Methocarbamol

241.24000

241.24

927-845-6

757112|170960

DTXSID6023286

Crystals from benzene

M - Musculo-skeletal system

2924299090

91.01000

0.6

Solid

1.256 g/cm3

92-94 °C

472.5ºC at 760 mmHg

239.6ºC

1.57

29.9 [ug/mL]

-20ºC Freezer

3.41X10-7 mm Hg at 25 deg C (est)

Henry's Law constant = 6.53X10-16 atm-cu m/mole at 25 °C (est)

Hydroxyl radical reaction rate constant = 4.51X10-11 cu cm/molec-sec at 25 °C (est)

NONH for all modes of transport

3

R22; R42/43

S36

TY8750000

Xn

Methocarbamol solutions containing 4 mg/mL in sterile water for injection or 5% dextrose or 0.9% sodium chloride injection are stable for 6 days at room temperature. Because formation of haze in diluted solutions of methocarbamol may be unpredictable, all diluted solutions of the drug should be inspected visually for presence of a haze prior to administration regardless of storage conditions. Because compatibility of methocarbamol injection with other drugs may depend on several factors (e.g., t

P261-P280-P284-P304 + P340-P333 + P313-P342 + P311

H302-H317-H334

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 methocarbamol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.|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. Methocarbamol is included on this list.|Oral dosage form new animal drugs. Methocarbamol tablets. ... Conditions of use: The drug is administered to dogs and cats as an adjunct to therapy for acute inflammatory and traumatic conditions of the skeletal muscles in order to reduce muscular spasms. ... For use only by or on the order of a licensed veterinarian.|Implantation or injectable dosage form new animal drugs. Methocarbamol injection. Conditions of use: (i) Dogs and cats. ... (ii) Horses. ... Indications for use. As an adjunct for treating acute inflammatory and traumatic conditions of the skeletal muscles and to reduce muscular spasms. ... Limitations. For intravenous use only.

|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P261, P264, P270, P271, P301+P312, P304+P340, P312, P330, P403+P233, P405, and P501

Overdose of methocarbamol may be associated with alcohol and other central nervous system depressants. Patients may experience nausea, drowsiness, blurred vision, hypotension, seizures, and coma. Treatment of overdose is generally through airway maintenance, monitoring urinary output, vital signs, and giving fluid intravenously if necessary. The oral LD50 in rats is 3576.2mg/kg. The FDA has classified methocarbamol as pregnancy category C. Animal and human studies have not been performed to determine the risks to a fetus, however fetal and congenital abnormalities have been reported. Methocarbamol is excreted in the milk of dogs, however it is unknown if this is also the case for humans. Caution should be exercised when taking methocarbamol while breastfeeding. Studies to assess the carcinogenicity, mutagenicity, or effects on fertility of methocarbamol have not been performed.

While the product label for methocarbamol states that it can cause jaundice (including cholestatic jaundice), there is little published evidence to suggest that methocarbamol is a cause of hepatic injury or clinically apparent drug induced liver disease. During clinical trials of methocarbamol, some patients had to stop treatment because of nausea, dizziness, or other nonspecific complaints, but no serum aminotransferase levels or other laboratory results were reported. Methocarbamol appears to be well tolerated, but the lack of monitoring of serum aminotransferase levels during clinical trials with methocarbamol makes it impossible to rule out the possibility of mild liver injury occurring with treatment.

Additive CNS depression may occur when methocarbamol is administered concomitantly with other CNS depressants, including alcohol. If methocarbamol is used concomitantly with other depressant drugs, caution should be used to avoid overdosage.|A case is presented of a fatal drug interaction caused by ingestion of methocarbamol (Robaxin) and ethanol. ... Therapeutic concentrations of methocarbamol are reported to be 24 to 41 ug/mL. Biological fluids were screened for ethanol ... and quantitated by gas-liquid chromatography (GLC). Determination of methocarbamol concentrations in biological tissue homogenates and fluids were obtained by colorimetric analysis of diazotized methocarbamol. Blood ethanol concentration was 135 mg/dL (0.135% w/v) and urine ethanol was 249 mg/dL (0.249% w/v). Methocarbamol concentrations were: blood, 257 ug/mL; bile, 927 ug/L; urine, 255 ug/L; gastric, 3.7 g; liver, 459 ug/g; and kidney, 83 ug/g. The combination of ethanol and carbamates is contraindicated since acute alcohol intoxication combined with carbamate usage can lead to combined central nervous system depression as a result of the interactive sedative-hypnotic properties of the compound|.../Methocarbamol/ is capable of inducing hepatic microsomal enzymes that metabolize warfarin in animals.|Imipramine enhances CNS effect of.../methocarbamol/ in animals...|Methocarbamol may inhibit the effects of pyridostigmine bromide. Use with caution in patients with myasthenia gravis receiving anticholinesterase agents.

