히드로코르티손

Pharmaceuticals -> Steroids

Pharmaceuticals -> Listed in ZINC15

Pharmaceuticals -> Steroids

log Kow = 1.61

1.61

Plates from alc or iso-propyl alc

Crystalline, striated blocks from absolute ethanol or isopropanol

White, crystalline powder

Amorphous, hygroscopic, white powder. Mp 169.0-171.2 °C. Solubility in water: approx 500 mg/mL. Similarly soluble in methanol, ethanol,; sparingly soluble in chloroform. /21-Sodium succinate/

Solubilities in various solvents [Table#4538]

Soluble in concentrated sulfuric acid with intense green flourescence

Soluble in dioxane

In water, 320 mg/L at 25 °C

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

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

FDA approved drugs -> Active ingredient

EMA approved medicines: Human medicine

EMA approved medicines: Human medicine

EMA approved medicines: Human medicine

Active Ingredients (Hydrocortisone) -> FDA Greenbook

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

This chemical does not meet GHS hazard criteria for 1.1% (3 of 274) of reports.

Warning

H361 (86.5%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

P203, P260, P280, P318, P319, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 274 reports by companies from 34 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: Pregn-4-ene-3,20-dione, 11,17,21-trihydroxy-, (11.beta.)-

Status: Active Update: 06-12-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/14486

Hydrocortisone: 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 hydrocortisone valerate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Hydrocortisone Valerate/

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

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

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

For more FDA Requirements (Complete) data for HYDROCORTISONE (9 total), please visit the HSDB record page.

Commercially available preparations of hydrocortisone should be stored at a temperature less than 40 °C, preferably between 15-30 °C; freezing of the oral suspension and sterile suspensions should be avoided. Hydrocortisone tablets should be stored in well-closed containers. Reconstituted solutions of hydrocortisone sodium succinate should be stored at 25 °C or below.

Hydrocortisone (80 mg/kg body weight, intraperitoneally for 4 days), both alone and in combination with acetylsalicylic acid (160 mg/kg body weight, orally, for 4 days), decreased acetylsalicylic acid general and specific toxicity via metabolic modulation of drug-metabolizing enzyme systems (intestinal acetylsalicylic acid-esterase and hepatic UDP-glucuronyltransferase) and did not change the acetylsalicylic acid analgesic effect.

The effect of glucocorticoids on oral anticoagulant therapy is variable, and the efficacy of oral anticoagulants has been reported to be enhanced or diminished with concomitant glucocorticoid administration. Patients receiving glucocorticoids and oral anticoagulants concomitantly should be monitored (e.g., using coagulation indices) in order to maintain desired anticoagulant effect. /Corticosteroids/

Estrogens may potentiate effects of hydrocortisone, possibly by increasing the concentration of transcortin and thus decreasing the amount of hydrocortisone available to be metabolized.

Potassium-depleting diuretics (e.g., thiazides, furosemide, ethacrynic acid) and other drugs that deplete potassium, such as amphotericin B, may enhance the potassium-wasting effect of glucocorticoids. Serum potassium should be closely monitored in patients receiving glucocorticoids and potassium-depleting drugs. /Corticosteroids/

For more Interactions (Complete) data for HYDROCORTISONE (7 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 180(SRC), determined from a log Kow of 1.61(2) and a regression-derived equation(3), indicates that hydrocortisone is expected to have moderate mobility in soil(SRC). Volatilization of hydrocortisone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.8X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Hydrocortisone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.3X10-13 mm Hg(SRC), determined from a fragment constant method(5). Biodegradation data were not available(SRC, 2007).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 180(SRC), determined from a log Kow of 1.61(2) and a regression-derived equation(3), indicates that hydrocortisone 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 5.8X10-8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from its log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2007).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), hydrocortisone, which has an estimated vapor pressure of 1.3X10-13 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 hydrocortisone may be removed from the air by wet or dry deposition(SRC). Hydrocortisone does not absorb at wavelengths >290 nm(4) and therefore is not expected to be susceptible to direct photolysis by sunlight(5).

The Koc of hydrocortisone is estimated as 180(SRC), using a log Kow of 1.61(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that hydrocortisone is expected to have moderate mobility in soil.

