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Triamcinolone

PubChem CID
31307
Structure
Triamcinolone_small.png
Triamcinolone_3D_Structure.png
Triamcinolone__Crystal_Structure.png
Molecular Formula
Synonyms
  • triamcinolone
  • 124-94-7
  • Fluoxyprednisolone
  • Aristocort
  • Triamcinolon
Molecular Weight
394.4 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Dates
  • Create:
    2005-03-26
  • Modify:
    2025-01-11
Description
Triamcinolone is a C21-steroid hormone that is 1,4-pregnadiene-3,20-dione carrying four hydroxy substituents at positions 11beta, 16alpha, 17alpha and 21 as well as a fluoro substituent at position 9. Used in the form of its 16,17-acetonide to treat various skin infections. It has a role as an anti-allergic agent and an anti-inflammatory drug. It is a fluorinated steroid, an 11beta-hydroxy steroid, a 20-oxo steroid, a 21-hydroxy steroid, a 3-oxo-Delta(4) steroid, a glucocorticoid, a 17alpha-hydroxy steroid, a 16alpha-hydroxy steroid, a C21-steroid hormone, a primary alpha-hydroxy ketone and a tertiary alpha-hydroxy ketone. It derives from a hydride of a pregnane.
Triamcinolone is a corticosteroid used to treat various inflammatory conditions in the body from allergic rhinitis to acute exacerbations of multiple sclerosis. Triamcinolone can be used as a one time adjunct treatment of osteoarthritic knee pain, or first line as a topical treatment of corticosteroid responsive dermatoses. Triamcinolone is more commonly seen in the forms triamcinolone hexacetonide, triamcinolone acetonide, and triamcinolone diacetate. Triamcinolone was granted FDA approval on 3 December 1957. In October 2021, a suspension of triamcinolone acetonide was approved for suprachoroidal injection - the first suprachoroidal injection to receive FDA approval - for the treatment of patients with macular edema associated with uveitis.
Triamcinolone is a Corticosteroid. The mechanism of action of triamcinolone is as a Corticosteroid Hormone Receptor Agonist.

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Triamcinolone.png

1.2 3D Conformer

1.3 Crystal Structures

CCDC Number
Associated Article
Crystal Structure Data
Crystal Structure Depiction
Crystal Structure Depiction

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

(8S,9R,10S,11S,13S,14S,16R,17S)-9-fluoro-11,16,17-trihydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,11,12,14,15,16-octahydrocyclopenta[a]phenanthren-3-one
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

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
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

GFNANZIMVAIWHM-OBYCQNJPSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

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
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C21H27FO6
Computed by PubChem 2.2 (PubChem release 2021.10.14)

2.3 Other Identifiers

2.3.1 CAS

124-94-7
51855-44-8

2.3.2 Deprecated CAS

83474-03-7

2.3.3 European Community (EC) Number

2.3.4 UNII

2.3.5 ChEBI ID

2.3.6 ChEMBL ID

2.3.7 DrugBank ID

2.3.8 DSSTox Substance ID

2.3.9 HMDB ID

2.3.10 KEGG ID

2.3.11 Metabolomics Workbench ID

2.3.12 NCI Thesaurus Code

2.3.13 Nikkaji Number

2.3.14 NSC Number

2.3.15 PharmGKB ID

2.3.16 Pharos Ligand ID

2.3.17 RXCUI

2.3.18 Wikidata

2.3.19 Wikipedia

2.4 Synonyms

2.4.1 MeSH Entry Terms

  • Aristocort
  • Triamcinolone
  • Volon

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
394.4 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
XLogP3
Property Value
1.2
Reference
Computed by XLogP3 3.0 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
4
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Acceptor Count
Property Value
7
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Rotatable Bond Count
Property Value
2
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
394.17916674 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
394.17916674 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
115 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
28
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
807
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
8
Reference
Computed by PubChem
Property Name
Undefined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Covalently-Bonded Unit Count
Property Value
1
Reference
Computed by PubChem
Property Name
Compound Is Canonicalized
Property Value
Yes
Reference
Computed by PubChem (release 2021.10.14)

3.2 Experimental Properties

3.2.1 Physical Description

Solid

3.2.2 Color / Form

Crystals
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1712
FINE, WHITE OR PRACTICALLY WHITE, CRYSTALLINE POWDER; POLYMORPHIC
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 897

3.2.3 Melting Point

270
Chemspider
269-271 °C
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1712
274 - 278 °C

3.2.4 Solubility

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/
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 898
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/
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 898
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/
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 898
1 G SOL IN 5000 ML WATER, 70 ML PROPYLENE GLYCOL, LESS THAN 20 ML DIMETHYL SULFOXIDE; SLIGHTLY SOL IN ALC & CHLOROFORM
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 897
Slightly sol in usual organic solvents; sol in dimethylformamide
Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 1116
In water, 80 mg/L at 25 °C
Yalkowsky, S.H., He, Yan., Handbook of Aqueous Solubility Data: An Extensive Compilation of Aqueous Solubility Data for Organic Compounds Extracted from the AQUASOL dATAbASE. CRC Press LLC, Boca Raton, FL. 2003., p. 1177
8.47e-01 g/L

3.2.5 Vapor Pressure

7.20X10-15 mm Hg at 25 °C
US EPA; Estimation Program Interface (EPI) Suite. Ver.3.12. Nov 30, 2004. Available from, as of Oct 16, 2007: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm

3.2.6 LogP

log Kow = 1.16
Hansch, C., Leo, A., D. Hoekman. Exploring QSAR - Hydrophobic, Electronic, and Steric Constants. Washington, DC: American Chemical Society., 1995., p. 173
0.2

