(+)-Ethambutol

204.31

204.31

200-810-6

8G167061QZ

DTXSID8023006

C61755

Crystals|WHITE, CRYSTALLINE POWDER

J04AK02|J - Antiinfectives for systemic use

2922191000

64.5

-0.1

Solid

1.0±0.1 g/cm3

87.5-88.8 °C

345℃

>110°(230°F)

1.478

soluble in water. Also soluble in chloroform and methylene chloride

-20°C

1.82X10-6 mm Hg at 25 deg C (est)

LD50 oral in rat: 998mg/kg

D25 +13.7° (c = 2 in water)

ESSENTIALLY ODORLESS

HAS BITTER TASTE

Henry's Law constant = 3.65X10-13 atm-cu m/mol at 25 °C (est)

pKa2 = 9.49 (est)

Hydroxyl radical reaction rate constant = 2.13X10-10 cu cm/molec-sec at 25 °C (est)|MP: 198.5-200.3 °C; also reported as mp 201.8-202.6 °C. Specific optical rotation: +7.6 deg at 20 °C/D ( c = 2 in water). Soluble in water, DMSO; sparingly soluble in ethanol; difficultly soluble in acetone, chloroform. /Dichloride/

EL3640000

STABLE IN LIGHT & HEAT BUT IS HYGROSCOPIC WHEN EXPOSED TO HIGH RELATIVE HUMIDITIES

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 ethambutol hydrochloride approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Ethambutol hydrochloride/

