulin Modulators.)|Substances used in the treatment or control of nematode infestations. They are used also in veterinary practice. (See all compounds classified as Antinematodal Agents.)

Poorly absorbed (approximately 5 to 10%) from gastrointestinal tract. Fatty food increases absorption.|In man, approximately 2% of administered mebendazole is excreted in urine and the remainder in the feces as unchanged drug or a primary metabolite.|Elimination: Fecal: Approximately 95% excreted unchanged or as the primary metabolite (2-amino derivative) in feces. Renal: Approximately 2 to 5% excreted unchanged or as the primary metabolite in urine.|Peak serum concentration: Following a dose of 100 mg twice a day for 3 days: Mebendazole: Not more than 0.03 ug/mL. 2-Amino metabolite: Not more than 0.09 ug/mL. Serum concentrations up to 0.5 ug/mL have been reported in chronic, high-dose therapy.|Time to peak serum concentration: 2 to 5 hours (range: 0.5 to 7 hours).|Mebendazole is highly bound to plasma proteins. It is not known if mebendazole is distributed into milk.|For more Absorption, Distribution and Excretion (Complete) data for MEBENDAZOLE (11 total), please visit the HSDB record page.

Primarily hepatic. Primary metabolite is 2-amino-5-benzoylbenzimidazole, but also metabolized to inactive hydroxy and hydroxyamino metabolites. All metabolites are devoid of anthelmintic activity.|Primarily hepatic; metabolized in inactive amino, hydroxy, and hydroxyamino metabolites; primary metabolite is 2-amino-5-benzoylbenzimidazole.|Although the exact metabolic fate of mebendazole has not been fully determined, the drug is metabolized via decarboxylation to 2-amino-5(6)-benzimidazolyl phenylketone; this metabolite does not have anthelmintic activity.|Mebendazole ... is extensively metabolized. Two major metabolites, methyl-5-(alpha-5-hydroxybenzyl)-2-benzimidazole carbamate and 2-amino-5-benzoylbenzimidazole, have lower rates of clearance than does mebendazole itself. Mebendazole, rather than its metabolites, appears to be the active drug form. Conjugates of mebendazole and its metabolites have been found in bile, but little unchanged mebendazole appears in the urine.

2.5 to 5.5 hours (range 2.5 to 9 hours) in patients with normal hepatic function. Approximately 35 hours in patients with impaired hepatic function (cholestasis).|Normal hepatic function: 2.5 to 5.5 hours (range: 2.5 to 9 hours). Impaired hepatic function (cholestasis): Approximately 35 hours.|The elimination half-life of mebendazole has been reported to be about 2.8-9 hours.

Mebendazole causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes their glycogen stores. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. Due to diminished energy production, the parasite is immobilized and eventually dies.|Although the exact mechanism of anthelmintic activity of mebendazole has not been fully elucidated, the drug appears to cause selective and irreversible inhibition of the uptake of glucose and other low molecular weight nutrients in susceptible helminths; inhibition of glucose uptake appears to result in endogenous depletion of glycogen stores in the helminth. Mebendazole does not inhibit glucose uptake in mammals. Mebendazole appears to cause degenerative changes in the intestine of nematodes and in the absorptive cells of cestodes. The principal anthelmintic effect of the drug appears to be degeneration of cytoplasmic microtubules within these intestinal and absorptive cells. Microtubular deterioration results in inhibition of organelle movement and interferes with the absorptive and secretory function. As a result of excessive accumulation of intracellular transport secretory granules, hydrolytic and proteolytic enzymes are released and cause cellular autolysis. This irreversible damage leads to death of the parasite.|Vermicidal; may also be ovicidal for ova or most helminths; mebendazole causes degeneration of parasite's cytoplasmic microtubules and thereby selectively and irreversibly blocks glucose uptake in susceptible adult intestine-dwelling helminths and their tissue-dwelling larvae; inhibition of glucose uptake apparently results in depletion of the parasite's glycogen stores; this, in turn, results in reduced formation of adenosine triphosphate (ATP) required for survival and reproduction of the helminth; corresponding energy levels are gradually reduced until death of the parasite ensues; mebendazole does not appear to affect serum glucose concentrations in humans, however.|Benzimidazoles produce many biochemical changes in susceptible nematodes, eg, inhibition of mitochondrial fumarate reductase, reduced glucose transport, and uncoupling of oxidative phosphorylation ... /but/ the primary action ... /should be/ to inhibit microtubule polymerization by binding to beta-tubulin. The selective toxicity of these agents derives from the fact that specific, high-affinity binding to parasite beta-tubulin occurs at much lower concn than does binding to the mammalian protein ... Benzimidazole-resistant Haemonchus contortus display reduced high-affinity drug binding to beta-tubulin and alterations in beta-tubulin isotype gene expression that correlate with drug resistance ... Two identified mechanisms of drug resistance in nematodes involve both a progressive loss of "susceptible" beta-tubulin gene isotypes together with emergence of a "resistant" isotype with a conserved point mutation that encodes a tyrosine instead of phenylalanine at position 200 of beta-tubulin. While this mutation may not be required for benzimidazole resistance in all parasites, eg, Giardia lamblia, benzimidazole resistance in parasitic nematodes is unlikely to be overcome by novel benzimidazole analogs, because tyrosine also is present at position 200 of human beta-tubulin. /Benzimidazoles/

