Methylprednisolone

Pharmaceuticals -> Listed in ZINC15

Pharmaceuticals -> Steroids

1.5

2.12

Crystals

White to practically white crystalline powder

MW 416.51, crystals, MP 205-208 °C, specific optical rotation: 101 deg at 20 °C (dioxane), uv max (95% ethanol): 243 nm (alpha m 14825), Sol in dioxane; sparingly sol in acetone, alcohol, chloroform, methanol; slightly sol in ether. Practically insol in water. /21-acetate/

SOL IN WATER /METHYLPREDNISOLONE 21-SUCCINATE SODIUM SALT/

Sparingly sol in alc, dioxane, methanol; slightly sol in acetone, chloroform; very slightly sol in ether.

In water, 1.20X10+2 mg/L at 25 °C

1.09e-01 g/L

Breast Feeding; Lactation; Milk, Human; Corticosteroids, Systemic; Glucocorticoids; Anti-Inflammatory Agents

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Hormones and antihormones

Active Ingredients (Methylprednisolone) -> FDA Greenbook

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

228-237 °C

232.5 °C

This chemical does not meet GHS hazard criteria for 0.9% (1 of 110) of reports.

Danger

H302 (16.4%): Harmful if swallowed [Warning Acute toxicity, oral]

P203, P260, P264, P270, P280, P301+P317, P302+P352, P317, P318, P319, P321, P330, P362+P364, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 110 reports by companies from 15 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Status: Active Update: 22-11-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/16624

Methylprednisolone: Does not have an individual approval but may be used under an appropriate group standard

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl methylprednisolone approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl methylprednisolone acetate approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Methylprednisolone acetate/

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl methylprednisolone sodium succinate approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Methylprednisolone sodium succinate/

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. Methylprednisolone is included on this list.

For more FDA Requirements (Complete) data for METHYLPREDNISOLONE (7 total), please visit the HSDB record page.

Commercially available preparations of methylprednisolone should be stored at a temperature less than 40 °C, preferably between 15-30 °C; freezing of methylprednisolone acetate sterile suspension should be avoided. Unreconstituted methylprednisolone sodium succinate sterile powder and reconstituted solutions of the drug, and methylprednisolone sodium acetate solution for injection should be stored at a controlled room temperature of 20-25 °C.

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.

PHENYTOIN IS ... KNOWN TO INCR METABOLISM OF ... METHYLPREDNISOLONE IN HUMANS.

SYSTEMIC EFFECTS OF ADMIN CORTICOSTEROIDS /METHYLPREDNISOLONE/ ... MAY BE DIMINISHED BY LARGE DOSES OF BARBITURATES SUCH AS PHENOBARBITAL.

HYPERGLYCEMIC ACTION OF CORTISONE /METHYLPREDNISOLONE/ MAY OFFSET HYPOGLYCEMIC ACTION OF CHLORPROPAMIDE.

Methylprednisolone clearance was reduced in asthmatic patients also taking troleandomycin.

For more Interactions (Complete) data for METHYLPREDNISOLONE (25 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 310(SRC), determined from a water solubility of 1.2X10+2 mg/L(2) and a regression-derived equation(3), indicates that methylprednisolone is expected to have moderate mobility in soil(SRC). Volatilization of methylprednisolone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.6X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Methylprednisolone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.9X10-14 mm Hg(SRC), determined from a fragment constant method(5). Biodegradation data for methylprednisolone were not available(SRC, 2007).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 310(SRC), determined from a water solubility of 1.20X10+2 mg/L(2) and a regression-derived equation(3), indicates that methylprednisolone is 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 3.6X10-8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 41(SRC), from its water solubility(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). Biodegradation data for methylprednisolone were not available(SRC, 2007).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), methylprednisolone, which has an estimated vapor pressure of 3.9X10-14 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 methylprednisolone may be removed from the air by wet or dry deposition(SRC). Methylprednisolone absorbs UV light at a maximum of 243 nm(3) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

The significant adverse effects of glucocorticoids stem from their hormonal actions, which can result in iatrogenic Cushing syndrome. Facial rounding, puffiness, fat deposition, and plethora (moon facies) are usually apparent. Fat redistributes from the extremities to the trunk, the back of the neck, and the supraclavicular fossae. Fine hair grows more quickly on the face, thighs, and trunk. Steroid-induced punctate acne may appear, and insomnia and increased appetite may be observed. With concurrent use of methylprednisolone, protein catabolism continues, diverting amino acids to glucose production, thus increasing the need for insulin and resulting in weight gain. Myopathy and muscle wasting can occur, as well as skin thinning, with striae and bruising. Hyperglycemia and osteoporosis can develop, as well as diabetes and aseptic necrosis of the hip.