The most commonly recognized toxic effect of ethambutol is optic neuropathy, which generally is considered uncommon and reversible in medical literature. Other side effects that have been observed are pruritus, joint pain, gastrointestinal upset, abdominal pain, malaise, headache, dizziness, mental confusion, disorientation, and possible hallucinations.|IDENTIFICATION: Ethambutol is used to treat tuberculosis. Ethambutol is an odorless crystalline hygroscopic powder. It is soluble in water, alcohol, chloroform, methyl alcohol, and very slightly soluble in ether. HUMAN EXPOSURE: Summary: Main risks and target organs: During chronic treatment ethambutol may produce visual and neurological disturbances, allergic reactions, gastrointestinal symptoms, psychiatric symptoms and transient impairment of liver function. This last event has a very low incidence. Increased serum uric acid levels and acute gouty arthritis have been reported. Summary of clinical effects: Acute overdosage may cause gastrointestinal symptoms, hallucinations and optic neuritis. Acute overdosage symptoms include nausea, abdominal pain, fever, mental confusion, visual hallucinations, and optic neuropathy (retrobulbar neuritis) with doses over 10 g. The effects of overdosage are not well established. During chronic treatment the following have been reported: Visual disturbances: Ethambutol may produce a reduction of visual acuity which appear to be due to optic neuritis. Central scotoma and green-red colour blindness may also occur. Allergic reactions: Rash, anaphylactoid reactions, dermatitis and pruritus. Gastrointestinal symptoms: Abdominal pain, anorexia, nausea, vomiting. Neurological disturbances and psychiatric symptoms: Headache, peripheral neuritis, dizziness, mental confusion, disorientation and hallucinations. Other side effects: Jaundice, transient impairment of liver function, fever, increase of serum uric acid levels, joint pain, acute gouty arthritis, malaise. Ethambutol may diffuse into milk. Ethambutol is a synthetic oral antibiotic derivative of ethylenediamine. Contraindications: Ethambutol hydrochloride is contraindicated in patients who are known to be hypersensitive to this drug. Renal impairment, old age and optic neuritis are relative contraindications. Routes of entry: Oral: Ethambutol is only available for oral use. Absorption by route of exposure: About 80% of an oral dose of ethambutol is absorbed from the gastro-intestinal tract, and the remainder appears in the feces unchanged. Absorption is not significantly impaired by food. Distribution by route of exposure: Ethambutol diffuses readily into red blood cells and into the cerebrospinal fluid when the meninges are inflamed. The concentration in erythrocytes at steady state is approximately twice the plasma concentration. It has been reported to cross the placenta and is excreted in breast milk. Biological half-life by route of exposure: The serum half-life in therapeutic doses is 3 hours, increasing in renal failure, as 80% is excreted renally. Metabolism: The main path of metabolism appears to be an initial oxidation of the alcohol to an aldehydic intermediate, followed by conversion to a dicarboxylic acid. Elimination by route of exposure: During the 24 hour period following oral administration of ethambutol, approximately 50% of the initial dose is excreted unchanged in the urine, while an additional 8% to 15% appears in the form of metabolites. From 20 to 22% of the initial dose is excreted in the feces as unchanged drug. Mode of action: Toxicodynamics: The underlying cause of visual alterations appears to be a disturbance of metabolism due to depletion of copper and zinc which serve as prosthetic groups for many enzymes. The eye normally contains a considerable store of zinc. Much of the zinc is in the pigmented cells of the outer zone of the retina, where it serves as a metal prosthetic group for retinol (alcohol) dehydrogenase. Pharmacodynamics: Ethambutol is an oral chemotherapeutic agent which is specifically effective against actively growing microorganisms of the genus Mycobacterium, including M. tuberculosis. Ethambutol is bacteriostatic and appears to inhibit the synthesis of one or more metabolites, thus causing impairment of cell metabolism, arrest of multiplication, and cell death. No cross resistance with other available antimycobacterial agents has been demonstrated. Ethambutol has been shown to be effective against strains of mycobacterium tuberculosis but does not seem to be active against fungi, viruses, or other bacteria. Ethambutol is also active against some atypical mycobacteria including M. kansasii. Primary resistance to ethambutol is uncommon in developed countries but resistant strains of M. tuberculosis are readily produced if the drug is used alone. Human data: Adults: Subclinical impairment of colour discrimination was reported to be relatively common in patients receiving ethambutol daily as part of antituberculous chemotherapy when compared with 50 patients receiving other antituberculous agents. Peripheral neuropathy has been reported in tubercular patients who had received ethambutol among other drugs. Interactions: Results of a crossover study involving 13 tuberculous patients suggest that concomitant administration of aluminium hydroxide may delay and reduce absorption of ethambutol in some patients. Untoward effects may be enhanced when ethambutol is combined with isoniazid or rifampicin. Main adverse effects: Ethambutol may produce decreased visual acuity which appear to be due to optic neuritis and to be related to dose and duration of treatment. The effects are generally reversible when administration of the drug is discontinued promptly. Ethambutol may produce constriction of visual field, central and peripheral scotoma, and green-red color blindness which may be associated with retrobulbar neuritis. Renal clearance of urate may be reduced in about 50% of patients receiving ethambutol and acute gout has been precipitated in patients with gout or impaired renal function. Cholestatic jaundice has been reported. ANIMAL/PLANT STUDIES: Relevant animal data: Toxicological studies in dogs on high prolonged doses, produced evidence of myocardial damage and failure, and depigmentation of the tapetum lucidum of the eyes, the significance of which is not known. Degenerative changes in the central nervous system, apparently not dose-related, have also been noted in dogs receiving ethambutol hydrochloride over a prolonged period. In the rhesus monkey, neurological signs appeared after treatment with high doses given daily over a period of several months. These correlated with specific serum levels of ethambutol hydrochloride and with definite neuro-anatomical changes in the central nervous system. Focal interstitial carditis was also noted in monkeys which received ethambutol hydrochloride in high doses for a prolonged period.

Because ethambutol is almost always used in combination with isoniazid, rifampin or other antituberculosis agents, the frequency of serum aminotransferase elevations attributable to ethambutol alone cannot be estimated with any confidence. The addition of ethambutol to isoniazid, rifampin or pyrazinamide does not appear to increase the rate of transient ALT elevations during therapy. In addition, ethambutol is a rare cause of acute, symptomatic liver injury. Despite 50 years of use, ethambutol has been linked to clinically apparent liver injury in only a few case reports. In the best described instance (Case 1), the onset of symptoms was 2 months after starting combination antituberculosis therapy and, in contrast to liver injury due to isoniazid or pyrazinamide, the pattern of serum enzymes was distinctly cholestatic. The recurrence of liver injury upon rechallenge with ethambutol but not isoniazid made the attribution convincing. Other case reports have described liver injury occurring in the context of DRESS syndrome, arising within 2 to 6 weeks of starting antituberculosis therapy with fever, rash, eosinophilia and other organ involvement such as liver, kidney and lung. Several published instances have described recurrence of injury after rechallenge with ethambutol.

