트라이엠시놀론

Pharmaceuticals -> Dermatologicals -> Corticosteroids, dermatological preparations

Pharmaceuticals -> Listed in ZINC15

Pharmaceuticals -> Cortico-adrenal hormones

log Kow = 1.16

0.2

Crystals

FINE, WHITE OR PRACTICALLY WHITE, CRYSTALLINE POWDER; POLYMORPHIC

FINE, WHITE OR SLIGHTLY OFF-WHITE CRYSTALS. SLIGHT, BITTER TASTE; SLIGHT ODOR; PRACTICALLY INSOL IN WATER. SOL IN CHLOROFORM; SLIGHTLY SOL IN ETHER; SPARINGLY SOL IN ALC & METHANOL. HYDRATED FORM MP 145-158 °C; ANHYDROUS FORM MP 170-185 °C /DIACETATE/

WHITE TO CREAM-COLORED CRYSTALLINE POWDER. ODORLESS & TASTELESS TO SLIGHTLY BITTER TASTING; DECOMP @ ABOUT 295 °C. PRACTICALLY INSOL IN WATER; 1 G SOL IN 167 ML METHANOL, LESS THAN 20 ML CHLOROFORM. /HEXACETONIDE/

WHITE TO CREAM-COLORED CRYSTALLINE POWDER. SLIGHT ODOR; PRACTICALLY INSOL IN WATER. VERY SOL IN DEHYDRATED ALC, CHLOROFORM, METHANOL; SLIGHTLY SOL IN ALC; SPARINGLY SOL IN ACETONE & ETHYL ACETATE /ACETONIDE/

1 G SOL IN 5000 ML WATER, 70 ML PROPYLENE GLYCOL, LESS THAN 20 ML DIMETHYL SULFOXIDE; SLIGHTLY SOL IN ALC & CHLOROFORM

Slightly sol in usual organic solvents; sol in dimethylformamide

In water, 80 mg/L at 25 °C

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

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

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

269-271 °C

274 - 278 °C

Crystals, mp 268-270 °C. Specific optical rotation at 23 °C: +92 deg (c= 0.59 chloroform). /21-Acetate/

SPECIFIC OPTICAL ROTATION: +75 DEG @ 25 °C/D (ACETONE); MAX ABSORPTION: 238 NM (E= 15,800)

Commercially available oral and parenteral preparations of triamcinolone should be stored at a temperature less than 40 °C, preferably between 15-30 °C; freezing of the sterile suspensions should be avoided. Exposure of sterile suspensions of the drug to freezing temperatures can result in irreversible clumping or agglomeration (granular appearance); such suspensions should not be used. Triamcinolone tablets should be stored in well-closed containers. Triamcinolone acetonide sterile suspension should be protected from light. Triamcinolone acetonide oral inhaler should be stored at controlled room temperature (20-25 °C). Because the contents of the oral inhaler are under pressure, the aerosol container should not be punctured, used or stored near heat or an open flame, exposed to temperatures greater than 49 °C, or placed into a fire or incinerator for disposal.

Warning

H351 (63.3%): Suspected of causing cancer [Warning Carcinogenicity]

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

Aggregated GHS information provided per 60 reports by companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

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

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

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products, incl triamcinolone.

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. Triamcinolone acetonide is included on this list. /Triamcinolone acetonide/

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

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.

Intranasal triamcinolone acetonide should be used with caution in patients receiving other inhaled or systemic corticosteroids (e.g., prednisone in an alternate-day regimen) for any disease, since concomitant use of the drugs could increase the likelihood of hypothalamic-pituitary-adrenal (HPA)-axis suppression compared with therapeutic dosages of either drug alone. /Triamcinolone acetonide/