3.2.7 Stability / Shelf Life

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.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3059

3.2.8 Optical Rotation

Crystals, mp 268-270 °C. Specific optical rotation at 23 °C: +92 deg (c= 0.59 chloroform). /21-Acetate/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1712
SPECIFIC OPTICAL ROTATION: +75 DEG @ 25 °C/D (ACETONE); MAX ABSORPTION: 238 NM (E= 15,800)
The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976., p. 1233

3.2.9 Collision Cross Section

184.21 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

210.98 Ų [M+Na]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

180.29 Ų [M+H-H2O]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

206.4 Ų [M+K]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

Ross et al. JASMS 2022; 33; 1061-1072. DOI:10.1021/jasms.2c00111
186.8 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

3.2.10 Other Experimental Properties

Crystals, mp 292-294 °C. Specific optical rotation at 23 °C: +109 deg (c = 0.75 chloroform). UV max (absolute alc): 238 nm (E 14600). Sparingly sol in methanol, acetone, ethyl acetate. /Acetonide/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1712
MP: 186-188 °C (with effervescence, mp 235 °C after drying); max absorption: 239 nm (e= 15,200); solvated crystals. Specific optical rotation: +22 deg at 25 °C/D (chloroform) /Diacetate/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1712
Fine, white, needle-like crystals, mp 295-296 °C (dec), also reported as mo 271-272 °C (dec). UV Max (ethanol): 238 nm (E 15,500). Specific optical rotation at 25 °C = +90 plus/minus 2 °C (c = 1.13% in chloroform). Solubility in g/100 mL at 25 °C: chloroform and dimethylacetamide > 5; ethyl acetate 0.77, methanol 0.59, diethyl carbonate 0.50, glycerin 0.42, propylene glycol 0.13, absolute alcohol 0.03, water 0.0004. /Hexacetonide/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1712

3.3 Chemical Classes

3.3.1 Drugs

Pharmaceuticals -> Cortico-adrenal hormones
S57 | GREEKPHARMA | Suspect Pharmaceuticals from the National Organization of Medicine, Greece | DOI:10.5281/zenodo.3248883
Pharmaceuticals -> Dermatologicals -> Corticosteroids, dermatological preparations
S92 | FLUOROPHARMA | List of ~340 ATC classified fluoro-pharmaceuticals | DOI:10.5281/zenodo.5979646
Pharmaceuticals -> Listed in ZINC15
S55 | ZINC15PHARMA | Pharmaceuticals from ZINC15 | DOI:10.5281/zenodo.3247749
3.3.1.1 Human Drugs
Breast Feeding; Lactation; Milk, Human; Corticosteroids, Topical; Glucocorticoids; Anti-Inflammatory Agents
Breast Feeding; Lactation; Milk, Human; Corticosteroids, Systemic; Glucocorticoids; Anti-Inflammatory Agents
Human drug -> Discontinued
Human drug -> Discontinued; Active ingredient (TRIAMCINOLONE)
3.3.1.2 Animal Drugs
Pharmaceuticals -> Animal Drugs -> Approved in Taiwan
S72 | NTUPHTW | Pharmaceutically Active Substances from National Taiwan University | DOI:10.5281/zenodo.3955664

3.3.2 Endocrine Disruptors

Potential endocrine disrupting compound
S109 | PARCEDC | List of 7074 potential endocrine disrupting compounds (EDCs) by PARC T4.2 | DOI:10.5281/zenodo.10944198

4 Spectral Information

4.1 1D NMR Spectra

4.1.1 1H NMR Spectra

1 of 2
Spectra ID
Instrument Type
JEOL
Frequency
400 MHz
Solvent
DMSO-d6
Shifts [ppm]:Intensity
1.36:66.00, 2.63:19.00, 2.20:41.00, 2.60:37.00, 0.85:803.00, 2.62:36.00, 4.15:40.00, 1.79:50.00, 7.29:193.00, 2.38:27.00, 4.48:121.00, 2.59:24.00, 1.78:49.00, 1.42:67.00, 7.26:202.00, 2.34:56.00, 4.53:91.00, 2.25:24.00, 6.21:160.00, 2.14:30.00, 4.12:125.00, 4.59:574.00, 4.11:101.00, 1.77:37.00, 6.01:192.00, 2.14:45.00, 1.74:38.00, 4.47:93.00, 4.06:78.00, 4.76:54.00, 2.23:30.00, 4.64:202.00, 2.31:59.00, 4.63:109.00, 5.28:109.00, 2.65:16.00, 2.28:21.00, 2.12:34.00, 2.17:20.00, 4.74:37.00, 4.78:48.00, 5.36:234.00, 1.45:77.00, 4.14:38.00, 1.48:1000.00, 1.81:42.00, 4.16:40.00, 4.74:44.00, 6.23:164.00, 4.78:39.00, 2.30:53.00, 2.57:21.00, 2.22:39.00, 4.07:87.00, 2.37:28.00, 2.41:11.00, 2.40:12.00, 1.85:19.00, 4.66:86.00, 2.11:50.00, 2.27:21.00, 5.37:231.00, 5.28:108.00, 1.33:62.00, 4.76:59.00, 1.34:67.00, 4.51:81.00, 6.20:166.00, 6.23:163.00, 1.76:48.00, 1.31:42.00
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2 of 2
Source of Spectrum
Sigma-Aldrich Co. LLC.
Source of Sample
Sigma-Aldrich Co. LLC.
Catalog Number
287334
Copyright
Copyright © 2021-2024 Sigma-Aldrich Co. LLC. - Database Compilation Copyright © 2021 John Wiley & Sons, Inc. All Rights Reserved.
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4.1.2 13C NMR Spectra