Patient administered digitoxin (0.1 mg/day orally) while taking ethambutol (20-25 mg/kg/day) had markedly decreased serum levels of digitoxin compared to controls (16.6 versus 35 ng/mL). Binding of digitoxin by blood proteins was same in both groups. Its metabolism was probably increased.|Concurrent administration of ethambutol with other neurotoxic medications may increase the potential for neurotoxicity, such as optic and peripheral neuritis.|Aluminum salts may delay and reduce the absorption of ethambutol.|The effect of repeated administration of rifabutin on the pharmacokinetics and metabolism of ethambutol was evaluated in ten healthy volunteers. The subjects received a single oral administration of 1200 mg ethambutol on days 1 and 10 and a single daily oral dose of 300 mg rifabutin from days 3 to 9. No statistically significant difference was found in plasma pharmacokinetics (C(max), t(max), AUC, half-life and MRT) and in the renal clearance, whereas a significant decrease in the amount of unchanged ethambutol excreted in urine was observed. The decrease observed in ethambutol urinary excretion may be accounted for by taking into consideration the variability of the urinary excretion of ethambutol reported in the literature. However, a slight, likely not clinically relevant, induction or activation of kidney alcohol and/or aldehyde dehydrogenase isoenzymes by rifabutin cannot be ruled out at present. Evidence exists in the present study for autoinduction of rifabutin metabolism; this is shown by the lower plasma concentrations obtained 24 hr after the seventh dose as compared to the theoretical concentrations.

LD50 Mouse oral 2800 mg/kg /Mixture with isoniazid methane sulfonate/|LD50 Mouse ip 2210 mg/kg /Mixture with isoniazid methane sulfonate/

20-30%

While data specific to ethambutol were not located(SRC, 2007), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2). Studies have indicated that several polar pharmaceutically active compounds can leach through soil(1).

Ethambutol is distributed into milk in concentrations approximately equal to plasma concentrations of the drug.

For use, as an adjunct, in the treatment of pulmonary tuberculosis.|FDA Label

Ethambutol is a first line but adjunctive antituberculosis medication which is used only in combination with other agents such as isoniazid and rifampin. Ethambutol therapy has been associated with minor, transient and asymptomatic elevations in serum aminotransferase levels, and is a reported but rare cause of clinically apparent acute liver injury.

Antituberculosis Agents

Antitubercular Agents|Ethambutol is indicated in combination with other antituberculosis medications in the treatment of all forms of tuberculosis, including tuberculous meningitis, caused by Mycobacterium tuberculosis. /Included in US product labeling/|Ethambutol is used in the treatment of atypical mycobacterial infections, such as Mycobacterium avium complex (MAC). /NOT included in US product labeling/

Appropriate studies on the relationship of age to the effects of ethambutol have not been performed in children up to 13 years of age. Ethambutol is generally not recommended in children whose visual acuity cannot be monitored (younger than 6 years of age). However, ethambutol should be considered for all children with organisms resistant to other medications, and in whom susceptibility to ethambutol has been demonstrated or is likely.|The most important adverse effect of ethambutol is optic neuritis with decreases in visual acuity, constriction of visual fields, central and peripheral scotomas, and loss of red-green color discrimination. The extent of ocular toxicity appears to be related to the dose and duration of ethambutol therapy. However, such toxicity also has been reported rarely after only a few days of therapy with the drug, and may represent an idiosyncratic reaction.|Other adverse effects of ethambutol include dermatitis, pruritus, headache, malaise, dizziness, fever, mental confusion, disorientation, possible hallucinations, joint pain, and rarely anaphylactoid reactions. GI upset, abdominal pain, nausea, vomiting, and anorexia have also occurred occasionally with ethambutol. Peripheral neuritis, with numbness and tingling of the extremities, has been reported infrequently. Increased serum uric acid concentrations and precipitation of acute gout have occurred occasionally in patients receiving ethambutol and are probably the result of decreased renal clearance of urate. Transient impairment of liver function, as indicated by abnormal liver function test results, has also occurred. Cholestatic jaundice, which appeared to be caused by ethambutol, has been reported in at least one patient who received the drug both alone and in conjunction with streptomycin.|Visual testing should be performed prior to initiating ethambutol therapy and then periodically during therapy with the drug. Testing should be done monthly in patients receiving more than 15 mg/kg daily. Examinations should include ophthalmoscopy, finger perimetry, and testing of color discrimination. Patients developing adverse ocular effects during ethambutol therapy may show subjective visual symptoms either before or simultaneously with decreases in visual acuity. All patients receiving the drug should be questioned periodically about blurred vision and other subjective visual symptoms and should be instructed to report to their physicians any such changes as soon as they are noticed. If substantial changes in visual acuity occur, ethambutol should be discontinued immediately.|For more Drug Warnings (Complete) data for ETHAMBUTOL (10 total), please visit the HSDB record page.