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/

Because corticosteroids inhibit antibody response, the drugs may cause a diminished response to toxoids and live or inactivated vaccines. In addition, corticosteroids may potentiate replication of some organisms contained in live, attenuated vaccines and supraphysiologic dosages of the drugs can aggravate neurologic reactions to some vaccines. Routine administration of vaccines or toxoids should generally be deferred until corticosteroid therapy is discontinued. Administration of live virus or live, attenuated vaccines, including smallpox vaccine, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. In addition, if inactivated vaccines are administered to such patients, expected serum antibody response may not be obtained. The Public Health Service Advisory Committee on Immunization Practices (ACIP) and American Academy of Family Physicians (AAFP) state that administration of live virus vaccines usually is not contraindicated in patients receiving corticosteroid therapy as short-term (less than 2 weeks) treatment, in low to moderate dosages, as long-term alternate-day treatment with short-acting preparations, in maintenance physiologic dosages (replacement therapy), or if corticosteroids are administered topically, ophthalmically, intra-articularly, bursally, or into a tendon. If immunization is necessary in a patient receiving corticosteroid therapy, serologic testing may be needed to ensure adequate antibody response and additional doses of the vaccine or toxoid may be necessary. Immunization procedures may be undertaken in patients receiving nonimmunosuppressive doses of glucocorticoids or in patients receiving glucocorticoids as replacement therapy (e.g., Addison's disease). /Corticosteroids/

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 TRIAMCINOLONE (18 total), please visit the HSDB record page.

Common adverse effects associated with the initial use of topical triamcinolone involve itchiness, burning, irritation, or skin drying. These symptoms resolve on their own within a few days of use. Other adverse effects may include headaches, dizziness, edema of the ankles or feet, or changes in urination or vision.

Glucocorticoids such as triamcinolone can cause variable neuropsychiatric symptoms to develop. Examples of these symptoms include mania, depression, delirium, and psychosis. These symptoms and other cognitive issues resulting from taking triamcinolone can be reversible after discontinuing the medication. An increased risk of suicide in patients on chronic glucocorticoid therapy has been recorded, so triamcinolone use warrants caution.

The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Firstly, however, these glucocorticoids bind to the glucocorticoid receptors which translocate into the nucleus and bind DNA (GRE) and change genetic expression both positively and negatively. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

/SIGNS AND SYMPTOMS/ The causes for an abnormal five-hour tetracosactrin test in 14 out of 75 patients (18.5% of the entire group), treated continuously with triamcinolone acetonide long-term (mean 3.2 years) for asthma or related syndromes, were investigated. The average daily dosage, duration of treatment and age of the patients were analyzed. Statistical analysis indicated that the risk of adrenocortical suppression was increased by the patient's age and the average patients under the age of 50, receiving less than 1.2 mg triamcinolone acetonide daily, only rarely develop adrenocortical functional impairment. /Triamcinolone acetonide/

/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 34-year-old man acquired visual field defects and severe vision loss in both eyes after intravitreal injection of triamcinolone for diabetic macular edema.

/CASE REPORTS/ In 2 patients, secondary intractable severe ocular hypertension occurred 2 months after a single 4-mg intravitreal injection of triamcinolone acetonide for macular edema. Both patients required trabeculectomy intervention to control intraocular pressure (IOP). /Triamcinolone acetonide/

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

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Administration of triamcinolone nasal aerosol to pregnant rats and rabbits resulted in embryotoxic and fetotoxic effects that were comparable to those produced by administration by other routes.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Pregnant rhesus macaques were treated with 0.5 or 2.5 mg/kg triamcinolone acetonide or 1.0 or 10.0 mg/kg dexamethasone sodium phosphate between 20 and 50 gestational days (GD). Treatment with triamcinolone acetonide at 2.5 mg/kg resulted in a fetal loss of 71%; 3/5 recovered fetuses displayed an encephalocele or meningocele. All other treatment groups displayed minor cranial skeletal abnormalities consistent with glucocorticoid-mediated teratogenesis. Dexamethasone sodium phosphate was shown to have a lower teratogenic potential than triamcinolone acetonide in this species. /Triamcinolone acetonide/

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Studies in non-human primates administered systemic doses of 500 ug/kg/day have shown teratogenic effects, including CNS and cranial malformations.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Studies in rats and rabbits administered systemic doses of 20 to 80 ug/kg/day have shown teratogenic effects, including a low incidence of cleft palate and/or internal hydrocephaly and axial skeletal defects.

For more Non-Human Toxicity Excerpts (Complete) data for TRIAMCINOLONE (6 total), please visit the HSDB record page.