1 of 2
Spectra ID
Instrument Type
JEOL
Frequency
100.40 MHz
Solvent
DMSO-d6
Shifts [ppm]:Intensity
16.58:552.00, 87.41:918.00, 124.07:315.00, 33.26:231.00, 33.58:323.00, 152.55:380.00, 70.25:202.00, 47.70:363.00, 166.78:218.00, 22.83:326.00, 166.77:237.00, 70.61:206.00, 43.04:299.00, 30.13:317.00, 22.77:320.00, 47.93:356.00, 46.42:1000.00, 128.89:451.00, 185.13:436.00, 66.49:419.00, 71.20:489.00, 27.22:242.00, 211.48:536.00, 100.07:157.00, 101.81:181.00, 27.21:255.00, 43.03:301.00, 33.07:235.00, 35.70:269.00
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2 of 2
Source of Spectrum
Sigma-Aldrich Co. LLC.
Source of Sample
Sigma-Aldrich Co. LLC.
Catalog Number
287334
Copyright
Copyright © 2021-2024 Sigma-Aldrich Co. LLC. - Database Compilation Copyright © 2021 John Wiley & Sons, Inc. All Rights Reserved.
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4.2 Mass Spectrometry

4.2.1 GC-MS

1 of 2
Source of Spectrum
Mass Spectrometry Committee of the Toxicology Section of the American Academy of Forensic Sciences
Copyright
Copyright © 2012-2024 John Wiley & Sons, Inc. Portions provided by AAFS, Toxicology Section. All Rights Reserved.
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2 of 2
Instrument Name
Finnigan 4000 quadrupole
Source of Spectrum
HRC-11-285-Triamcinolone (DOI: 10.1002/jhrc.1240110312)
Copyright
Copyright © 2020-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.2.2 MS-MS

1 of 6
View All
Spectra ID
Ionization Mode
Negative
Top 5 Peaks

345.15 100

325.1397 84.76

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2 of 6
View All
Spectra ID
Ionization Mode
Positive
Top 5 Peaks

357.1681 100

225.1258 66.33

339.1583 44.66

237.127 33.67

321.1478 33.28

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4.2.3 LC-MS

1 of 25
View All
Authors
Nikiforos Alygizakis, Katerina Galani, Nikolaos Thomaidis, University of Athens
Instrument
Bruker maXis Impact
Instrument Type
LC-ESI-QTOF
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
10 eV
Fragmentation Mode
CID
Column Name
Acclaim RSLC C18 2.2um, 2.1x100mm, Thermo
Retention Time
6.376 min
Precursor m/z
395.1864
Precursor Adduct
[M+H]+
Top 5 Peaks

375.18 999

395.187 867

357.1692 481

376.1825 282

396.1887 243

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License
CC BY
2 of 25
View All
Authors
Nikiforos Alygizakis, Katerina Galani, Nikolaos Thomaidis, University of Athens
Instrument
Bruker maXis Impact
Instrument Type
LC-ESI-QTOF
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
20 eV
Fragmentation Mode
CID
Column Name
Acclaim RSLC C18 2.2um, 2.1x100mm, Thermo
Retention Time
6.382 min
Precursor m/z
395.1864
Precursor Adduct
[M+H]+
Top 5 Peaks

357.1681 999

225.1258 662

339.1583 446

237.127 336

321.1478 332

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License
CC BY

4.2.4 Other MS

1 of 2
MS Category
Experimental
MS Type
Other
Precursor Type
[M+H]+
Precursor m/z
395.1864432
Instrument
Agilent 6560
Ionization Mode
positive
Collision Energy
20
Retention Time
5.188783
Top 5 Peaks

357.16901 100

225.12694 91.19

339.15826 65.12

321.14761 64.19

147.07985 60.04

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2 of 2
MS Category
Experimental
MS Type
Other
Precursor Type
[M+H]+
Precursor m/z
395.1864432
Instrument
Agilent 6560
Ionization Mode
positive
Collision Energy
40
Retention Time
5.189517
Top 5 Peaks

147.08086 100

223.11201 49.88

171.08051 46.05

121.06519 39.95

225.1274 39.09

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4.3 IR Spectra

4.3.1 FTIR Spectra

Instrument Name
Bio-Rad FTS
Technique
KBr1 0.82mg
Source of Spectrum
Forensic Spectral Research
Source of Sample
Steraloids
Catalog Number
P0550-000
Lot Number
G041
Copyright
Copyright © 2008-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.3.2 ATR-IR Spectra

1 of 2
Instrument Name
Bio-Rad FTS
Technique
ATR-Neat (DuraSamplIR II)
Source of Spectrum
Forensic Spectral Research
Source of Sample
Steraloids Inc.
Catalog Number
P0550-000
Lot Number
G041
Copyright
Copyright © 2009-2024 John Wiley & Sons, Inc. All Rights Reserved.
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2 of 2
Source of Sample
Aldrich
Catalog Number
287334
Copyright
Copyright © 2018-2024 Sigma-Aldrich Co. LLC. - Database Compilation Copyright © 2018-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.4 Raman Spectra

Technique
FT-Raman
Source of Spectrum
Forensic Spectral Research
Source of Sample
Steraloids Inc.
Catalog Number
P0550-000
Lot Number
G041
Copyright
Copyright © 2013-2024 John Wiley & Sons, Inc. All Rights Reserved.
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6 Chemical Vendors