Ethambutol is a highly specific agent and is active only against organisms of the genus Mycobacterium. The drug is active in vitro and in vivo against M. tuberculosis, M. bovis, M. marinum, and some strains of M. kansasii, M. avium, M. fortuitum, and M. intracellulare. In vitro, the minimum inhibitory concentration (MIC) of ethambutol for most susceptible mycobacteria is 1-8 mcg/mL, depending on the culture media used.|Natural and acquired resistance to ethambutol have been demonstrated in vitro and in vivo in strains of M. tuberculosis. In vitro, resistance to ethambutol appears to occur in a stepwise manner. Resistant strains of initially susceptible M. tuberculosis develop rapidly if ethambutol is used alone in the treatment of clinical tuberculosis. When ethambutol is combined with other antituberculosis agents in the treatment of the disease, emergence of resistant strains may be delayed or prevented. There is no evidence of cross-resistance between ethambutol and other antituberculosis agents currently available in the US.

Ethambutol is an oral chemotherapeutic agent which is specifically effective against actively growing microorganisms of the genus Mycobacterium, including M. tuberculosis. Ethambutol inhibits RNA synthesis and decreases tubercle bacilli replication. Nearly all strains of M. tuberculosis and M. kansasii as well as a number of strains of MAC are sensitive to ethambutol.

Drugs used in the treatment of tuberculosis. They are divided into two main classes: "first-line" agents, those with the greatest efficacy and acceptable degrees of toxicity used successfully in the great majority of cases; and "second-line" drugs used in drug-resistant cases or those in which some other patient-related condition has compromised the effectiveness of primary therapy. (See all compounds classified as Antitubercular Agents.)

About 75% to 80% of an orally administered dose of ethambutol is absorbed from the gastrointestinal tract.|During the 24-hour period following oral administration of ethambutol hydrochloride approximately 50 percent of the initial dose is excreted unchanged in the urine, while an additional 8 to 15 percent appears in the form of metabolites. From 20 to 22 percent of the initial dose is excreted in the feces as unchanged drug.|Approximately 75-80% of an oral dose of ethambutol hydrochloride is rapidly absorbed from the GI tract. Absorption is not substantially affected when the drug is administered with food. Following a single oral ethambutol hydrochloride dose of 25 mg/kg, peak serum ethambutol concentrations of 2-5 mcg/mL are attained within 2-4 hours; serum concentrations of the drug are undetectable 24 hours after the dose.|There is no evidence that accumulation of the drug occurs when ethambutol doses of 25 mg/kg are given once daily in patients with normal renal function. Serum concentrations of the drug are higher and accumulation may occur when ethambutol is used in patients with impaired renal function.|Ethambutol is widely distributed into most body tissues and fluids. Highest concentrations of the drug are found in erythrocytes, kidneys, lungs, and saliva; lower drug concentrations are found in ascitic fluid, pleural fluid, brain, and CSF. Peak intracellular concentrations of ethambutol in erythrocytes are about twice peak plasma concentrations and maintain this ratio for at least 24 hours after a single oral dose. In patients with meningitis, administration of an oral ethambutol hydrochloride dose of 25 mg/kg has produced peak CSF concentrations of the drug ranging from 0.15-2.0 ug/mL.|/Ethambutol/ does not penetrate intact meninges, but 10 to 50% may penetrate the meninges of patients with tuberculous meningitis. Volume of distribution is 1.6 liters per kg|For more Absorption, Distribution and Excretion (Complete) data for ETHAMBUTOL (9 total), please visit the HSDB record page.

Hepatic. Up to 15% of administered drug is metabolized to inactive metabolites. The main path of metabolism appears to be an initial oxidation of the alcohol to an aldehydic intermediate, followed by conversion to a dicarboxylic acid.|... Up to 15% is excreted in the form of two metabolites, an aldehyde and a dicarboxylic acid derivative.|Ethambutol is partially inactivated in the liver by oxidation to an aldehyde intermediate, 2,2?-(ethylenediimino)-di-butyraldehyde, which is converted to the decarboxylic acid derivative, 2,2?-(ethylenediimino)-di-butyric acid.