The Koc of methylprednisolone is estimated as 310(SRC), using a water solubility of 1.20X10+2 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that methylprednisolone is expected to have moderate mobility in soil.

/SIGNS AND SYMPTOMS/ Glucocorticoids may cause fetal damage when administered to pregnant women. One retrospective study of 260 women who received pharmacologic dosages of glucocorticoids during pregnancy revealed 2 instances of cleft palate, 8 stillbirths, 1 spontaneous abortion, and 15 premature births. Another study reported 2 cases of cleft palate in 86 births. Occurrence of cleft palate in these studies is higher than in the general population but could have resulted from the underlying diseases as well as from the steroids. Other fetal abnormalities that have been reported following glucocorticoid administration in pregnant women include hydrocephalus and gastroschisis. Women should be instructed to inform their physicians if they become or wish to become pregnant while receiving glucocorticoids. If glucocorticoids must be used during pregnancy or if the patient becomes pregnant while taking one of these drugs, the potential risks should be carefully considered. /Corticosteroids/

/CASE REPORTS/ A 16-year-old poorly compliant, steroid-dependent subject with asthma received two courses of high-dose intravenous methylprednisolone during a 3-week period, followed by a tapering schedule of oral prednisone. During this time, she was exposed to chickenpox. She subsequently developed a classic varicella rash, sever back pain, rapidly progressive hepatic failure, pneumonitis, and encephalopathy. Death ensued 3 days after the onset of the rash. Evidence of disseminated varicella infection was confirmed at autopsy. This case illustrates that a small number of subjects with severe asthma receiving high-dose corticosteroids need to be considered as a separate, high-risk group for developing disseminated varicella. We recommend that the immune status of these patients to varicella-zoster virus be assessed by a serum titer. If these patients are nonimmune, they would be candidates for varicella-zoster immune globulin on exposure, and for acyclovir therapy should varicella dissemination occur.

/CASE REPORTS/ Two patients with recalcitrant ocular hypertension persisting 6 and 4 months, respectively, after periocular injection of methylprednisolone acetate despite maximum medical therapy /were described/. White sub-Tenon's plaques of residual methylprednisolone acetate were excised surgically and analyzed for steroid activity using spectrophotometry. In both cases, intraocular pressure was normalized promptly after surgical removal of visible steroid. In both instances, biochemical analysis of the excised samples revealed residual steroid. Surgical removal of a residual methylprednisolone depot is an effective management choice in patients developing persistent intraocular pressure elevation after periocular injection. /Methylprednisolone acetate/

/CASE REPORTS/ A 47-year-old woman was admitted to our clinic with weakness, fatigue, pruritus, and scleral icterus that had developed 10 days prior to presentation. She had been taking topiramate for one year for treatment of chronic isolated central nervous system vasculitis. One week before her symptoms developed, she had completed a self-prescribed 7 day course of oral methylprednisolone for treatment of left arm weakness. She believed that methylprednisolone was appropriate since it had been used previously for acute episodes of vasculitis. Results of liver function tests performed on admission were alanine aminotransferase 2478 U/L, aspartate aminotransferase 1600 U/L, total bilirubin 10 mg/dL, direct bilirubin 8 mg/dL, alkaline phosphatase 138 U/L, and gamma-glutamyl transferase 242 U/L. Topiramate and methylprednisolone were the only drugs she had been taking before admission, and no other causes of liver dysfunction (eg, infection, ischemia, systemic disease) were identified. Topiramate was stopped, and enzyme levels decreased to normal values within 45 days without treatment. There had been no increase in enzyme levels during hospitalization upon the accidental use of topiramate. Based on the history and laboratory findings, the final diagnosis was mixed hepatocellular and cholestatic liver injury caused by methylprednisolone. DISCUSSION: Steroids have rarely been associated with hepatotoxicity; moreover, they are the treatment of choice for severe hepatitis. To date, only 2 cases of methylprednisolone-induced hepatotoxicity have previously been reported. Our case is similar to those with regard to mixed hepatocellular and cholestatic liver injury. Resolution of the hepatotoxicity occurred after discontinuation of the drug, with conservative treatment measures. An objective causality assessment based on the Naranjo scale suggests that hepatotoxicity was probably related to methylprednisolone. Although rare, hepatotoxicity related to methylprednisolone should be considered in patients who develop elevated enzyme levels while receiving this steroid.