Methocarbamol is 46-50% protein bound in healthy patients and 47.3-48.9% protein bound in hemodialysis patients.

Methocarbamol's production and use as an muscle relaxant in humans and animals(1) 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 51(SRC), determined from a log Kow of 0.61(2) and a regression-derived equation(3), indicates that methocarbamol is expected to have high mobility in soil(SRC). Volatilization of methocarbamol from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 6.5X10-16 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Methocarbamol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.4X10-7 mm Hg(SRC), determined from a fragment constant method(5). Methocarbamol is not expected to readily biodegrade in the environment based on the results of a Japanese MITI test where methocarbamol reached 4% of its theoretical BOD in activated sludge after 4 weeks(6).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 51(SRC), determined from a log Kow of 0.61(2) and a regression-derived equation(3), indicates that methocarbamol is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 6.5X10-16 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 1.7(SRC), from its log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Methocarbamol is not expected to readily biodegrade in the environment based on the results of a Japanese MITI test where methocarbamol reached 4% of its theoretical BOD in activated sludge after 4 weeks(7).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), methocarbamol, which has an estimated vapor pressure of 3.4X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase methocarbamol is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 8.5 hours(SRC), calculated from its rate constant of 4.5X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase methocarbamol may be removed from the air by wet or dry deposition(SRC). Methocarbamol does not contain chromophores that absorb at wavelengths >290 nm(4) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of methocarbamol with photochemically-produced hydroxyl radicals has been estimated as 4.5X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 8.5 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Methocarbamol contains hydrolyzable functional groups(2), however, using a structure estimation method, the base-catalyzed second-order hydrolysis half-life was estimated to be greater than 1 year(3). Therefore, hydrolysis is not expected to be an important fate process(SRC). Methocarbamol does not contain chromophores that absorb at wavelengths >290 nm(2) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 1.7 was calculated for methocarbamol(SRC), using a log Kow of 0.61(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Koc of methocarbamol is estimated as 51(SRC), using a log Kow of 0.61(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that methocarbamol is expected to have high mobility in soil.

The Henry's Law constant for methocarbamol is estimated as 6.5X10-16 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that methocarbamol is expected to be essentially nonvolatile from water surfaces(2). Methocarbamol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.4X10-7 mm Hg(SRC), determined from a fragment constant method(3).

While data specific to methocarbamol were not located(SRC, 2008), 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).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 9,546 workers (8,341 of these are female) are potentially exposed to methocarbamol in the US(1). Occupational exposure to methocarbamol may occur through inhalation of dust and dermal contact with this compound at workplaces where methocarbamol is produced or used. Exposure to methocarbamol among the general population may be limited to those administered the drug (Robaxin), a muscle relaxant(SRC).

Methocarbamol tablets and intramuscular injections are indicated in the United States as an adjunct to rest, physical therapy, and other measures for the relief of discomforts associated with acute, painful musculoskeletal conditions. Oral methocarbamol in America may be given up to 1500mg 4 times daily for 2-3 days. In Canada, methocarbamol containing oral formulations are sold over the counter for pain associated with muscle spasm. However, if these combination formulations include codeine, they are prescription only.|FDA Label

Methocarbamol is a commonly used, centrally acting muscle relaxant and has not been linked to instances of liver injury.

Autonomic Agents: Muscle Relaxants, Central

Muscle Relaxants, Central|Skeletal muscle relaxants are indicated as adjunts to other measures, such as rest and physical therapy, for the relief of muscle spasm associated with acute, painful musculoskeletal conditions. /Included in US product label/|Methcarbamol is also FDA-approved for control of the neuromuscular manifestations of tetanus. However it has largely been replaced in the treatment of tetanus by diazepam, or, in severe cases a neuromuscular blocking agent such as pancuronium. Such therapy is used as an adjunct to other measures, such as debridement, tetanus antitoxin, penicillin, tracheotomy, fluid and electrolyte replacement, and supportive treatment.|VET: In dogs, cats, and horses, methocarbamol is indicated as adjunct therapy of acute inflammatory and traumatic conditions of skeletal muscle and to reduce muscle spasms.|For more Therapeutic Uses (Complete) data for METHOCARBAMOL (6 total), please visit the HSDB record page.