7 Drug and Medication Information

7.1 Drug Indication

Triamcinolone hexacetonide injections are indicated for intralesional administration in alopecia areata, discoid lupus erythematosus, keloids, and necrobiosis lipoidica diabeticorum. This formulation can also be used for localized hypertrophic infiltrated inflammatory lesions of granuloma annulare, lichen planus, lichen simplex chronicus, and psoriatic plaques. Triamcinolone acetonide spray and cream are indicated for the treatment of inflammatory and pruritic manifestations of corticosteroid responsive dermatoses. A triamcinolone acetonide 10mg/mL or 40mg/mL injection is indicated intra-articularly for acute gouty arthritis, acute and subacute bursitis, acute nonspecific tenosynovitis, epicondylitis, rheumatoid arthritis, and synovitis of osteoarthritis. The same 10mg/mL injection is indicated by the intralesional route for the treatment of alopecia areata, discoid lupus erythematosus, keloids, necrobiosis lipoidica diabeticorum, and tumors of an aponeurosis or tendon. This formulation can also be used for localized hypertrophic infiltrated inflammatory lesions of granuloma annulare, lichen planus, lichen simplex chronicus, and psoriatic plaques. The 40mg/mL injection is indicated intramuscularly for controlling severe allergic conditions such as asthma, atopic dermatitis, contact dermatitis, drug hypersensitivity, perennial or seasonal allergic rhinitis, serum sickness, and transfusion reactions; treatment of bullous dermatitis herpetiformis, exfoliative erythroderma, mycosis fungoides, pemphigus, Stevens-Johnson syndrome, congenital adrenal hyperplasia, hypercalcemia in cancer, nonsuppurative thyroiditis, autoimmune hemolytic anemia, Diamond-Blackfan anemia, pure red cell aplasia, secondary thrombocytopenia, trichinosis, tuberculous meningitis, acute exacerbations of multiple sclerosis or cerebral edema, sympathetic ophthalmia, temporal arteritis, uveitis, ocular inflammation, berylliosis, idiopathic eosinophilic pneumonias, symptomatic sarcoidosis, dermatomyositis, polymyositis, and systemic lupus erythematosus; adjunct treatment of adrenocortical insufficiency, regional enteritis, ulcerative colitis, fulminating or disseminated pulmonary tuberculosis, acute gouty arthritis, acute rheumatic carditis, ankylosing spondylitis, psoriatic arthritis, rheumatoid arthritis; palliative management of leukemia and lymphoma; induction of diuresis or remission of proteinuria in idiopathic nephrotic syndrome or lupus erythematosus. A triamcinolone intravitreal injection is indicated for the treatment of sympathetic ophthalmia, temporal arteritis, uveitis, and ocular inflammatory conditions. The intravitreal injection is also used for visualization during vitrectomy. An extended release suspension is indicated intra-articularly for management of pain in osteoarthritis of the knee. A triamcinolone acetonide suspension for injection into the suprachoroidal space is indicated for the treatment of macular edema associated with uveitis.

7.2 Drug Classes

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

7.3 FDA Approved Drugs

7.4 FDA Orange Book

7.5 Drug Labels

Active ingredient and drug

7.6 Clinical Trials

7.6.1 ClinicalTrials.gov

7.6.2 EU Clinical Trials Register

7.6.3 NIPH Clinical Trials Search of Japan

7.7 Therapeutic Uses

Anti-Inflammatory Agents, Steroidal; Glucocorticoids, Synthetic; Glucocorticoids, Topical
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)
MEDICATION (VET): ... Triamcinolone acetonide /is/ effective /in the treatment of acute traumatic synovitis and capsulitis in horses/ with no deleterious side effects.
Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 861
... 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/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 889
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.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3535
For more Therapeutic Uses (Complete) data for TRIAMCINOLONE (27 total), please visit the HSDB record page.

7.8 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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3058
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.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2835
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.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2835
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.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2835
For more Drug Warnings (Complete) data for TRIAMCINOLONE (46 total), please visit the HSDB record page.

8 Pharmacology and Biochemistry

8.1 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.

8.2 MeSH Pharmacological Classification

Glucocorticoids
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. (See all compounds classified as Glucocorticoids.)
Anti-Inflammatory Agents
Substances that reduce or suppress INFLAMMATION. (See all compounds classified as Anti-Inflammatory Agents.)

8.3 FDA Pharmacological Classification

FDA UNII
1ZK20VI6TY
Active Moiety
TRIAMCINOLONE
Pharmacological Classes
Established Pharmacologic Class [EPC] - Corticosteroid
Pharmacological Classes
Mechanisms of Action [MoA] - Corticosteroid Hormone Receptor Agonists
FDA Pharmacology Summary
Triamcinolone is a Corticosteroid. The mechanism of action of triamcinolone is as a Corticosteroid Hormone Receptor Agonist.