For more Human Toxicity Excerpts (Complete) data for METHYLPREDNISOLONE (12 total), please visit the HSDB record page.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Methylprednisolone

vLess-DILI-concern

3

Adverse reactions

DOI:10.1016/j.drudis.2016.02.015

An estimated BCF of 41 was calculated for methylprednisolone(SRC), using a water solubility of 1.20X10+2 mg/L(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 Henry's Law constant for methylprednisolone is estimated as 3.6X10-8 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that methylprednisolone is expected to be essentially nonvolatile from water surfaces(2). Methylprednisolone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.9X10-14 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Repeated dose toxicity studies were carried out with methylprednisolone in dogs using daily oral doses of 0, 2.5 and 5 mg/kg body weight/day for 42 days and daily intramuscular administration of 1.1 to 1.5 mg/kg body weight/day methylprednisolone for 5 weeks. In a special study to investigate adrenal gland function, groups of dogs were dosed orally with 2 or 4 mg/day or intramuscularly with 2.5 mg/kg body weight once a week. The main effects in these studies were reduced body weight, skeletal muscle atrophy, increased glycogen deposition in the liver and adrenal atrophy.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ A 14 week repeated dose toxicity study was carried out in Sprague-Dawley rats given daily subcutaneous doses of 0, 0.4, 4, 40 or 400 ug/kg body weight/day of methylprednisolone aceponate. Body weight gain and food consumption were reduced in males given 40 ug/kg body weight and above and females given 400 ug/kg body weight and above. Leucocyte counts were reduced in both sexes given 400 ug/kg body weight and bone marrow lymphocytes were reduced in males given 400 ug/kg body weight and females given 4 ug/kg body weight and above. Changes in serum clinical chemistry values at 400 ug/kg were indicative of effects on the liver and kidney. Atrophy of the thymus and adrenal glands was observed in the 400 ug/kg body weight group at necropsy. The NOEL was 0.4 ug/kg body weight/day. /Methylprednisolone aceponate/

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A 52 week repeated-dose toxicity study was carried out in the Sprague Dawley rat using subcutaneous doses of 0, 0.16, 0.8, 4, 20 or 100 ug/kg body weight methylprednisolone aceponate. At 100 ug/kg body weight, the main effects were reduced body weight and food consumption, reduced erythrocyte, hematocrit and lymphocyte counts and atrophy of the spleen and adrenals. At 20 ug/kg body weight, body weight gain and food consumption were reduced and there were some minor effects on oran weight and clinical chemistry values. The NOEL was 4 ug/kg body weight/day. /Methylprednisolone aceponate/

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ A fertility study of methylprednisolone aceponate, anti-inflammatory corticosteroid, was performed using Jcl:SD rats at doses of 0.004, 0.02 and 0.1 mg/kg body wt. Methylprednisolone aceponate was administered sc to male rats from 60 days before mating until successful copulation, and to female rats from 14 days before mating until day 7 of gestation. On day 21 of gestation, all dams were killed and their fetuses were examined for external, internal and skeletal abnormalities. The following results were obtained. Suppression of body wt gain and food consumption, and increase in dead embryos and fetuses were observed in the 0.02 and 0.1 mg/kg groups. From the above results, the no-effect dose of methylprednisolone aceponate was estimated to be 0.004 mg/kg body wt for general toxicity in parent animals, 0.1 mg/kg body wt for reproductive toxicity in parent animals, and 0.004 mg/kg body wt for developmental toxicity in the fetuses. /Methylprednisolone aceponate/

For more Non-Human Toxicity Excerpts (Complete) data for METHYLPREDNISOLONE (9 total), please visit the HSDB record page.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl methylprednisolone approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl methylprednisolone acetate approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Methylprednisolone acetate/

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl methylprednisolone sodium succinate approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Methylprednisolone sodium succinate/

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. Methylprednisolone is included on this list.