In patients with normal renal function, 3 to 4 hours. In patients with impaired renal function, up to 8 hours.|The plasma half-life of ethambutol is approximately 3.3 hours in patients with normal renal function. The half-life is prolonged in patients with impaired renal or hepatic function. In patients with renal failure, the half-life may be 7 hours or longer.|Six normal adult volunteers were administered 15 mg/kg of ethambutol (EMB) by a constant-rate 1-hr infusion. Plasma and urine samples were collected up to 24 and 72 hr, respectively. ... Subsequent postinfusion EMB levels exhibited multiphasic decay. In the 12-hr period following infusion, EMB levels showed biexponential decay. However, 24-hr plasma levels in all subjects were observed to be higher than those predicted using a two-compartment body model. The alpha phase in these subjects had a mean half-life of 8.6 min while the half-life of the beta phase ranged from 2.5 to 3.6 hr (mean 3.1). The half-life of the gamma phase estimated from plasma data points between 12 and 24 hr averaged 1.2 +/- 3.6 hr. A terminal gamma t1/2 of 15.4 +/- 1.7 hr was calculated from 12-72 hr urine data. ... Plasma EMB clearance ranged from 7.47 to 8.87 mL/min/kg (mean 8.57). ...

Ethambutol inhibits arabinosyl transferases which is involved in cell wall biosynthesis. By inhibiting this enzyme, the bacterial cell wall complex production is inhibited. This leads to an increase in cell wall permeability.|Ethambutol is bacteriostatic in action. Although the exact mechanism of action has not been fully elucidated, the drug appears to inhibit the synthesis of one or more metabolites in susceptible bacteria resulting in impairment of cellular metabolism, arrest of multiplication, and cell death. Ethambutol is active against susceptible bacteria only when they are undergoing cell division.

Decontamination: Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. /Antibacterial agents/|Emergency and supportive measures: Maintain an open airway and assist ventilation if necessary. Treat coma, seizures, hypotension, anaphylaxis, and hemolysis if they occur. Replace fluid losses resulting from gastroenteritis with intravenous crystalloids. ... /Antibacterial agents/|Enhanced elimination: Most antibiotics are excreted unchanged in the urine, so maintenance of adequate urine flow is important. The role of forced diuresis in unclear. Hemodialysis is not usually indicated, except perhaps in patients with renal dysfunction and a high level of a toxic agent. /Antibacterial agents/