The most frequent adverse effects of methocarbamol are drowsiness, dizziness, and lightheadedness. Blurred vision, headache, fever, and nausea may occur after oral, IM, or IV administration of the drug. Anorexia has been reported after oral administration. Adynamic ileus occurred in one patient who received a total of 10 g of methocarbamol orally. Metallic taste, GI upset, nystagmus, diplopia, flushing, vertigo, mild muscular incoordination, syncope, hypotension, and bradycardia have occurred in patients receiving the drug IM or IV.|Allergic reactions such as urticaria, pruritus, rash, skin eruptions, and conjunctivitis with nasal congestion may occur in patients receiving methocarbamol. Anaphylactic reactions have occurred following IM or IV administration of the drug. Although most patients with methocarbamol-induced syncope recover with supportive treatment, epinephrine, corticosteroids, and/or antihistamines have been used to increase the rate of recovery in some of these patients.|When methocarbamol is administered IV, thrombophlebitis, sloughing, and pain at the injection site may result from extravasation. IM injection of the drug may also cause local irritation. IV injection of methocarbamol may cause a small amount of hemolysis and increased hemoglobin and red blood cells in the urine. Leukopenia may occur rarely.|Parenteral dosage forms should be used with caution in patients with epilepsy.|For more Drug Warnings (Complete) data for METHOCARBAMOL (14 total), please visit the HSDB record page.

The subjective and behavioral effects of po administered methocarbamol, lorazepam and placebo were studied in a nonresidential group of adult male volunteers with histories of recreational substance abuse including sedative/hypnotics. In the first phase of the investigation, a dose run-up of methocarbamol (up to 12 g) was conducted in six subjects to determine appropriate doses. In the second phase, a randomized block cross-over study using 14 subjects was conducted. The following drug conditions were tested in the cross-over phase: placebo, lorazepam 1, 2 and 4 mg, and methocarbamol 2.25, 4.5 and 9 g. Drug conditions were tested under double-blind conditions. Psychomotor and cognitive performance measures and subject- and observer-rated behavioral responses were measured daily before dosing and for 5.5 hr after drug administration. The results showed that both lorazepam and methocarbamol produced statistically significant dose-related increases in subjects' ratings of drug effect and liking, although only lorazepam increased morphine-benzedrine group (MGB) scale scores. Methocarbamol also increased ratings on measures indicating the emergence of dysphoric and other side effects at high doses. Both drugs impaired psychomotor and cognitive performance, with lorazepam generally producing greater effects than methocarbamol. The results indicate that methocarbamol, at doses well above those used therapeutically, has some potential to be abused by persons with histories of sedative/hypnotic abuse; however, this potential for abuse is probably decreased by the accompanying side effects at high doses and is probably less than that of lorazepam.

Methacarbamol is a skeletal muscle relaxant with an unknown mechanism of action. Methacarbamol has been shown to block spinal polysynaptic reflexes, decrease nerve transmission in spinal and supraspinal polysynaptic pathways, and prolong the refractory period of muscle cells. Methocarbamol does not act as a local anesthetic upon injection. In animal studies, methocarbamol also prevents convulsions after electric shock.

A heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358) (See all compounds classified as Muscle Relaxants, Central.)

The time to maximum concentration is 1.1 hours for both healthy patients and those on hemodialysis. The maximum plasma concentration is 21.3mg/L for healthy patients and 28.7mg/L in hemodialysis patients. The area under the curve for healthy patients is 52.5mg/L\*hr and 87.1mg/L*hr in hemodialysis patients. AUC% based on terminal elimination half life is 2% for healthy patients and 4% for hemodialysis patients. Older studies report maximum plasma concentrations in 0.5 hours.|In humans the majority of the dose is eliminated in the urine. In dogs, 88.85% of the dose is eliminated in urine and 2.14% in the feces. In rats, 84.5-92.5% of the dose is eliminated in the urine and 0-13.3% is eliminated in the feces.|Volume of distribution data in humans is scarce. In horses, the volume of distribution is 515-942mL/kg at steady state or 724-1130mL/kg.|0.2-0.8L/h/kg.|Methocarbamol is rapidly and almost completely absorbed from the GI tract. Blood or serum concentrations of methocarbamol required for sedative, skeletal muscle relaxant, or toxic effects are not known.|Following oral administration of a single dose of methocarbamol, peak blood or serum concentrations of the drug appear to be attained in approximately 1-2 hours; the onset of action is usually within 30 minutes. Data from an unpublished study indicate that peak blood concentrations (measured as total carbamates and expressed in terms of methocarbamol) average 16.5 mcg/mL following a single 2-g oral dose, while data from a published study (using an assay relatively specific for methocarbamol) indicate that peak serum concentrations average 29.8 mcg/mL following the same dose. Data from the unpublished study also indicate that after IV administration of 1 g of methocarbamol at a rate of 300 mg/minute, blood concentrations of 19 mcg/mL are attained immediately and that the onset of action is almost immediate.|In dogs, methocarbamol is widely distributed, with highest concentrations attained in the kidney and liver; lower concentrations are attained in the lungs, brain, and spleen, and low concentrations are attained in heart and skeletal muscle.|The drug and/or its metabolites cross the placenta in dogs. It is not known if methocarbamol is distributed into milk in humans.|For more Absorption, Distribution and Excretion (Complete) data for METHOCARBAMOL (8 total), please visit the HSDB record page.