SYMPTOMS: Symptoms of exposure to this compound may include headache, dizziness, gastrointestinal disturbances, pruritus, drowsiness, abnormalities in liver-function test, eosinophilia, lowered hemoglobin concentrations, leucopenia, hematuria and casts, cough, fever, glomerulonephritis, abdominal pain, diarrhea, nausea and vomiting. It may also cause allergic reactions, alopecia and reversible neutropenia. ACUTE/CHRONIC HAZARDS: When heated to decomposition this compound emits very toxic fumes of NOx. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. If symptoms (such as redness or irritation) develop, immediately transport the victim to a hospital. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Overdosage of mebendazole may result in GI symptoms lasting up to a few hours.

Anti Worm

Oral: Tablets, chewable: 100 mg Mebendazole Tablets, (Teva); Vermox, (McNeil).

RELATIVE SPECIFICITY OF ANTHELMINTIC DRUGS USUALLY NECESSITATES ACCURATE DIAGNOSIS, BUT WITH DEVELOPMENT OF NEW, BROADER SPECTRUM AGENTS (EG, MEBENDAZOLE...) IMPORTANCE OF DETERMINING SPECIFIC HELMINTH MAY DIMINISH IN FUTURE.

ESTIMATION BY DISSOLVING IN ETHANOL & TITRATING WITH PERCHLORIC ACID USING CRYSTAL VIOLET AS INDICATOR.|MEBENDAZOLE SEPARATED BY HIGH-PRESSURE LIQUID CHROMATOGRAPHY.|Analyte: mebendazole; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards|Analyte: mebendazole; matrix: chemical purity; procedure: dissolution in glacial acetic acid; potentiometric titration with perchloric acid using a calomel-glass electrode system|For more Analytic Laboratory Methods (Complete) data for MEBENDAZOLE (9 total), please visit the HSDB record page.

HUMAN PLASMA ANALYZED FOR MEBENDAZOLE BY HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY USING A REVERSED-PHASE COLUMN.|Analyte: mebendazole; matrix: blood (plasma), body fluid (abomasal, duodenal, rumen); procedure: high-performance liquid chromatography with ultraviolet detection at 292 nm; limit of detection: 20 ng/mL|Analyte: mebendazole; matrix: blood (plasma); procedure: high-performance liquid chromatography with electrochemical detection at 300 nm|Analyte: mebendazole; matrix: blood (serum); procedure: high-performance liquid chromatography with electrochemical detection; limit of detection: 0.25 ng/mL|For more Clinical Laboratory Methods (Complete) data for MEBENDAZOLE (13 total), please visit the HSDB record page.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients|Pharmaceuticals -> Animal Drugs -> Approved in Taiwan