For more FDA Requirements (Complete) data for METHYLPREDNISOLONE (7 total), please visit the HSDB record page.

H02AB04

D - Dermatologicals

D - Dermatologicals

H - Systemic hormonal preparations, excl. sex hormones and insulins

QD - Dermatologicals

QD - Dermatologicals

Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections.

The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.

Glucocorticoids are capable of suppressing the inflammatory process through numerous pathways. They interact with specific intracellular receptor proteins in target tissues to alter the expression of corticosteroid-responsive genes. Glucocorticoid-specific receptors in the cell cytoplasm bind with steroid ligands to form hormone-receptor complexes that eventually translocate to the cell nucleus. There these complexes bind to specific DNA sequences and alter their expression. The complexes may induce the transcription of mRNA leading to synthesis of new proteins. Such proteins include lipocortin, a protein known to inhibit PLA2a and thereby block the synthesis of prostaglandins, leukotrienes, and PAF. Glucocorticoids also inhibit the production of other mediators including AA metabolites such as COX, cytokines, the interleukins, adhesion molecules, and enzymes such as collagenase. /Glucocorticoids/

Methylprednisolone has a half life of 2.3h.

IV HALF-LIFE IS APPROX 80 MIN IN DOGS.

PLASMA HALF-LIFE IS 3-4 HR.

SINGLE DOSE STUDY OF 12 NORMAL MALE VOLUNTEERS. HALF-LIFE OF 2.39 HR.

The metabolism of methylprednisolone is thought to be mostly mediated by 11beta-hydroxysteroid dehydrogenases and 20-ketosteroid reductases.

METAB OF 6ALPHA-METHYLPREDNISOLONE NA SUCCINATE IN RATS; METABOLITES; 6ALPHA-METHYLPREDNISOLONE, 6ALPHA-METHYL-11BETA,17ALPHA,20BETA- TRIHYDROXY-1,4-PREGNADIEN-3-ONE,21-OIC ACID, & 6ALPHA-METHYL-11BETA,17ALPHA,20,21-TETRAHYDROXY-1,4-PREGNADIEN-3-ONE 21-SUCCINATE.

Prednisone, prednisolone, and methylprednisolone are currently administered in association with cyclosporin A in the postoperative treatment of transplant patients. The aim of this work was to evaluate the effects of these corticosteroids on the expression of several forms of cytochromes p450, including p450 1A2, 2D6, 2E1, and 3A, and on cyclosporin A oxidase activity in human liver. For this purpose, human hepatocytes prepared from lobectomies were maintained in culture in a serum-free medium, in collagen-coated dishes, for 96-144 hr, in the absence or presence of 50-100 uM corticosteroids, rifampicin, or dexamethasone. To mimic more closely the current clinical protocol, hepatocyte cultures were also co-treated with corticosteroids and cyclosporin A or ketoconazole (a selective inhibitor of cytochromes p450 3A). Cyclosporin A oxidase activity, intracellular retention of cyclosporin A oxidized metabolites within hepatocytes, accumulation of cytochromes p450 proteins and corresponding messages, and de novo synthesis and half-lives of these cytochromes p450 were measured in parallel in these cultures. Our results, obtained from seven different hepatocyte cultures, showed that 1) dexamethasone and prednisone, but not prednisolone or methylprednisolone, were inducers of cytochrome p450 3A, at the level of protein and mRNA accumulation, as well as of cyclosporin A oxidase activity, known to be predominantly catalyzed by these cytochromes p450; 2) although corticosteroids are known to be metabolized in human liver, notably by cytochrome p450 3A, partial or total inhibition of this cytochromes p450 by cyclosporin or ketoconazole, respectively, did not affect the inducing efficiency of these molecules; 3) corticosteroids did not affect the half-life of cytochrome p450 3A or the accumulation of other forms of cytochromes p450, including 1A2, 2D6, and 2E1; 4) chronic treatment of cells with cyclosporin did not affect cytochrome p450 3A accumulation; 5) corticosteroids were all competitive inhibitors of cyclosporin A oxidase in human liver microsomes, with Ki values of 61 + or - 12, 125 + or - 25, 190 + or - 38, and 210 + or - 42 uM for dexamethasone, prednisolone, prednisone, and methylprednisolone, respectively; and 6) chronic treatment of cells with corticosteroids did not influence the excretion of oxidized metabolites of cyclosporin from the cells.