Methocarbamol is metabolized in the liver by demethylation to 3-(2-hydroxyphenoxy)-1,2-propanediol-1-carbamate or hydroxylation to 3-(4-hydroxy-2-methoxyphenoxy)-1,2-propanediol-1-carbamate. Methocarbamol and its metabolites are conjugated through glucuronidation or sulfation.|Methocarbamol is extensively metabolized, presumably in the liver, by dealkylation and hydroxylation.|Based on limited data, about 10-15% of a single oral dose is excreted in urine as unchanged drug, about 40-50% as the glucuronide and sulfate conjugates of 3-(2-hydroxyphenoxy)-1,2-propanediol-1-carbamate and 3-(4-hydroxy-2-methoxyphenoxy)-1,2-propanediol-1-carbamate, and the remainder as unidentified metabolites.|In dogs, rats and in man, methocarbamol gave p-hydroxymethocarbamol and o-demethylation product. All three substances were excreted in urine as glucuronic acid and ester sulfate conjugates.|Permethylation and g.l.c.-mass spectrometric analysis of bile from an isolated rat liver perfusion to which methocarmol was added showed seven components not present in control bile: methocarbamol, glucuronides of methocarbamol and desmethyl-methocarbamol, and four glucuronides of hydroxylated methocarbamol metabolites. 2. An interesting rearrangement of a methyl group has been found in the mass spectrum of 3-(2-methoxyphenyloxy)-1,2-dimethoxypropane, the permethylation product from methocarbamol.

The elimination half life is 1.14 hours in healthy subjects and 1.24 hours in subjects with renal insufficiency. Older studies report half lives of 1.6-2.15 hours.|Methocarbamol has a serum half-life of 0.9-1.8 hours.|... Pharmacokinetics of methocarbamol were studied in eight healthy, adult horses after intravenous (iv) and oral administration of large dosages. ... Plasma methocarbamol concentration declined very rapidly during the initial or rapid disposition phase after iv administration; the terminal elimination half-life ranged from 59 to 90 mins. ...|/Investigators/ determined plasma methocarbamol concentrations over 24 hr following a 1.5 g methocarbamol dose (off-dialysis day) to 8 chronic hemodialysis patients and compared these results to those from 17 healthy male volunteers. The harmonic mean elimination half-life was similar between the two groups, 1.24 and 1.14 hr, respectively. ...

The mechanism of action of methocarbamol is thought to be dependant on its central nervous system depressant activity. This action may be mediated through blocking spinal polysynaptic reflexes, decreasing nerve transmission in spinal and supraspinal polysynaptic pathways, and prolonging the refractory period of muscle cells. Methocarbamol has been found to have no effect on contraction of muscle fibres, motor end plates, or nerve fibres.|Precise mechanism of action has not been determined. These agents act in the central nervous system (CNS) rather than directly on skeletal muscle. Several of these medications have been shown to depress polysynaptic reflexes preferentially. The muscle relaxant effects of most of these agents may be related to their CNS depressant (sedative) effects. /Skeletal Muscle Relaxants/

Emergency and supportive measures: Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat coma, hypothermia, hypotension, and pulmonary edema if they occur. Hypotension usually responds promptly to supine position and intravenous fluids. Monitor patients for at least 6 hours after ingestion, because delayed absorption may occur. /Skeletal muscle relaxants/|The usefulness of forced diuresis or hemodialysis in treating overdose has not been determined.|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/|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/|Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ Methocarbamol, a compound related to mephenesin, has in vitro hemolytic potential. A study was performed to determine whether any hemolysis was detectable after intravenous injection. Methocarbamol and its vehicle (50% polyethylene glycol-300) was compared with vehicle alone and with normal saline controls in high- and low-dose regimens in normal volunteers. Significant increases in plasma hemoglobin were detected 30 min after intravenous injection of methocarbamol or its vehicle alone. Maximum initial plasma hemoglobin levels were approximately 10 mg/dL with vehicle alone, but only 4 mg/dL with the methocarbamol added. Serum haptoglobin levels fell after both high-dose methocarbamol and vehicle during the 3-day period of treatment. Hemolysis, though detectable, did not exceed levels found under physiologic circumstances such as exercise, and represents only a small fraction of the normal daily hemolysis of aged erythrocytes.|/SIGNS AND SYMPTOMS/ Limited information is available on the acute toxicity of methocarbamol. Extreme drowsiness reportedly occurred in one adult who ingested 22-30 g of the drug; treatment was symptomatic and recovery was uneventful. Another adult survived an ingestion of 30-50 g; the principal symptom was drowsiness.|/CASE REPORTS/ A case is presented of a fatal drug interaction caused by ingestion of methocarbamol (Robaxin) and ethanol. ... Therapeutic concentrations of methocarbamol are reported to be 24 to 41 ug/mL. Biological fluids were screened for ethanol ... and quantitated by gas-liquid chromatography (GLC). Determination of methocarbamol concentrations in biological tissue homogenates and fluids were obtained by colorimetric analysis of diazotized methocarbamol. Blood ethanol concentration was 135 mg/dL (0.135% w/v) and urine ethanol was 249 mg/dL (0.249% w/v). Methocarbamol concentrations were: blood, 257 ug/mL; bile, 927 ug/L; urine, 255 ug/L; gastric, 3.7 g; liver, 459 ug/g; and kidney, 83 ug/g. The combination of ethanol and carbamates is contraindicated since acute alcohol intoxication combined with carbamate usage can lead to combined central nervous system depression as a result of the interactive sedative-hypnotic properties of the compounds.|/OTHER TOXICITY INFORMATION/ The mean elimination half-life of methocarbamol in elderly healthy volunteers was slightly prolonged and the fraction of bound methocarbamol was slightly decreased compared to younger healthy volunteers.

Carbamate, Guaiphenesin

Oral /formulations/: Tablets 500 mg methocarbamol, (Global, Sandoz, United Research, Watson, West-Ward); 750 mg methocarbamol Tablets, (Global, Sandoz, United Research, Watson, West-Ward); Tablets, film-coated 500 mg Robaxin with povidone and propylene glycol, (Schwarz); 750 mg Robaxin with povidone and propylene glyco), (Schwarz); Parenteral Injection 100 mg/mL Robaxin with 50% polyethylene glycol 300, (Baxter).|METHOCARBAMOL, NF (ROBAXIN) TABLETS, 500 & 750 MG; INJECTION, 1 G/10 ML. /FROM TABLE/

1,2-Propanediol, 3-(2-methoxyphenoxy)-, 1-carbamate: ACTIVE

THIN LAYER CHROMATOGRAPHY; DAVIS, TW MCCONNELL, J CHROMATOGR 29, 286 (1967).|LIQUID CHROMATOGRAPHY FOR DETERMINATION IN PHARMACEUTICAL PREPARATIONS.|Analyte: methocarbamol; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards|Analyte: methocarbamol; matrix: chemical identification; procedure: ultraviolet absorption spectrophotometry with comparison to standards|For more Analytic Laboratory Methods (Complete) data for METHOCARBAMOL (7 total), please visit the HSDB record page.

Analyte: methocarbamol; matrix: blood (plasma); procedure: high-performance liquid chromatography with ultraviolet detection at 272 nm|Analyte: methocarbamol; matrix: blood (serum), urine; procedure: high-performance liquid chromatography with ultraviolet detection at 280 nm and atmospheric pressure ionization-mass spectrometric confirmation; limit of detection: 200 ng/mL (serum); 700 ng/mL (urine)|Analyte: methocarbamol; matrix: blood (whole, plasma); procedure: high-performance liquid chromatography with ultraviolet detection at 223 nm; limit of detection: <120 ng/mL|Analyte: methocarbamol; matrix: blood (serum), urine; procedure: high-performance liquid chromatography with ultraviolet detection at 280 nm; limit of detection: 10 ng/mL

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