8.4 ATC Code

S76 | LUXPHARMA | Pharmaceuticals Marketed in Luxembourg | Pharmaceuticals marketed in Luxembourg, as published by d'Gesondheetskeess (CNS, la caisse nationale de sante, www.cns.lu), mapped by name to structures using CompTox by R. Singh et al. (in prep.). List downloaded from https://cns.public.lu/en/legislations/textes-coordonnes/liste-med-comm.html. Dataset DOI:10.5281/zenodo.4587355

D - Dermatologicals

D07 - Corticosteroids, dermatological preparations

D07X - Corticosteroids, other combinations

D07XB - Corticosteroids, moderately potent, other combinations

D07XB02 - Triamcinolone

A - Alimentary tract and metabolism

A01 - Stomatological preparations

A01A - Stomatological preparations

A01AC - Corticosteroids for local oral treatment

A01AC01 - Triamcinolone

C - Cardiovascular system

C05 - Vasoprotectives

C05A - Agents for treatment of hemorrhoids and anal fissures for topical use

C05AA - Corticosteroids

C05AA12 - Triamcinolone

D - Dermatologicals

D07 - Corticosteroids, dermatological preparations

D07A - Corticosteroids, plain

D07AB - Corticosteroids, moderately potent (group ii)

D07AB09 - Triamcinolone

R - Respiratory system

R01 - Nasal preparations

R01A - Decongestants and other nasal preparations for topical use

R01AD - Corticosteroids

R01AD11 - Triamcinolone

S - Sensory organs

S01 - Ophthalmologicals

S01B - Antiinflammatory agents

S01BA - Corticosteroids, plain

S01BA05 - Triamcinolone

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

H02 - Corticosteroids for systemic use

H02A - Corticosteroids for systemic use, plain

H02AB - Glucocorticoids

H02AB08 - Triamcinolone

R - Respiratory system

R03 - Drugs for obstructive airway diseases

R03B - Other drugs for obstructive airway diseases, inhalants

R03BA - Glucocorticoids

R03BA06 - Triamcinolone

8.5 Absorption, Distribution and Excretion

Absorption
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.
Route of Elimination
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.
Volume of Distribution
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.
Clearance
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 Chemical Society. Foreign Compound Metabolism in Mammals. Volume 2: A Review of the Literature Published Between 1970 and 1971. London: The Chemical Society, 1972., p. 128
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.
Kripalani KJ et al; J Pharm Sci 64 (8): 1351-9 (1975)
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/
Argenti D et al; J Clin Pharmacol 40 (7): 770-80 (2000)
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.
Argenti D et al; J Clin Pharmacol 39 (7): 695-702 (1999)
For more Absorption, Distribution and Excretion (Complete) data for TRIAMCINOLONE (9 total), please visit the HSDB record page.

8.6 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/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 898
Hepatic. Half Life: 88 minutes

8.7 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/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 898
88 minutes (plasma) NOTE: The plasma half-life of the inhaled corticosteroids does not correspond well with the biologic half-life.
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 890

8.8 Mechanism of Action

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/
Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2128
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)/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 919
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/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 890

8.9 Human Metabolite Information

8.9.1 Cellular Locations

  • Cytoplasm
  • Extracellular
  • Membrane

9 Use and Manufacturing

9.1 Uses

Glucocorticoid used for systemic or local anti-inflammatory activity
Hinz B et al; Ullmann's Encyclopedia of Industrial Chemistry. 7th ed. (2005). NY, NY: John Wiley & Sons; Anti-Inflammatory-Antirheumatic Drugs. Online Posting Date: June 15, 2000.
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/
FDA; Database of Approved Animal Drug Products, FDA Center for Veterinary Medicine, VMRCVM Drug Information Lab, CFR Product Abstract for: 030-434, Available from, as of Oct 12, 2007: https://dil.vetmed.vt.edu/
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/
FDA; Database of Approved Animal Drug Products, FDA Center for Veterinary Medicine, VMRCVM Drug Information Lab, CFR Product Abstract for: 012-258, Available from, as of Oct 12, 2007: https://dil.vetmed.vt.edu/
The drug is recommended ... for topical treatment of summer eczema. /Acetonide; Vetalog Cream/
FDA; Database of Approved Animal Drug Products, FDA Center for Veterinary Medicine, VMRCVM Drug Information Lab, CFR Product Abstract for: 046-146, Available from, as of Oct 12, 2007: https://dil.vetmed.vt.edu/
For more Uses (Complete) data for TRIAMCINOLONE (8 total), please visit the HSDB record page.

Use (kg) in USA (2002): 2300

Consumption (g per capita) in the USA (2002): 0.00815

Calculated removal (%): 45.6

For the treatment of perennial and seasonal allergic rhinitis.

9.1.1 Use Classification

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients
Pharmaceuticals -> Animal Drugs -> Approved in Taiwan
S72 | NTUPHTW | Pharmaceutically Active Substances from National Taiwan University | DOI:10.5281/zenodo.3955664

9.2 Methods of Manufacturing

Bernstein et al, Allen et al, US 2789118; US 3021347 (1957, 1962, both to American Cyanamid).
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1650
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.
Sandow J et al; Ullmann's Encyclopedia of Industrial Chemistry. 7th ed. (2005). NY, NY: John Wiley & Sons; Hormones. Online Posting Date: June 15, 2000.

9.3 Impurities

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)
Council of Europe, European Directorate for the Quality of Medicines. European Pharmacopoeia, 5th Ed., Volume 2; Strasbourg, France, p.2613 (2007)

9.4 Formulations / Preparations

Oral: Tablets: 4 mg Aristocort (scored), (Astellas).
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3059
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)/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3060
Oral Inhalation: Aerosol 100 ug/metered spray Azmacort Oral Inhaler (with dehydrated alcohol 1% w/w and dichlorodifluoromethane propellant), (Kos). /Triamcinolone acetonide (microcrystalline)/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3060
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3059
For more Formulations/Preparations (Complete) data for TRIAMCINOLONE (6 total), please visit the HSDB record page.

9.5 General Manufacturing Information

Marketed as its acetonide (76-25-5) in Vetalog cream, oral powder, tablets, and parenteral solution.
Sams R et al; Ullmann's Encyclopedia of Industrial Chemistry. 7th ed. (2005). NY, NY: John Wiley & Sons; Veterinary Drugs. Online Posting Date: June 15, 2000.