/SIGNS AND SYMPTOMS/ Glucocorticoids should be used with caution in patients with seizure disorders, renal insufficiency, osteoporosis, or herpes simplex infections of the eye; some manufacturers state that glucocorticoids should not be used in patients with active ocular herpes simplex infections /SRP: due to the risk of corneal ulceration/. /Corticosteroids/

/CASE REPORTS/ A 66-year-old man who complained of generalized muscle weakness, shallow respiration, and palpitations after receiving high-dose intravenous hydrocortisone (total dose, 2400 mg over 4 days) to treat a severe asthma attack /is described/. During this therapy, there was a weight gain of 1.0 kg. An electrocardiogram revealed ventricular arrhythmia with frequent premature ventricular contractions. Hypokalemia was profound, with plasma potassium (K+) concentration of 1.7 mEq/L, and associated with renal potassium wasting, as evidenced by a transtubular potassium concentration gradient of 12; metabolic alkalosis (plasma hydrocortisone O3-, 37 mEq/L) was also present. When treated with spironolactone, KCl supplementation, and substitution of hydrocortisone with prednisolone, his plasma K+ concentration rapidly normalized, metabolic alkalosis was corrected, and arrhythmia disappeared within 3 days. Because of unwanted mineralocorticoid side-effects, high-dose hydrocortisone may cause life-threatening hypokalemia in asthmatic patients. Because of these potential risks, plasma acid-base and electrolyte concentrations should be monitored frequently in any patient treated with high-dose hydrocortisone.

/CASE REPORTS/ A 62-year-old asthmatic patient with evidence of aspirin sensitivity ... /was/ administered 100 mg of hydrocortisone-21-hemisuccinate dissolved in 100 mL 0.9% sodium chloride solution for perioperative corticoid substitution. The patient immediately developed severe bronchospasm and anaphylactic shock requiring intubation and mechanical ventilation. He received adrenaline, isoflurane, ketamine and inhalational fenoterol. He then developed atrioventricular block type III for which he was transcutaneously paced. Subsequently he was tested via skin prick tests, intracutaneous tests and IV-challenges resulting in the patient having positive reactions to hydrocortisone-21-hemisuccinate. /Hydrocortisone-21-hemisuccinate/

/CASE REPORTS/ Glucocorticoids may indirectly cause convulsions by the induction of electrolytes abnormalities, severe hypertension, or severe hyperglycemia. These agents may rarely cause convulsions by a direct toxicity to the central nervous system (CNS). We describe a 23-yr-old patient with Crohn's disease in whom generalized convulsions developed on two occasions while receiving intravenous hydrocortisone.

For more Human Toxicity Excerpts (Complete) data for HYDROCORTISONE (8 total), please visit the HSDB record page.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

hydrocortisone

DILI Negative

Oral

DOI:10.1016/j.drudis.2019.09.022

An estimated BCF of 3 was calculated in fish for hydrocortisone(SRC), using a log Kow of 1.61(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 Henry's Law constant for hydrocortisone is estimated as 5.8X10-8 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that hydrocortisone is expected to be essentially nonvolatile from water surfaces(2). Hydrocortisone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.3X10-13 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The effects of hydrocortisone during the prenatal period and its later repercussion on reproductive aspects of female rats /were investigated/. Pregnant rats were treated (s.c.) with hydrocortisone acetate, at 1.5 mg/day on the 17th, 18th, and 19th days of pregnancy. Although the present study was not intended to identify mechanisms of toxicity, the treatment with hydrocortisone in the last period of pregnancy presented no signs of toxicity. The efficacy of the hydrocortisone in reducing the adrenal wet mass and plasma corticosterone levels immediately after delivery in both the treated mothers and in respective pups at birth may indicate impairment of the hypothalamus-pituitary-adrenal axis. In addition, the treatment with hydrocortisone did not interfere in the development of the female descendants until puberty. However, it affected the estrous cycle and fertility. Probably, the prenatal exposure to corticosteroids had altered at least partially the hypothalamus-pituitary-gonadal axis, resulting in the damages observed in adult life. These results indicate that the use of the hydrocortisone at a dose that apparently does not endanger the neonate led to undesirable effects in the adult reproductive phase, resulting in later deleterious alteration of the reproductive physiology in female rats. /Hydrocortisone acetate/

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The aim of the present study was to investigate the effects of hydrocortisone during the prenatal period and its later repercussions on the fertility and sexual behavior of male rats. Pregnant rats were treated (sc) with hydrocortisone acetate, at 1.5 mg/day on the 17th, 18th, and 19th days of gestation. Decreased body weight and no alteration in anogenital distance were observed in male offspring. Adulthood, presented reductions of body weight, plasma testosterone levels, and seminal-vesicle wet weight without secretion as well as no alteration in the wet weights of the testes, epididymis, and seminal vesicle with secretion in the treated group. Males exposed to hydrocortisone during the prenatal period were able to mate with normal females, which became pregnant but exhibited an increased number of post-implantation losses. In spite of this, these treated males exhibited decreased male sexual behavior and the appearance of female sexual behavior after these male rats were castrated and pretreated with exogenous estrogen. These results indicate that exposure to hydrocortisone in the later stages of pregnancy may have a long-term effect on the fertility and sexual behavior of male rats, suggesting an incomplete masculinization and defeminization of the central nervous system.