Glucocorticoids should be used with caution in patients with hypothyroidism or cirrhosis, because such patients often show exaggerated response to the drugs. Glucocorticoids should be used with caution in psychotic patients or patients with hypertension or congestive heart failure. /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/

Because glucocorticoids increase susceptibility to and mask symptoms of infection, the drugs should not be used, except in life-threatening situations, in patients with viral infections or bacterial infections not controlled by anti-infectives. Manufacturers state that glucocorticoid oral inhalation therapy should be used with caution, if at all, in patients with untreated systemic fungal, bacterial, viral, or parasitic infections. Patients whose susceptibility to infection is high, such as those receiving glucocorticoids as immunosuppressive therapy, are especially likely to develop secondary infections. Patients receiving glucocorticoids who are potentially immunosuppressed should be warned of the risk of exposure to certain infections (e.g., chickenpox, measles) and of the importance of obtaining medical advice if such exposure occurs. Since glucocorticoid therapy can reactivate tuberculosis, treatment of latent tuberculosis infection should be included in the regimen of patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy. If glucocorticoids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary. Use of glucocorticoids in patients with active tuberculosis should be restricted to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate antimycobacterial chemotherapy. Manufacturers state that glucocorticoid oral inhalation therapy should be used with caution, if at all, in patients with clinical or asymptomatic Mycobacterium tuberculosis infections of the respiratory tract. Since glucocorticoids can reactivate latent amebiasis, any patient who has been in the tropics or who has unexplained diarrhea should be evaluated for amebiasis to exclude these patients prior to initiating therapy. In the treatment of acute or disseminated tuberculosis, glucocorticoids should only be used as part of a total antituberculosis regimen. ... /Corticosteroids/

Corticosteroids should be used with caution in patients with active or latent peptic ulcer, diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), and in those with recent intestinal anastomoses. Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving glucocorticoids. /Corticosteroids/

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/

While data specific to triamcinolone 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).

/SRP:/ 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/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

◉ Summary of Use during Lactation

◉ Summary of Use during Lactation

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

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

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products, incl triamcinolone.

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. Triamcinolone acetonide is included on this list. /Triamcinolone acetonide/

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

H02AB08

D - Dermatologicals

A - Alimentary tract and metabolism

C - Cardiovascular system

D - Dermatologicals

R - Respiratory system

Corticosteroids like triamcinolone inhibit phospholipase A2 on cell membranes, preventing the breakdown of lysosomal membranes of leukocytes, which in turn prevent the formation of arachidonic acid, which decrease expression of cyclooxygenase and lipoxygenase, inhibiting synthesis of prostaglandins and leukotrienes. Anti-inflammatory activity occurs via reversal of vascular dilation and reducing permeability, which prevents macrophage and leukocyte migration. Triamcinolone also inhibits nuclear factor kappa-B, which decreases the production of pro-inflammatory signals such as interleukin-6, interleukin-8, and monocyte chemoattractant protein-1.

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/

Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA (chromatin), and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various inhibitory enzymes responsible for the anti-inflammatory effects of topical corticosteroids. These anti-inflammatory effects include inhibition of early processes such as edema, fibrin deposition, capillary dilatation, movement of phagocttes into the area, and phagocytic activities. Later processes, such as capillary production, collagen deposition, and keloid formation also are inhibited by corticosteroids. The overall actions of topical corticosteroids are catabolic. /Corticosteroids (topical)/

The potent anti-inflammatory action may be due to an inhibition of the secretion of growth factors, endothelial activating and other cytokines from lymphocytes, eosinophils, macrophages, fibroblasts, and mast cells. The results are decreased influx of inflammatory cells into the bronchial walls, due in part to inhibition of expression of adhesion molecules on the endothelium and in the tissue. Decreased activation and survival of eosinophils in the lung tissue and a reduction in numbers of mast cells are further effects. Corticosteroids may inhibit release of mediators from basophils and enzymes from macrophages. There is decreased permeability through vasoconstriction and direct inhibition of endothelial cell contradiction. Beta-adrenergic-receptor numbers may be increased, which results in an enhanced response to beta-adrenergic bronchodilators and reduced down-regulation of beta-receptors after prolonged beta-agonist exposure. Inhaled corticosteroids also inhibit mucus secretion in airways, possibly by a direct action on submucosal gland cells and an indirect inhibitory effect caused by the reduction in inflammatory mediators that stimulate mucus secretion. The amount and viscosity of sputum are reduced. /Corticosteroids (inhalation-local/

The half life of triamcinolone is 2.7h. The mean terminal elimination half life following an inhaled dose of triamcinolone acetonide is 2.4h. The half life of triamcinolone diacetate is 2.8h.

Intravenous: Approximately 90 minutes (plasma). Intranasal: Apparent half-life is 4 hours (plasma) (range, 1 to 7 hours); however, this value probably reflects lingering absorption; 3.1 hours with aqueous formulation. /Triamcinolone acetonide/

88 minutes (plasma) NOTE: The plasma half-life of the inhaled corticosteroids does not correspond well with the biologic half-life.

The major metabolite of triamcinolone is 6-beta-hydroxy-triamcinolone. Data regarding the metabolism of triamcinolone is not readily available.

Hepatic to 3 less active metabolites, 6-beta-hydroxytriamcinolone acetonide, 21-carboxytriamcinolone acetonide, and 21-carboxy-6-beta-hydroxytriamcinolone acetonide. /Triamcinolone acetonide/

Hepatic. Half Life: 88 minutes

1ZK20VI6TY

TRIAMCINOLONE

Established Pharmacologic Class [EPC] - Corticosteroid

Mechanisms of Action [MoA] - Corticosteroid Hormone Receptor Agonists

Triamcinolone is a Corticosteroid. The mechanism of action of triamcinolone is as a Corticosteroid Hormone Receptor Agonist.

Substances that reduce or suppress INFLAMMATION.

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.

A 16mg oral dose of triamcinolone reaches a Cmax of 5.23±0.84ng/mL with a Tmax of 2.24±0.78h and an AUC of 36.0±6.2ng\*h/mL. A 2mg intravenous dose of triamcinolone acetonide has an AUC of 57.7ng\*h/mL. The bioavailability of 800µg of inhaled triamcinolone acetonide is 25%, with 10.4% coming from pulmonary absorption and the rest being accounted for by deposition on the oral mucosa and other underlying factors. An inhaled dose of triamcinolone acetonide reaches a Cmax of 0.92ng/mL with a Tmax of 1.74h and an AUC of 5.12ng\*h/mL. The fraction of an inhaled dose that is actually absorbed via the pulmonary route reaches a Cmax of 0.55ng/mL with a Tmax of 0.66h and an AUC of 2.15ng\*h/mL. A 16mg oral dose of triamcinolone diacetate reaches a Cmax of 5.33±1.55ng/mL with a Tmax of 1.86±0.47h and an AUC of 32.7±9.9ng\*h/mL.

Approximately 20% of a dose of triamcinolone is recovered in the urine as the unchanged drug, 25% is recovered as 6-beta-hydroxy-triamcinolone, and 5% is recovered as unidentified metabolites.

The apparent volume of distribution of triamcinolone is 115.2±10L. The mean apparent volume of distribution of triamcinolone acetonide is 1.96L/kg. The apparent volume of distribution of triamcinolone diacetate is 119.7±33.14L.

The clearance of triamcinolone is 28.6±5.6L/h. The mean total body clearance of triamcinolone acetonide is 0.57L/h. The clearance of triamcinolone diacetate is 34.4±10.6L/h.

TOPICAL APPLICATIONS OF CREAM...CONTAINING...[(14)C]TRIAMCINOLONE ACETONIDE... IN RABBIT. ...9%...OF (14)C WERE ABSORBED FROM OCCLUDED/ABRADED SKIN, THROUGH WHICH PERCUTANEOUS ABSORPTION WOULD BE MAXIMALLY ENHANCED. /TRIAMCINOLONE ACETONIDE/

The absorption, distribution and metabolic fate of triamcinolone acetonide-(14)C-21-phosphate were studied in the dog, monkey, and rat. A comparison of levels of radioactivity in blood or plasma, reached after intramuscular or intravenous administration, indicated that the drug was completely absorbed from the site of intramuscular injection within 10-15 min in all three species. Within 1-5 min after intramuscular or intravenous administration, the 21-phosphate ester was completely hydrolyzed to triamcinolone acetonide, which was present in the blood. The radioactivity was eliminated rapidly (t1/2 = 1-2 hr) from plasma (dogs, monkeys, and rats) and tissues (rats) after intramuscular or intravenous administration. In the three species, the major route of excretion was via the bile; however, the ratio of biliary to urinary excretion among the species varied considerably (from 1.5 to 15). In rats, excretion of radioactivity as expired carbon dioxide accounted for only 2-3 percent of the dose. 6beta-Hydroxytriamcinolone acetonide was the major metabolite in urine of the three species. Hydrolytic cleavage of the acetonide group did not appear to be significant.

Glucocorticoid used for systemic or local anti-inflammatory activity

Treatment of inflammation and related disorders in dogs and cats; and management and treatment of acute arthritis and allergic and dermatologic disorders in dogs and cats. Treatment of inflammation and related disorders in horses. /Acetonide; Vetalog Parenteral Veterinary/

Topically: Use either ointment in cats for anti-inflammatory, antipruritic, antifungal, and antibacterial treatment of superficial bacterial infections, and for dermatologic disorders characterized by inflammation and dry or exudative dermatitis, particularly associated with bacterial or candidal (Candida albicans) infections. /Acetonide; Panolog Ointment/

The drug is recommended ... for topical treatment of summer eczema. /Acetonide; Vetalog Cream/

For more Uses (Complete) data for TRIAMCINOLONE (8 total), please visit the HSDB record page.

Use (kg) in USA (2002): 2300

9-fluoro-11beta,17-dihydroxy-3,20-dioxopregna-1,4-diene-16alpha,21-diyl diacetate (triamcinolone 16,21-diacetate); 9-fluoro-11beta,16alpha,17-trihydroxy-3,20-dioxopregna-1,4-diene-21-diyl acetate (triamcinolone 21-acetate); 9-fluoro-11beta,17,21-tetrahydroxypregn-4-ene-3,20-dione (pretriamcinolone)

Bernstein et al, Allen et al, US 2789118; US 3021347 (1957, 1962, both to American Cyanamid).

Triamcinolone is prepared commercially via a method developed by Bernstein and coworkers. By starting with cortisol 21-acetate, reaction with ethylene glycol gives the 3,20-bisethylene ketal. The 11b- and 17a-hydroxyl groups of this compound are then dehydrated with thionyl chloride in pyridine, followed by alkaline saponification of the 21-acetate group, acid deketalization of the cyclic acetal groups at positions 3 and 20, and reacetylation of the 21-hydroxyl group ... Selective hydroxylation of the double bond at position 16 with osmium tetroxide in pyridine - benzene ... The 9,11-double bond of this compound is converted to a 9a-fluoro-11b-hydroxyl group ... Triamcinolone is obtained after alkaline saponification of the 21-acetate group and microbiological introduction of the D1 double bond with Corynebacterium simplex.

Oral: Tablets: 4 mg Aristocort (scored), (Astellas).

Parenteral: Injectable suspension: 5 mg/mL Aristospan Intralesional (with benzyl alcohol), (Sabex); 20 mg/mL Aristospan Intra-articular (with benzyl alcohol), (Sabex). /Triamcinolone hexacetonide (microcrystalline)/

Oral Inhalation: Aerosol 100 ug/metered spray Azmacort Oral Inhaler (with dehydrated alcohol 1% w/w and dichlorodifluoromethane propellant), (Kos). /Triamcinolone acetonide (microcrystalline)/

Parenteral: Injectable suspension: 3 mg/mL Tac (with benzyl alcohol), (Parnell); 10 mg/mL Kenalog (with benzyl alcohol), (Bristol-Myers Squibb); 40 mg/mL Kenalog (with benzyl alcohol), (Bristol-Myers Squibb). /Triamcinolone acetonide/

For more Formulations/Preparations (Complete) data for TRIAMCINOLONE (6 total), please visit the HSDB record page.