10 Identification

10.1 Analytic Laboratory Methods

Analyte: triamcinolone; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards
U.S. Pharmacopeia. The United States Pharmacopeia, USP 30/The National Formulary, NF 25; Rockville, MD: U.S. Pharmacopeial Convention, Inc., p.3390 (2007)
Analyte: triamcinolone; matrix: chemical identification; procedure: ultraviolet absorption spectrophotometry with comparison to standards
U.S. Pharmacopeia. The United States Pharmacopeia, USP 30/The National Formulary, NF 25; Rockville, MD: U.S. Pharmacopeial Convention, Inc., p.3390 (2007)
Analyte: triamcinolone; matrix: chemical purity; procedure: liquid chromatography with detection at 254 nm and comparison to standards
U.S. Pharmacopeia. The United States Pharmacopeia, USP 30/The National Formulary, NF 25; Rockville, MD: U.S. Pharmacopeial Convention, Inc., p.3390 (2007)
Analyte: triamcinolone; matrix: pharmaceutical preparation (tablet); procedure: infrared absorption spectrophotometry with comparison to standards (chemical identification)
U.S. Pharmacopeia. The United States Pharmacopeia, USP 30/The National Formulary, NF 25; Rockville, MD: U.S. Pharmacopeial Convention, Inc., p.3391 (2007)
For more Analytic Laboratory Methods (Complete) data for TRIAMCINOLONE (35 total), please visit the HSDB record page.

10.2 Clinical Laboratory Methods

Analyte: triamcinolone; matrix: urine; procedure: high-performance liquid chromatography with ultraviolet detection at 245 nm
Santos-Montes A et al; J Chromatogr B 652: 83-89 (1994). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: triamcinolone; matrix: urine; procedure: high-performance liquid chromatography with ultraviolet detection at 246 nm; limit of detection: 10 ng/mL
Park SJ et al; J Anal Toxicol 14: 102-108 (1990). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: triamcinolone; matrix: tissue (muscle, liver); procedure: high-performance liquid chromatography with ultraviolet (at 245 nm) or mass spectrometric detection; limit of detection: 100 ppb
Huopalahti RP, Henion JD; J Liq Chromatogr Rel Technol 19: 69-87 (1996). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: triamcinolone acetonide; matrix: blood (plasma); procedure: high-performance liquid chromatography with ultraviolet detection at 252 nm; limit of quantitation: 600 pg/mL /triamcinolone acetonide/
Doppenschmitt SA et al; J Chromatogr B 682: 79-88 (1996). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
For more Clinical Laboratory Methods (Complete) data for TRIAMCINOLONE (10 total), please visit the HSDB record page.

11 Safety and Hazards

11.1 Hazards Identification

11.1.1 GHS Classification

Pictogram(s)
Health Hazard
Signal
Warning
GHS Hazard Statements

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

H361 (31.7%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

Precautionary Statement Codes

P203, P280, P318, P405, and P501

(The corresponding statement to each P-code can be found at the GHS Classification page.)

ECHA C&L Notifications Summary

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.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown.

11.1.2 Hazard Classes and Categories

Carc. 2 (63.3%)

Repr. 2 (31.7%)

11.2 Accidental Release Measures

11.2.1 Disposal Methods

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.

11.3 Regulatory Information

11.3.1 FDA Requirements

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/
DHHS/FDA; Electronic Orange Book-Approved Drug Products with Therapeutic Equivalence Evaluations. Available from, as of November 9, 2007: https://www.fda.gov/cder/ob/
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/
DHHS/FDA; Electronic Orange Book-Approved Drug Products with Therapeutic Equivalence Evaluations. Available from, as of November 9, 2007: https://www.fda.gov/cder/ob/
The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products, incl triamcinolone.
DHHS/FDA; Electronic Orange Book-Approved Drug Products with Therapeutic Equivalence Evaluations. Available from, as of November 9, 2007: https://www.fda.gov/cder/ob/
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/
US FDA/Center for Veterinary Medicine; The Green Book - FDA Approved Animal Drug Products. Available from, as of November 9, 2007: https://www.fda.gov/cvm/Green_Book/greenbook.html
For more FDA Requirements (Complete) data for TRIAMCINOLONE (9 total), please visit the HSDB record page.

11.4 Other Safety Information

Chemical Assessment

IMAP assessments - Pregna-1,4-diene-3,20-dione, 9-fluoro-11,16,17,21-tetrahydroxy-, (11.beta.,16.alpha.)-: Environment tier I assessment

IMAP assessments - Pregna-1,4-diene-3,20-dione, 9-fluoro-11,16,17,21-tetrahydroxy-, (11.beta.,16.alpha.)-: Human health tier I assessment

12 Toxicity

12.1 Toxicological Information

12.1.1 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.

12.1.2 Carcinogen Classification

Carcinogen Classification
No indication of carcinogenicity to humans (not listed by IARC).

12.1.3 Effects During Pregnancy and Lactation

◉ Summary of Use during Lactation

Topical triamcinolone has not been studied during breastfeeding. Since only extensive application of the most potent corticosteroids may cause systemic effects in the mother, it is unlikely that short-term application of topical corticosteroids would pose a risk to the breastfed infant by passage into breastmilk. However, it would be prudent to use the least potent drug on the smallest area of skin possible. It is particularly important to ensure that the infant's skin does not come into direct contact with the areas of skin that have been treated. Current guidelines allow topical corticosteroids to be applied to the nipples just after nursing for eczema, with the nipples cleaned gently before nursing. Only water-miscible cream or gel products should be applied to the breast because ointments may expose the infant to high levels of mineral paraffins via licking.