Because cortisone has been reported rarely to increase blood coagulability and to precipitate intravascular thrombosis, thromboembolism, and thrombophlebitis, corticosteroids should be used with caution in patients with thromboembolic disorders. Glucocorticoids should be used with caution in patients with seizure disorders, renal insufficiency, osteoporosis, or herpes simplex infections of the eye; some manufacturers state that glucocorticoids should not be used in patients with active ocular herpes simplex infections. /Corticosteroids/

Because an apparent association has been suggested between use of corticosteroids and left ventricular free-wall rupture after a recent myocardial infarction, corticosteroids should be used with extreme caution in these patients. /Corticosteroids/

This study examined the hypothesis/ that subjects with posttraumatic stress disorder, as compared to nonpsychiatric controls, would show greater impairments in verbal declarative memory and working memory, but not attention, following exogenous glucocorticoid administration. ... The hydrocortisone administration led to impairment in working memory in the group of subjects with posttraumatic stress disorder, but not in the control subject group.

Hydrocortisone is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze readily under environmental conditions(1). Hydrocortisone does not absorb at wavelengths >290 nm(2) and therefore is not expected to be susceptible to direct photolysis by sunlight(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 36,900 workers (21,576 of these are female) are potentially exposed to hydrocortisone in the US(1). Occupational exposure to hydrocortisone may occur through inhalation and dermal contact with this compound at workplaces where hydrocortisone is produced or used(SRC). Use data indicate that the general population may be exposed to hydrocortisone via dermal contact with this compound and other consumer products containing hydrocortisone(SRC).

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

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

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

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

For more FDA Requirements (Complete) data for HYDROCORTISONE (9 total), please visit the HSDB record page.

D07AA02

D - Dermatologicals

S - Sensory organs

S - Sensory organs

S - Sensory organs

A - Alimentary tract and metabolism

Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes. Hydrocortisone has a wide therapeutic index and a moderate duration of action. Patients should stop taking the medication if irritation or sensitization occurs.

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.

Following topical application, corticosteroids produce anti-inflammatory, antipruritic, and vasoconstrictor actions. The activity of the drugs is thought to result at least in part from binding with a steroid receptor. Corticosteroids decrease inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes; inhibiting macrophage accumulation in inflamed areas; reducing leukocyte adhesion to capillary endothelium; reducing capillary wall permeability and edema formation; decreasing complement components; antagonizing histamine activity and release of kinin from substrates; reducing fibroblast proliferation, collagen deposition, and subsequent scar tissue formation; and possibly by other mechanisms as yet unknown. Corticosteroids, especially the fluorinated corticosteroids, have antimitotic activity on cutaneous fibroblasts and the epidermis. /Corticosteroids/

Reactive oxygen species (ROS) generation by polymorphonuclear leukocytes (PMNL) and mononuclear cells (MNC) is inhibited following the intravenous administration of hydrocortisone. This is associated with a parallel decrease in intranuclear NFkappaB, known to modulate inflammatory responses including ROS generation. Plasma levels of interleukin-10 (IL-10), an anti-inflammatory and immunosuppressive cytokine produced by TH2 cells, are also increased after hydrocortisone administration. In this study, we have investigated the effect of hydrocortisone on p47(phox) subunit, a key component of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in MNC and the pharmacodynamics of this effect with ROS generation and plasma IL-10 levels /were investigated/. p47(phox) subunit protein levels in MNC showed a progressive decrease after hydrocortisone administration. It reached a nadir at 4 hours and increased thereafter to a baseline level at 24 hours. ROS generation also decreased, reached a nadir between 2 and 4 hours, and returned to a baseline level at 24 hours. IL-10 concentrations increased, peaked at 4 hours, and reverted to the baseline levels at 24 hours. In conclusion, p47(phox) subunit suppression may contribute to the inhibition of ROS generation in MNC after hydrocortisone administration. This suppression occurs in parallel with the suppression of NFkappaB and an increase in IL-10 plasma levels. Therefore, it would appear that the decrease in intranuclear NFkappaB and an increase in IL-10 may cause the inhibitory modulation on p47(phox) subunit and ROS generation by MNC following hydrocortisone and other glucocorticoids.