X4W7ZR7023

METHYLPREDNISOLONE

Established Pharmacologic Class [EPC] - Corticosteroid

Mechanisms of Action [MoA] - Corticosteroid Hormone Receptor Agonists

Methylprednisolone is a Corticosteroid. The mechanism of action of methylprednisolone is as a Corticosteroid Hormone Receptor Agonist.

METHYLPREDNISOLONE

Substances that reduce or suppress INFLAMMATION.

Drugs used to prevent NAUSEA or VOMITING.

A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.

Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.

Oral methylprednisolone has 89.9% the bioavailability of oral methylprednisolone acetate, while rectal methylprednisolone has 14.2% the bioavailability. Intravitreal methylprednisolone has a Tmax of 2.5h. Approximately 1/10 of an oral or IV dose of methylprednisolone will reach the vitreous humor. Further data regarding the absorption of methylprednisolone are not readily available.

Methylprednisolone and its metabolites have been collected in urine in humans. A study in dogs showed 25-31% elimination in urine and 44-52% elimination in feces.

The average volume of distribution of methylprednisolone is 1.38L/kg.

The average plasma clearance of methylprednisolone is 336mL/h/kg.

ORAL ABSORPTION IN SINGLE-DOSE STUDY OF 12 NORMAL MALE VOLUNTEERS. MEAN BIOAVAIL AFTER ORAL ADMIN 89.9%, INDICATING BETTER SYSTEMIC AVAIL OF ESTER THAN ALC. AVG ELIMINATION RATE CONSTANT AFTER ORAL ADMIN OF ESTER & ALC 0.290 H-1, HALF-LIFE OF 2.39 HR.

The pharmacokinetics of methylprednisolone (MP) were studied in five normal subjects following intravenous doses of 20, 40 and 80 mg methylprednisolone sodium succinate (MPSS) and an oral dose of 20 mg methylprednisolone as 4 x 5 mg tablets. Plasma concentrations of MP and MPSS were measured by both high performance thin layer (h.p.t.l.c.) and high pressure liquid chromatography (h.p.l.c.). 2. The mean values (+/- s.d.) of half-life, mean residence time (MRT), systemic clearance (CL) and volume of distribution at steady state (Vss) of MP following intravenous administration were 1.93 +/- 0.35 h, 3.50 +/- 1.01 h, 0.45 +/- 0.12 lh-1 kg-1 and 1.5 +/- 0.63 1 kg-1, respectively. There was no evidence of dose-related changes in these values. The plasma MP concentration-time curves were superimposable when normalized for dose. 3. The bioavailability of methylprednisolone from the 20 mg tablet was 0.82 +/- 0.11 (s.d.). 4. In vivo hydrolysis of MPSS was rapid with a half-life of 4.14 +/- 1.62 (s.d.) min, and was independent of dose. In contrast, in vitro hydrolysis in plasma, whole blood and red blood cells was slow; the process continuing for more than 7 days. Sodium fluoride did not prevent the hydrolysis of MPSS.

Used to treat rheumatoid arthritis

Used in dogs and cats as an anti-inflammatory agent. /Medrol Tablets/

Used in dogs as an analgesic agent. /Cortoba Tablets/

Treatment of inflammation and related disorders in cats and dogs; treatment of allergic and dermatologic disorders in cats and dogs; and as supportive therapy to antibacterial treatment of severe infections in cats and dogs. Treatment of inflammation and related disorders in horses. /Depo-Medrol Sterile Aqueous Suspension/

For more Uses (Complete) data for METHYLPREDNISOLONE (9 total), please visit the HSDB record page.