◉ Effects in Breastfed Infants

Topical application of a corticosteroid with relatively high mineralocorticoid activity (isofluprednone acetate) to the mother's nipples resulted in prolonged QT interval, cushingoid appearance, severe hypertension, decreased growth and electrolyte abnormalities in her 2-month-old breastfed infant. The mother had used the cream since birth for painful nipples.

◉ Effects on Lactation and Breastmilk

Relevant published information was not found as of the revision date. Adequate endogenous adrenocorticoid levels are necessary for normal lactation.

◉ Summary of Use during Lactation

Because no information is available on the use of oral triamcinolone during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant. Use of triamcinolone as a nasal spray or local injections, such as for tendinitis, would not be expected to cause any adverse effects in breastfed infants. Expert opinion considers inhaled and oral corticosteroids acceptable to use during breastfeeding. Local injections, such as for tendinitis, would not be expected to cause any adverse effects in breastfed infants. Single injections of triamcinolone acetonide into the breast for treating granulomatous mastitis appear to be acceptable. Medium to large doses of corticosteroids given systemically or injected into joints or the breast have been reported to cause temporary reduction of lactation. See also Triamcinolone, Topical.

◉ Effects in Breastfed Infants

None reported with any corticosteroid.

◉ Effects on Lactation and Breastmilk

A mother was nursing her 14-month-old 3 to 7 times daily. She had 5.7 mg of betamethasone sodium phosphate and acetate mixture injected into her shoulder for bursitis with no effect on lactation. Four weeks later, she continued to have pain in her thoracic cervical regions and was diagnosed with neural sensitization. She had 80 to 120 mg of triamcinolone diacetate injected into her cervical and thoracic spine epidurally and into the facets. Three days later, she noticed a decrease in milk supply and a reduced ejection reflex which continued to worsen over the next 5 days. She began using a breast pump with frequent pumping and domperidone as a galactogogue. Her milk slowly increased over several days and was normal by 21 days after the injection when she stopped domperidone. At that time, her serum prolactin levels were elevated. The decrease in the mother's milk supply was possibly caused by the corticosteroid injections. Medium to large doses of corticosteroids given systemically or injected into joints or the breast have been reported to cause temporary reduction of lactation.

A study of 46 women who delivered an infant before 34 weeks of gestation found that a course of another corticosteroid (betamethasone, 2 intramuscular injections of 11.4 mg of betamethasone 24 hours apart) given between 3 and 9 days before delivery resulted in delayed lactogenesis II and lower average milk volumes during the 10 days after delivery. Milk volume was not affected if the infant was delivered less than 3 days or more than 10 days after the mother received the corticosteroid. An equivalent dosage regimen of triamcinolone might have the same effect.

A study of 87 pregnant women found that betamethasone given as above during pregnancy caused a premature stimulation of lactose secretion during pregnancy. Although the increase was statistically significant, the clinical importance appears to be minimal. An equivalent dosage regimen of triamcinolone might have the same effect.

A nursing mother who was 7 months postpartum had triamcinolone 40 mg injected into the first dorsal compartment of the wrist along with 2 mL of 1% lidocaine for de Quervain tenosynovitis. Twenty-four hours after the injection, the patient reported a 90% decrease in lactation as measured by breast pumping before and after the injection. She continued to pump her breasts and began taking fenugreek to stimulate lactation. Within 1 week, her milk supply increased by 50% and by 1 month after the injection, she was able to meet her infants breastfeeding needs.

A woman with idiopathic granulomatous mastitis received an injection of 40 mg of triamcinolone acetonide into erythematous areas of the affected breast. Her milk production decreased from the injected left breast. She had originally been able to express 60 mL on that side with an electric breast pump, and after the injection she was only able to express 10 mL. Her milk supply on the affected side recovered over the course of 2 weeks. Production on the unaffected right breast did not decrease.

12.1.4 Exposure Routes

Rapid absorption following oral administration

12.1.5 Acute Effects

12.1.6 Toxicity Data

LD<sub>50</sub>=>500mg/kg (in rats)

12.1.7 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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2835
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3036
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3036
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3036
For more Interactions (Complete) data for TRIAMCINOLONE (18 total), please visit the HSDB record page.

12.1.8 Antidote and Emergency Treatment

/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/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
/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/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
/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/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160-1

12.1.9 Human Toxicity Excerpts

/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/
Droszcz W et al; Ann Allergy 44 (3): 174-6 (1980)
/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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3035
/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.
Quiram PA et al; Am J Ophthalmol 141 (3): 580-2 (2006)
/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/
Yang CS et a; Ophthalmologica 219 (6): 413-5 (2005)
For more Human Toxicity Excerpts (Complete) data for TRIAMCINOLONE (12 total), please visit the HSDB record page.

12.1.10 Non-Human Toxicity Excerpts

/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.
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 899
/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/
Jerome CP et al; J Med Primatol. 17 (4): 195-203 (1988)
/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.
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 899
/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.
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 899
For more Non-Human Toxicity Excerpts (Complete) data for TRIAMCINOLONE (6 total), please visit the HSDB record page.

12.1.11 Populations at Special Risk

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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3035
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3034
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3035
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3035
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/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3035

12.1.12 Protein Binding

Triamcinolone is mostly bound to corticosteroid-binding globulin or serum albumin. Triamcinolone acetonide is approximately 68% protein bound in plasma.