Total hydrocortisone via the oral route has a half life of 2.15h while the free fraction has a half life of 1.39h. A 20mg IV dose of hydrocortisone has a terminal half life of 1.9±0.4h.

... After IV administration, hydrocortisone was eliminated with a total body clearance of 18 L/hr and a half-life of 1.7 hr.

Hydrocortisone is metabolised to 6-beta hydrocortisol via CYP3A, 5-beta tetrahydrocortisol via 3-oxo-5-beta-steroid 4-dehydrogenase, 5-alpha tetrahydrocortisol via 3-oxo-5-alpha-steroid 4-dehydrogenase 2, cortisone via Corticosteroid 11-beta-dehydrogenase isozyme 1 and Corticosteroid 11-beta-dehydrogenase isozyme 2, and glucuronide products. Cortisone is further metabolized to tetrahydrocortisone and dihydrocortisol.

A study was made of the absorption of exogenous hydrocortisone and formation of its metabolites in isolated liver of intact and exposed rats in conditions of recirculating perfusion. It was shown that the absorption of the hormone by the liver of irradiated rats was greatly lowered but the content of most metabolites found in the perfused medium of irradiated liver increased as compared to the control. It is suggested that irradiation inhibits subsequent transformations of the hydrocortisone metabolism products.

Subcellular distribution of (3)H-hydrocortisone and its metabolites in the liver and kidney of intact and alloxan diabetic rats was investigated. Ten minutes after the administration of this hormone several metabolites (mostly tetrahydrocortisol) and the native hormone were found in liver cytosol, microsomes, mitochondria and nuclei, the relative content of individual compounds in various subcellular fractions being different. In liver mitochondria, microsomes and nuclei of alloxan diabetic rats the concentration of tetrahydrocortisol was decreased, while that of native hormone was increased as compared to normal animals. It was suggested that such changes found in diabetic animals may be one of the causes of increased sensitivity of transcription and translation processes to glucocorticoids. In kidney cytosol and microsomes of intact rats cortisone and tetrahydrocortisol were found. In diabetic animals, however, the concentration of tetrahydrocortisol increased, while that of cortisone was undetectable.

WI4X0X7BPJ

HYDROCORTISONE

Established Pharmacologic Class [EPC] - Corticosteroid

Mechanisms of Action [MoA] - Corticosteroid Hormone Receptor Agonists

Hydrocortisone is a Corticosteroid. The mechanism of action of hydrocortisone is as a Corticosteroid Hormone Receptor Agonist.

ANTI ITCH

The pharmacokinetics of hydrocortisone can vary by 10 times from patient to patient. Following the oral administration of hydrocortisone at a dose of 0.2-0.3 mg/kg/day, the mean Cmax and AUC of plasma free cortisol were 32.69 nmol/L and 90.63 h x nmol/L, respectively. The mean Cmax and AUC of plasma total cortisol were 514.47 nmol/L and 1743.93 h x nmol/L, respectively. Following the dose of 0.4-0.6 mg/kg/day, the mean Cmax and AUC of plasma free cortisol were 70.81 nmol/L and 199.11 h x nmol/L. The mean Cmax and AUC of plasma total cortisol were 754.94 nmol/L and 2533.02 h x nmol/L, respectively. Topical hydrocortisone cream is 4-19% bioavailable with a Tmax of 24h. Hydrocortisone retention enemas have a bioavailability of 0.810 for slow absorbers and 0.502 for rapid absorbers. Slow absorbers take up hydrocortisone at a rate of 0.361±0.255/h while fast absorbers take up hydrocortisone at a rate of 1.05±0.255/h. A 20mg IV dose of hydrocortisone has an AUC of 1163±277ng\*h/mL.

Corticosteroids are eliminated predominantly in the urine. However, data regarding the exact proportion is not readily available.

Total hydrocortisone has a volume of distribution of 39.82L, while the free fraction has a volume of distribution of 474.38L.

Total hydrocortisone by the oral route has a mean clearance of 12.85L/h, while the free fraction has a mean clearance of 235.78L/h. A 20mg IV dose of hydrocortisone has a clearance of 18.2±4.2L/h.

Following percutaneous penetration of a topical corticosteroid, the drug that is systemically absorbed probably follows the metabolic pathways of systemically administered corticosteroids. Corticosteroids usually are metabolized in the liver and excreted by the kidneys. Some topical corticosteroids and their metabolites are excreted in bile. /Topical corticosteroids/

Topical application of corticosteroids to the mucosa of the genitourinary or lower intestinal tract may result in substantial systemic absorption of the drugs. In healthy individuals, as much as 30-90% of rectally administered hydrocortisone as a retention enema may be absorbed. Greater amounts of hydrocortisone may be absorbed rectally if the intestinal mucosa is inflamed.

Medicine (antiinflammatory agent), also used as the acetate and sodium succinate salts

THERAP CAT: Glucocorticoid

THERAP CAT (VET): Glucocorticoid

MEDICATION (VET)

MEDICATION

Use (kg; approx.) in Germany (2009): >1000

ISOLATION FROM ADRENAL GLANDS

Preparation by microbioal transformation: H.C. Murrary, D.H. Perterson, US 2602769 (1952 to Upjohn)

Ointment: 0.5% Cortizone-5, (Pfizer), 1% Cortizone-10, (Pfizer), HydroSKIN, (Rugby), 2.5% Hytone, (Dermik). Pledgets (saturated with solution): 0.5% Massengill Medicated Soft Cloth Towelette (with parabens and propylene glycol), (GlaxoSmithKline). Solution: 1% Cortaid FastStick Maximum Strength (with alcohol and methylparaben), (Pfizer), Cortaid Spray Maximum Strength (with alcohol and methylparaben), (Pfizer), Cortizone-10 Scalp Itch Formula Liquid (with alcohol SD 40-2 60% v/v, benzyl alcohol, and propylene glycol), (Pfizer), Penecort (with alcohol SD 40-2 57%, benzyl alcohol, and propylene glycol), (Allergan), Texacort (with SD alcohol 33% and propylene glycol), (Sirius), 2.5% Texacort, (Sirius).

Lotion: 0.5% HydroSKIN, (Rugby). 1% Ala-Cort, (Del-Ray), Aquanil HC (with benzyl alcohol), (Person & Covey), Cetacort (with parabens), (Healthpoint), Dermacort (with benzyl alcohol), (Solvay) HydroSKIN, (Rugby) LactiCare-HC, (Stiefel) Nutracort (with parabens), (Healthpoint), Sarnol HC, (Stiefel), 2% Ala-Scalpt, (Del-Ray); 2.5% Hydrocortisone Lotion, (Glades), Hydrocortisone Lotion, (Major), Hytone (with propylene glycol), (Dermik), LactiCare-HC, (Stiefel), Nutracort (with parabens), (Healthpoint), ProctoCream-HC (with benzyl alcohol), (Physicians Total Care).

Topical: Cream: 0.5% Cortizone-5 (with aloe and parabens), (Pfizer), Cortizone for Kids ( with aloe and parabens), (Pfizer); 1% Ala-Cort, (Del-Ray), Cortaid Intensive Therapy (with parabens and propylene glycol), (Pfizer), Cortizone-10 (with aloe and parabens), (Pfizer), Cortizone-10 External Anal Itch Relief Creme ( with aloe and parabens), (Pfizer), Dermacort, (Solvay), DermiCort (Republic), HydroSKIN, (Rugby), Hytone (with propylene glycol), (Dermik), Penecort (with benzyl alcohol and propylene glycol), (Allergan), Preparation H Hydrocortisone (with parabens and propylene glycol), (Wyeth); 2.5% Anusol-HC (with benzyl alcohol and propylene glycol), (Pfizer), Hytone (with propylene glycol), (Dermik). Gel: 1% CortaGel Extra Strength, (Norstar).

Rectal: Cream: 1 Proctocort ( with benzyl alcohol and propylene glycol), (Monarch); Suspension: 100 mg/60 mL Cortenema ( with methylparaben), (Solvay), Hydrocortisone Enema, (Copley).

For more Formulations/Preparations (Complete) data for HYDROCORTISONE (14 total), please visit the HSDB record page.

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

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

Pharmaceuticals -> Hormones -> Steroid hormones

Pregn-4-ene-3,20-dione, 11,17,21-trihydroxy-, (11.beta.)-: ACTIVE

RELATIVE ANTIINFLAMMATORY POTENCY= 1; RELATIVE SODIUM RETAINING POTENCY= 1. /FROM TABLE/