Use (kg) in Switzerland (2009): >25

17,21-dihydroxy-6alpha-methylpregna-1,4-diene-3,11,20-trione; 11beta,17,21,21-tetrahydroxy-6alpha-methylpregna-1,4-diene-3,20-dione; 11beta-hydroxy-6alpha-methylandrosta-1,4-diene-3,17-dione; (E)- and (Z)-11beta,20-dihydroxy-6alpha-methylpregna-1,4,17(20)-triene-3,21-dione

(20RS)-11beta,17,20-trihydroxy-6alpha-methyl-3-oxopregna-1,4-diene-21-yl acetate; methylprednisolone; 11beta,17-dihydroxy-6alpha-methylpregna-1,4-diene-3,20,21-trione; 11beta-hydroxy-6alpha-methylpregna-1,4-diene-3,20,21-trione; prednisolone acetate; 6alpha-methyl-3,11,20-trioxopregna-1,4-dien-21-yl acetate; 11beta,17-dihydroxy-6alpha-methyl-3,20-dioxopregn-4-ene-21-yl acetate; 11beta-hydroxy-6alpha-methyl-3-oxopregna-1,4,17(20)-trien-21-yl acetate /methylprednisolone acetate/

methylprednisolone; 4-[(11beta,21-dihydroxy-6alpha-methyl-3,20-dioxopregna-1,4-dien-17-yl)oxy]-4-oxobutanoic acid (methylprednisolone 17-(hydrogen succinate)); methylprednisolone acetate; 4-[(11beta,17-dihydroxy-6alpha-methyl-3,20-dioxopregna-4-en-21-yl)oxy]-4-oxobutanoic acid (methylhydrocortisone 21-(hydrogen succinate)) /methylprednisolone hydrogen succinate/

Preparation: Sebek, Spero, US 2897218 (1959 to Upjohn); Gould, US 3053832 (1962 to Schering)

Cortisone is first converted to the 6-keto derivative via suitable intermediates. Subsequent Grignard reaction with methylmagnesium bromide and further reaction steps then yield 6a-methylprednisolone.

Oral: Tablets: 2 mg Medrol (scored), (Pfizer), 4 mg Medrol (scored), (Pfizer), Medrol Dosepak, (Pfizer), Meprolone Unipak, (Major), Methylprednisolone, (Barr), Methylprednisolone, (Par), Methylprednisolone, (Trigen); 8 mg Medrol (scored), (Pfizer), Methylprednisolone, (Par); 16 mg Medrol (scored), (Pfizer); 32 mg Medrol (scored), (Pfizer).

Parenteral: Injectable suspension: 20 mg/mL Depo-Medrol, (Pfizer); 40 mg/mL Depo-Medrol, (Pfizer), Methylprednisolone Acetate Injection, (Sicor), Methylprednisolone Acetate Injection, (Teva); 80 mg/mL Depo-Medrol, (Pfizer) Methylprednisolone Acetate Injection, (Sicor), Methylprednisolone Acetate Injection, (Teva). /Methylprednisolone acetate/

Parenteral: For injection: 40 mg (of methylprednisolone) A-methaPred ( with benzyl alcohol in Univial), (Hospira), Methylprednisolone Sodium Succinate Injection (with benzyl alcohol), (Abraxis) Solu-Medrol (with benzyl alcohol 8.8 mg in Act-O-Vial), (Pfizer); 125 mg (of methylprednisolone) A-methaPred (with benzyl alcohol in Univial), (Hospira), Methylprednisolone Sodium Succinate Injection (with benzyl alcohol), Abraxis Solu-Medrol (with benzyl alcohol 17.6 mg in Act-O-Vial), (Pfizer); 500 mg (of methylprednisolone) A-methaPred (with benzyl alcohol in Univial), (Hospira), A-methaPred ADD-Vantage, (Hospira) Solu-Medrol (with and without diluent containing benzyl alcohol 70.2 mg), (Pfizer); 1 g (of methylprednisolone) A-methaPred (with benzyl alcohol in Univial), (Hospira), A-methaPred ADD-Vantage, (Hospira), Methylprednisolone Sodium Succinate Injection (with benzyl alcohol), (Abraxis), Solu-Medrol (with benzyl alcohol 141 mg and with benzyl alcohol 66.8 mg in Act-O-Vial), (Pfizer); 2 g (of methylprednisolone) Solu-Medrol (with and without diluent containing benzyl alcohol 273 mg), (Pfizer). /Methylprednisolone sodium succinate/

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

Pregna-1,4-diene-3,20-dione, 11,17,21-trihydroxy-6-methyl-, (6.alpha.,11.beta.)-: INACTIVE

US REGULATIONS CURRENTLY LIMIT MILK RESIDUES @ 10 PPB.