12.2 Ecological Information

12.2.1 Environmental Water Concentrations

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).
(1) Heberer T; Tox Lett 131: 5-17 (2002)
(2) Koplin DW et al; Environ Sci Toxicol 36: 1202-211 (2002)

12.2.2 Milk Concentrations

Corticosteroids may be distributed into milk ... . /Corticosteroids/
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 3036

13 Associated Disorders and Diseases

14 Literature

14.1 Consolidated References

14.2 NLM Curated PubMed Citations

14.3 Springer Nature References

14.4 Thieme References

14.5 Nature Journal References

14.6 Chemical Co-Occurrences in Literature

14.7 Chemical-Gene Co-Occurrences in Literature

14.8 Chemical-Disease Co-Occurrences in Literature

15 Patents

15.1 Depositor-Supplied Patent Identifiers

15.2 WIPO PATENTSCOPE

15.3 Chemical Co-Occurrences in Patents

15.4 Chemical-Disease Co-Occurrences in Patents

15.5 Chemical-Gene Co-Occurrences in Patents

16 Interactions and Pathways

16.1 Chemical-Target Interactions

16.2 Drug-Drug Interactions

17 Biological Test Results

17.1 BioAssay Results

18 Classification

18.1 MeSH Tree

18.2 NCI Thesaurus Tree

18.3 ChEBI Ontology

18.4 KEGG: Drug

18.5 KEGG: USP

18.6 KEGG: ATC

18.7 KEGG: Target-based Classification of Drugs

18.8 KEGG: JP15

18.9 KEGG: Drug Groups

18.10 KEGG: Drug Classes

18.11 WHO ATC Classification System

18.12 FDA Pharm Classes

18.13 ChemIDplus

18.14 IUPHAR / BPS Guide to PHARMACOLOGY Target Classification

18.15 ChEMBL Target Tree

18.16 UN GHS Classification

18.17 NORMAN Suspect List Exchange Classification

18.18 CCSBase Classification

18.19 EPA DSSTox Classification

18.20 PFAS and Fluorinated Organic Compounds in PubChem

18.21 MolGenie Organic Chemistry Ontology

19 Information Sources

  1. Australian Industrial Chemicals Introduction Scheme (AICIS)
    Pregna-1,4-diene-3,20-dione, 9-fluoro-11,16,17,21-tetrahydroxy-, (11.beta.,16.alpha.)-
    https://services.industrialchemicals.gov.au/search-assessments/
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    https://creativecommons.org/licenses/by-nc/4.0/
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  4. DrugBank
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  7. European Chemicals Agency (ECHA)
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    https://echa.europa.eu/web/guest/legal-notice
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  9. Hazardous Substances Data Bank (HSDB)
  10. Human Metabolome Database (HMDB)
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    http://www.hmdb.ca/citing
  11. CCSbase
    CCSbase Classification
    https://ccsbase.net/
  12. ChEBI
  13. FDA Pharm Classes
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  16. Toxin and Toxin Target Database (T3DB)
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  20. IUPHAR/BPS Guide to PHARMACOLOGY
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    https://www.fda.gov/about-fda/about-website/website-policies#linking
  26. EU Clinical Trials Register
  27. FDA Orange Book
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  28. NORMAN Suspect List Exchange
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    https://creativecommons.org/licenses/by/4.0/
    Triamcinolone
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  29. SpectraBase
    9.alpha.-fluoro-11.beta.,16.alpha.,17.alpha.,21-tetrahydroxy-pregna-1,4-diene-3-one
    https://spectrabase.com/spectrum/EXPueI2VwPQ
  30. Japan Chemical Substance Dictionary (Nikkaji)
  31. KEGG
    LICENSE
    Academic users may freely use the KEGG website. Non-academic use of KEGG generally requires a commercial license
    https://www.kegg.jp/kegg/legal.html
    Therapeutic category of drugs in Japan
    http://www.genome.jp/kegg-bin/get_htext?br08301.keg
    Anatomical Therapeutic Chemical (ATC) classification
    http://www.genome.jp/kegg-bin/get_htext?br08303.keg
    Target-based classification of drugs
    http://www.genome.jp/kegg-bin/get_htext?br08310.keg
    Drugs listed in the Japanese Pharmacopoeia
    http://www.genome.jp/kegg-bin/get_htext?br08311.keg
  32. MassBank Europe
  33. MassBank of North America (MoNA)
    LICENSE
    The content of the MoNA database is licensed under CC BY 4.0.
    https://mona.fiehnlab.ucdavis.edu/documentation/license
  34. Metabolomics Workbench
  35. Nature Chemical Biology
  36. NIPH Clinical Trials Search of Japan
  37. NLM RxNorm Terminology
    LICENSE
    The RxNorm Terminology is created by the National Library of Medicine (NLM) and is in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from NLM. Credit to the U.S. National Library of Medicine as the source is appreciated but not required. The full RxNorm dataset requires a free license.
    https://www.nlm.nih.gov/research/umls/rxnorm/docs/termsofservice.html
  38. WHO Anatomical Therapeutic Chemical (ATC) Classification
    LICENSE
    Use of all or parts of the material requires reference to the WHO Collaborating Centre for Drug Statistics Methodology. Copying and distribution for commercial purposes is not allowed. Changing or manipulating the material is not allowed.
    https://www.whocc.no/copyright_disclaimer/
  39. PharmGKB
    LICENSE
    PharmGKB data are subject to the Creative Commons Attribution-ShareALike 4.0 license (https://creativecommons.org/licenses/by-sa/4.0/).
    https://www.pharmgkb.org/page/policies
  40. Pharos
    LICENSE
    Data accessed from Pharos and TCRD is publicly available from the primary sources listed above. