Absorption, Distribution and Excretion
Following oral administration of 16 mg triamcinolone acetonide, the peak plasma concentration (Cmax) was 5.23 ± 0.84 ng/mL, the time to peak concentration (Tmax) was 2.24 ± 0.78 h, and the area under the curve (AUC) was 36.0 ± 6.2 ngh/mL. After intravenous administration of 2 mg triamcinolone acetonide, the AUC was 57.7 ngh/mL. The bioavailability of inhaled 800 µg triamcinolone acetonide was 25%, of which 10.4% was absorbed from the lungs, and the remainder was due to oral mucosal deposition and other factors. After inhalation of triamcinolone acetonide, the peak plasma concentration (Cmax) was 0.92 ng/mL, the time to peak concentration (Tmax) was 1.74 h, and the AUC was 5.12 ngh/mL. The inhaled dose, after actual absorption by the lungs, reached peak plasma concentration (Cmax) of 0.55 ng/mL, with a time to peak concentration (Tmax) of 0.66 hours and an area under the curve (AUC) of 2.15 ng·h/mL. Oral administration of 16 mg triamcinolone acetonide resulted in a peak plasma concentration (Cmax) of 5.33 ± 1.55 ng/mL, a time to peak concentration (Tmax) of 1.86 ± 0.47 hours, and an AUC of 32.7 ± 9.9 ng·h/mL. Approximately 20% of triamcinolone acetonide is excreted unchanged in the urine, 25% as 6-β-hydroxytriamcinolone, and 5% as unidentified metabolites. The apparent volume of distribution of triamcinolone acetonide is 115.2 ± 10 L. The mean apparent volume of distribution of triamcinolone acetonide was 1.96 L/kg. The apparent volume of distribution of triamcinolone acetonide diacetate was 119.7 ± 33.14 L. The clearance of triamcinolone acetonide was 28.6 ± 5.6 L/h. The mean systemic clearance of triamcinolone acetonide was 0.57 L/h. The clearance of triamcinolone acetonide diacetate was 34.4 ± 10.6 L/h. Topical application of a cream containing [(14)C]triamcinolone acetonide in rabbits…9%…(14)C was absorbed by occluded/abraded skin, and transdermal absorption was maximized through this pathway. /triamcinolone/ This study investigated the absorption, distribution, and metabolic pathways of triamcinolone acetonide-(14)C-21-phosphate in dogs, monkeys, and rats. By comparing the levels of radioactivity in blood or plasma after intramuscular or intravenous injection, the results showed that the drug was completely absorbed within 10–15 minutes at the intramuscular injection site in all three animals. Within 1–5 minutes after intramuscular or intravenous injection, the 21-phosphate ester was completely hydrolyzed to triamcinolone and entered the bloodstream. Following intramuscular or intravenous injection, the radioactive material was rapidly eliminated from plasma (dogs, monkeys, and rats) and tissues (rat) (half-life 1–2 hours). In all three animals, the primary route of excretion was bile; however, the ratio of bile to urine excretion differed significantly among species (1.5–15). In rats, only 2–3% of the dose was exhaled as carbon dioxide. 6β-hydroxytriamcinolone was the major metabolite in the urine of all three animals. Hydrolysis of the acetone group appeared to be insignificant. Six healthy male subjects each received a single oral dose of 100 μCi (approximately 800 μg) of 14C-triamcinolone. Plasma, urine, and fecal samples were collected at selected time points, and the radioactivity of triamcinolone and ¹⁴C-derived triamcinolone was analyzed. The plasma protein binding rate of triamcinolone was also determined. Metabolites in plasma and excrement were analyzed and identified. The activity of major metabolites was assessed using an in vitro anti-inflammatory model. (14)C-triamcinolone is systemically absorbed after oral administration. First-pass metabolism and clearance of triamcinolone are extensive, with only a small amount of triamcinolone present in total plasma radioactivity. The parent compound was almost undetectable in plasma 24 hours after administration. Most of the (14)C-derived radioactivity in urine and feces was also eliminated within 24 hours and 72 hours after administration, respectively. The mean plasma protein binding rate of triamcinolone was constant and predictable, at a relatively low 68% over a 24-fold plasma concentration range. Three major triamcinolone metabolites in plasma, urine, and feces were analyzed. These metabolites were identified as 6β-hydroxytriamcinolone, 21-carboxylic acid triamcinolone, and 6β-hydroxy-21-acid triamcinolone. None of these three metabolites showed any concentration-dependent effects in anti-inflammatory models assessing IL-5-maintained eosinophil viability and IgE-induced basophil histamine release. /Triamcinolone/
Triamcinolone is a glucocorticoid administered via inhalation for the treatment of asthma. After inhalation, glucocorticoids can be absorbed systemically via deposition in the oropharynx, gastrointestinal tract, or airways. This study aimed to determine the absolute bioavailability of triamcinolone after inhalation and to elucidate the contribution of airway absorption to triamcinolone absorption and its relationship to absolute bioavailability. All subjects received a 5-minute intravenous infusion of 400 micrograms of triamcinolone, and a single inhalation of 800 micrograms of triamcinolone, in a randomized, three-period crossover trial with or without oral activated charcoal. Oral activated charcoal separated the pulmonary absorption component by adsorbing drug deposits in the oropharynx and gastrointestinal tract. The mean (± standard deviation) absolute bioavailability of inhaled triamcinolone was 25% (8.75%). Airway contribution analysis of triamcinolone absorption indicated that 10.4% of the inhaled dose was absorbed from the lungs as triamcinolone. The mean (± standard deviation) systemic clearance was rapid, at 0.57 (0.12) L/hr/kg. The mean (± standard deviation) apparent volume of distribution after intravenous administration was low, at 1.96 (0.31) L/kg. There was no significant difference in the apparent terminal elimination half-life (approximately 2.4 hours) of triamcinolone among different treatment regimens. For more complete data on absorption, distribution, and excretion of triamcinolone (9 types in total), please visit the HSDB record page. Metabolism/Metabolites The major metabolite of triamcinolone is 6-β-hydroxytriamcinolone. Data on triamcinolone metabolism are not available.
It is metabolized in the liver to produce three less active metabolites: 6-β-hydroxytriamcinolone, 21-carboxytriamcinolone, and 21-carboxy-6-β-hydroxytriamcinolone. /triamcinolone/
Hepatic metabolism.
Half-life: 88 minutes