/HUMAN EXPOSURE STUDIES/ The aim of the present study was to describe the side effects related to combined Pyrazinamide (PZA) and ethambutol (EMB) treatment given for LTBI, in contacts previously exposed to MDR-TB. In total, 12 consecutive contacts, all of African origin and aged 38+/-5 yrs, were treated with daily PZA (23+/-4 mg.kg(-1)) and EMB (17+/-4 mg.kg(-1)) at Geneva University Hospital outpatient clinic (Switzerland), as a result of contact-tracing procedures for two patients with contagious MDR-TB. Clinical status and liver function tests (aspartate aminotransferase (ALAT) and alanine aminotransferase (ASAT)) were monitored monthly. In seven cases (58%) treatment was discontinued after a median of 119 days, due to hepatic toxicity in six cases (ALAT or ASAT elevation more than four times the upper normal limit), and gastrointestinal symptoms in one case.|/HUMAN EXPOSURE STUDIES/ Seventy patients with pulmonary tuberculosis and 12 healthy controls were included in a study to observe the effect of ethambutol on serum uric acid level. In ethambutol-treated cases a statistically significant increase in mean serum uric acid levels was observed in the second, third and fourth week of treatment. This increase was independent of dosage of ethambutol. However, 22 of the 52 (42%) ethambutol-treated cases showed no increase. ... Hyperuricemia due to ethambutol was reversed with probenecid but not by salicylates. No patient developed acute gouty arthritis although two developed arthralgia.|/EPIDEMIOLOGY STUDIES/ A retrospective observational case series from a single neuro-ophthalmology practice. 8 patients with a history of ethambutol-induced optic neuropathy were examined within 3 months after stopping ethambutol treatment. All patients underwent a neuro-ophthalmologic examination, including visual acuity, color vision, visual fields and funduscopy. Optical coherence tomography (OCT) was performed on both eyes of each patient using the retinal nerve fibre layer analysis protocol. The interval between cessation of ethambutol treatment and the initial visit ranged from 1 week to 3 months. All patients had visual deficits characteristic of ethambutol-induced optic neuropathy at their initial visit, and the follow-up examination was performed within 12 months. Compared with the initial retinal nerve fibre layer thickness (RNFLT), there was a statistically significant decrease in the mean RNFLT of the temporal, superior and nasal quadrants (p = 0.009, 0.019 and 0.025, respectively), with the greatest decrease in the temporal quadrant (mean decrease 26.5 mum). A decrease in RNFLT is observed in all quadrants in patients with ethambutol-induced optic neuropathy who have recently discontinued the medication. This decrease is most pronounced in the temporal quadrant of the optic disc.|/HUMAN EXPOSURE STUDIES/ From January 1984-December 1987, 1783 patients received combination therapy of isoniazid, rifampin, and ethambutol for the control of tuberculosis. Forty-two developed symptomatic hepatitis during the period of treatment. Fifteen were hepatitis B virus carriers, and the remaining 27 were noncarriers. The peak serum transaminase and bilirubin levels were higher in carriers. Seven carriers died of fulminant or subacute hepatic failure, and only 1 noncarrier died. Eleven carriers had detectable serum hepatitis B virus deoxyribonucleic acid during the acute stage of hepatitis.|For more Human Toxicity Excerpts (Complete) data for ETHAMBUTOL (12 total), please visit the HSDB record page.

Dexambutol

Oral Tablets, film-coated 100 mg ethambutol Tablets, VersaPharm; Myambutol, X-Gen. Oral Tablets, film-coated 400 mg ethambutol Tablets, Barr; VersaPharm; West-Ward; Myambutol (scored), X-Gen.|Available commercially as the free base or hydrochloride.|Dexambutol; Ebutol; Etibi; Etapiam; Myambutol; Mycobutol; Sural; Tibutol /Ethambutol dihydrochloride/

...IN-VITRO & IN-VIVO STUDIES REVEALED THAT D FORM OF THIS SUBSTANCE (ETHAMBUTOL) EXHIBITED 200 TIMES MORE ACTIVITY THAN DID L ISOMER.

Analyte: ethambutol hydrochloride; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards /ethambutol hydrochloride/|Analyte: ethambutol hydrochloride; matrix: chemical purity; procedure: dissolution in glacial acetic acid and mercuric acetate; addition of crystal violet indicator; titration with perchloric acid to a blue to blue-green endpoint /ethambutol hydrochloride/|Analyte: ethambutol hydrochloride; matrix: pharmaceutical preparation (tablet); procedure: infrared absorption spectrophotometry with comparison to standards (chemical identification) /ethambutol hydrochloride/|Analyte: ethambutol hydrochloride; matrix: pharmaceutical preparation (tablet); procedure: liquid chromatography with detection at 200 nm and comparison to standards (chemical purity)|For more Analytic Laboratory Methods (Complete) data for ETHAMBUTOL (8 total), please visit the HSDB record page.

GC METHOD OF CS LEE & LZ BENET (1976) FOR DETECTION OF ETHAMBUTOL IN BLOOD SERUM WAS MODIFIED TO IMPROVE RELIABILITY OF RESULTS.|WITH A DUAL-COLUMN & DUAL-DETECTOR GAS-LIQ CHROMATOGRAPH, SIMULATANEOUS MICR (PLASMA & DIALYZATE) & MACRO (URINE) DETECTIONS OF ETHAMBUTOL ARE POSSIBLE.|DETERMINATION OF ETHAMBUTOL IN PLASMA & URINE BY CHEM IONIZATION GC-MS USING DEUTERATED INTERNAL STD. ASSAY IS SENSITIVE TO APPROX 10 NG/ML.|Analyte: ethambutol; matrix: blood (plasma); procedure: high-performance liquid chromatography with ultraviolet detection at 270 nm; limit of detection: 150 ng/mL|For more Clinical Laboratory Methods (Complete) data for ETHAMBUTOL (6 total), please visit the HSDB record page.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients