Absorption, Distribution and Excretion
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.
Six healthy male subjects each received a single 100 uCi (approximately 800 ug) oral dose of (14)C-triamcinolone acetonide. Plasma, urine, and fecal samples were collected at selected times and analyzed for triamcinolone acetonide and (14)C-derived radioactivity. Plasma protein binding of triamcinolone acetonide was also determined. Metabolite profiling and identification were carried out in plasma and excreta. Principle metabolites were assessed for activity with in vitro anti-inflammatory models. (14)C-triamcinolone acetonide was found to be systemically absorbed following oral administration. The presystemic metabolism and clearance of triamcinolone acetonide were extensive, with only a small fraction of the total plasma radioactivity being made up of triamcinolone acetonide. Little to no parent compound was detected in the plasma 24 hours after administration. Most of the urinary and fecally (14)C-derived radioactivity was also excreted within 24 and 72 hours postdose, respectively. Mean plasma protein binding of triamcinolone acetonide was constant, predictable, and a relatively low 68% over a 24-fold range of plasma concentrations. Three principle metabolites of triamcinolone acetonide were profiled in plasma, urine, and feces. These metabolites were identified as 6 beta-hydroxy triamcinolone, 21-carboxylic acid triamcinolone acetonide, and 6 beta-hydroxy-21-oic triamcinolone acetonide. All three metabolites failed to show any concentration-dependent effects in anti-inflammatory models evaluating IL-5-sustained eosinophil viability and IgE-induced basophil histamine release. /Triamcinolone acetonide/
Triamcinolone acetonide is a glucocorticoid administered by oral inhalation in the management of asthma. With oral inhalation of glucocorticoids, systemic absorption can come from oropharyngeal, gastrointestinal, or airway deposition of the drug. The objectives of this study were to determine the absolute bioavailability of triamcinolone acetonide following inhalation administration and to delineate the airway contribution of triamcinolone acetonide absorption relative to the absolute bioavailability. All subjects received a 5-minute 400 mcg intravenous infusion of triamcinolone acetonide and a single 800 mcg dose of inhaled triamcinolone acetonide with and without oral charcoal administration in a randomized three-way crossover fashion. The oral charcoal allowed for isolating the pulmonary component of absorption by adsorbing the oropharyngeal and gastrointestinal deposited drug. The mean (+/- SD) absolute bioavailability value for inhaled triamcinolone acetonide was 25% (8.75%). Delineation of the airway contribution of triamcinolone acetonide absorption showed that 10.4% of an inhaled dose is absorbed as triamcinolone acetonide from the lungs. Mean (+/- SD) total body clearance was rapid at 0.57 (0.12) L/hr/kg. The mean (+/- SD) apparent volume of distribution following the intravenous dose was a low 1.96 (0.31) L/kg. No significant differences were noted in the apparent terminal elimination half-life of triamcinolone acetonide (approximately 2.4 hr) between treatments.
For more Absorption, Distribution and Excretion (Complete) data for TRIAMCINOLONE (9 total), please visit the HSDB record page.

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Metabolism / Metabolites
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

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Biological Half-Life
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.

Toxicity Summary
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.

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Toxicity Data
LD₅₀=>500mg/kg (in rats)

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Interactions
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.

Ann Pharmacother.2015Apr;49(4):387-97.

Therapeutic Uses
Anti-Inflammatory Agents, Steroidal; Glucocorticoids, Synthetic; Glucocorticoids, Topical
MEDICATION (VET): ... Triamcinolone acetonide /is/ effective /in the treatment of acute traumatic synovitis and capsulitis in horses/ with no deleterious side effects.
... Triamcinolone /is/ indicated as primary maintenance treatment in patients with persistent symptoms of chronic bronchial asthma. Treatment with inhaled corticosteroids is indicated in asthmatic patients whose conditions require anti-inflammatory treatment and in patients dependent on oral corticosteroids who may benefit from a gradual withdrawal from oral corticosteroids to decrease the likelihood of side effects. Regular, continuous use of inhaled corticosteroids controls chronic airway inflammation, decreases airway hyperresponsiveness, prevents asthma symptoms, reduces the frequency of asthma exacerbations, and reduces hospital admissions for asthma. Clinical studies have also reported that regular use with inhaled corticosteroids is associated with decreased mortality. Inhaled corticosteroids are effective in all types of asthma and in patients of all ages. /Included in US product labeling/
Triamcinolone shares the actions of the other topical corticosteroids and is used for the relief of the inflammatory manifestations of corticosteroid-responsive dermatoses. The drug is also used as a paste for adjunctive treatment to provide temporary relief of symptoms associated with oral inflammatory or ulcerative lesions resulting from trauma.
For more Therapeutic Uses (Complete) data for TRIAMCINOLONE (27 total), please visit the HSDB record page.

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Drug Warnings
Triamcinolone acetonide oral inhalation therapy should not be used in the treatment of nonasthmatic bronchitis. Orally inhaled triamcinolone acetonide should not be used for the primary treatment of severe acute asthmatic attacks or status asthmaticus when intensive measures (e.g., oxygen, parenteral bronchodilators, IV corticosteroids) are required. Triamcinolone acetonide oral inhaler is not a bronchodilator, and patients should be warned that the drug should not be used for rapid relief of bronchospasm. /Triamcinolone acetonide/
Patients who are taking immunosuppressant drugs have increased susceptibility to infections compared with healthy individuals, and certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients, particularly in children. In patients who have not had these diseases or been properly immunized, particular care should be taken to avoid exposure. If exposure to varicella or measles occurs in such individuals, administration of varicella zoster immune globulin (VZIG) or immune globulin, respectively, may be indicated. If varicella develops, treatment with an antiviral agent may be considered.
Patients who have received systemic corticosteroids for prolonged periods and are being switched to treatment with intranasal triamcinolone acetonide should be carefully monitored, since corticosteroid withdrawal symptoms (e.g., joint pain, muscular pain, lassitude, depression), acute adrenal insufficiency, or severe symptomatic exacerbation of asthma or other clinical conditions may occur. Systemic corticosteroid dosage should be tapered, and patients should be carefully monitored during dosage reduction. In general, the greater the dosage and duration of systemic corticosteroid therapy, the greater the time required for withdrawal of systemic corticosteroids and replacement by intranasal corticosteroids.
Adverse effects occurring in at least 2% of patients receiving triamcinolone acetonide nasal aqueous suspension (Nasacort AQ) in clinical trials and more frequently than with placebo included pharyngitis, epistaxis, and increased cough.
For more Drug Warnings (Complete) data for TRIAMCINOLONE (46 total), please visit the HSDB record page.

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Pharmacodynamics
Triamcinolone is a corticosteroid with anti-inflammatory properties. These properties are used to treat inflammation in conditions that affect various organs and tissues. Triamcinolone should not be administered as an epidural injection.

C21H27FO6

394.43

394.179

124-94-7

Triamcinolone (Standard);124-94-7

31307

White to off-white solid powder

1.4±0.1 g/cm3

587.5±50.0 °C at 760 mmHg

262-263 °C(lit.)

309.1±30.1 °C

0.0±3.7 mmHg at 25°C

1.618

0.83

4

7

2

28

807

8

C[C@]12C[C@@H]([C@]3([C@H]([C@@H]1C[C@H]([C@@]2(C(=O)CO)O)O)CCC4=CC(=O)C=C[C@@]43C)F)O

GFNANZIMVAIWHM-OBYCQNJPSA-N

InChI=1S/C21H27FO6/c1-18-6-5-12(24)7-11(18)3-4-13-14-8-15(25)21(28,17(27)10-23)19(14,2)9-16(26)20(13,18)22/h5-7,13-16,23,25-26,28H,3-4,8-10H2,1-2H3/t13-,14-,15+,16-,18-,19-,20-,21-/m0/s1

(8S,9R,10S,11S,13S,14S,16R,17S)-9-fluoro-11,16,17-trihydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,9,10,11,12,13,14,15,16,17-dodecahydro-3H-cyclopenta[a]phenanthren-3-one

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.34 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.34 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.34 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)