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Biological half-life
The half-life of triamcinolone is 2.7 hours. The mean terminal elimination half-life after inhalation of triamcinolone is 2.4 hours. The half-life of triamcinolone diacetate is 2.8 hours.
Intravenous injection: Approximately 90 minutes (plasma). Intranasal administration: Apparent half-life is 4 hours (plasma) (range: 1 to 7 hours); however, this value may reflect sustained absorption; the half-life of aqueous formulations is 3.1 hours. /triamcinolone/
88 minutes (plasma) Note: The plasma half-life of inhaled corticosteroids does not necessarily correlate with the biological half-life.

Toxicity Summary
The anti-inflammatory effects of corticosteroids are thought to be related to lipocorticoids, phospholipase A2 inhibitory proteins that control the biosynthesis of prostaglandins and leukotrienes by inhibiting arachidonic acid. However, firstly, these glucocorticoids bind to glucocorticoid receptors, which translocate into the cell nucleus and bind to DNA (GRE), thereby positively or negatively altering gene expression. Corticosteroids suppress the immune system by reducing lymphatic system function, decreasing immunoglobulin and complement concentrations, inducing lymphopenia, and interfering with antigen-antibody binding.

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Toxicity Data
LD₅₀=>500 mg/kg (rat)

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Interactions
Intranasal triamcinolone should be used with caution in patients receiving other inhaled or systemic corticosteroids (e.g., prednisone every other day) for any disease, as concomitant use may increase the likelihood of hypothalamic-pituitary-adrenal (HPA) axis suppression compared to therapeutic doses of either drug alone. Triamcinolone/
The effect of glucocorticoids on oral anticoagulation therapy varies from person to person; concomitant use of glucocorticoids has been reported to either enhance or diminish the efficacy of oral anticoagulants. Patients receiving both glucocorticoids and oral anticoagulants should be monitored (e.g., using coagulation indicators) to maintain the desired anticoagulation effect. /Corticosteroids/
Because corticosteroids suppress antibody responses, these drugs may lead to a diminished response to toxoids and live or inactivated vaccines.
Furthermore, corticosteroids may enhance the replication of microorganisms contained in some live or attenuated vaccines, and supraphysiological doses can exacerbate neurological responses induced by certain vaccines. Routine vaccinations or toxoid administration should generally be postponed until corticosteroid treatment is discontinued. Live virus vaccines or live attenuated vaccines, including smallpox vaccines, are contraindicated in patients receiving immunosuppressive doses of glucocorticoids. Additionally, administering inactivated vaccines to such patients may not produce the expected serum antibody response. The Advisory Committee on Immunization Practice (ACIP) of the U.S. Public Health Services and the American Academy of Family Physicians (AAFP) state that live virus vaccination is generally not a contraindication for patients receiving short-term (less than 2 weeks), low- to moderate-dose glucocorticoid therapy; it is also not a contraindication for patients receiving short-term (every other day), low-dose, low-dose, low-dose, low-dose glucocorticoid therapy; it is not a contraindication for patients receiving maintenance doses (replacement therapy) of glucocorticoids; and it is not a contraindication for patients receiving topical, ocular, intra-articular, intrabursal, or intratendinous injections of glucocorticoids. If patients receiving corticosteroid therapy require immunization, serological testing may be necessary to ensure an adequate antibody response, and additional doses of vaccine or toxoid may be required. Immunization may be performed for patients receiving non-immunosuppressive doses of glucocorticoids or receiving glucocorticoid replacement therapy (e.g., Addie's disease). /Corticosteroids/
Potassium-depleting diuretics (e.g., thiazide diuretics, furosemide, ethacrynic acid) and other potassium-depleting drugs (e.g., amphotericin B) may enhance the potassium-depleting effects of glucocorticoids. Patients receiving glucocorticoids and potassium-depleting drugs should have their serum potassium levels closely monitored. /Corticosteroids/
For more complete data on interactions of triamcinolone (18 in total), please visit the HSDB records page.

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

Therapeutic Uses
Anti-inflammatory drugs, steroids; synthetic corticosteroids; topical corticosteroids. Veterinary drugs: ... Triamcinolone acetonide is effective in treating acute traumatic synovitis and capsulitis in horses without harmful side effects. ... Triamcinolone acetonide is indicated for primary maintenance therapy in patients with persistent chronic bronchial asthma. Inhaled corticosteroids are indicated for asthma patients requiring anti-inflammatory treatment, as well as patients dependent on oral corticosteroids who may benefit from gradually discontinuing oral corticosteroids to reduce the risk of side effects. Regular, continuous use of inhaled corticosteroids can control chronic airway inflammation, reduce airway hyperresponsiveness, prevent asthma symptoms, reduce the frequency of acute asthma exacerbations, and reduce asthma hospitalizations. Clinical studies have also reported that regular use of inhaled corticosteroids is associated with reduced mortality. Inhaled corticosteroids are effective for all types of asthma and patients of all ages. /US product label includes/
Triamcinolone acetonide acts similarly to other topical corticosteroids to relieve the inflammatory manifestations of corticosteroid-responsive dermatitis. This medication can also be used as an adjunct to ointment therapy to temporarily relieve symptoms associated with oral inflammation or ulcerative lesions caused by trauma. For more complete data on the therapeutic uses of triamcinolone (out of 27), please visit the HSDB record page. Drug Warnings Triamcinolone acetone inhalation therapy should not be used to treat non-asthmatic bronchitis. Oral inhaled triamcinolone should not be used as first-line treatment for severe acute asthma attacks or status asthmaticus, especially when intensive treatment measures (such as oxygen therapy, parenteral bronchodilators, or intravenous corticosteroids) are required. Oral triamcinolone inhaler is not a bronchodilator, and patients should be informed that this medication should not be used for rapid relief of bronchospasm. Patients taking immunosuppressants are more susceptible to infections than healthy individuals, and certain infections (such as chickenpox and measles) can lead to more serious consequences, even life-threatening ones, in these patients, especially in children. Special care should be taken to avoid exposure to these pathogens in patients who have not had these diseases or have not been vaccinated. If such individuals are exposed to the varicella-zoster virus, they can be treated with varicella-zoster immunoglobulin (VZIG) or immunoglobulin, respectively. If chickenpox occurs, antiviral medication may be considered. Patients on long-term systemic corticosteroid therapy who are switching to intranasal triamcinolone should be closely monitored, as corticosteroid withdrawal symptoms (e.g., arthralgia, muscle pain, fatigue, depression), acute adrenal insufficiency, or severe exacerbations of asthma or other clinical conditions may occur. The dose of systemic corticosteroids should be gradually reduced, and the patient should be closely monitored during the tapering period. Generally, the higher the dose and the longer the duration of systemic corticosteroid therapy, the longer it takes to discontinue systemic corticosteroids and switch to intranasal corticosteroids. In clinical trials, at least 2% of patients receiving nasal triamcinolone nasal aqueous suspension (Nasacort AQ) experienced adverse reactions, with a higher incidence than in the placebo group. These adverse reactions included pharyngitis, epistaxis, and exacerbation of cough. For more complete data on drug warnings for triamcinolone (46 in total), please visit the HSDB Records page.

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Pharmacodynamics
Triamcinolone is a corticosteroid with anti-inflammatory properties. These properties make it suitable for treating inflammation affecting a variety of organs and tissues. Triamcinolone should not be administered via 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.)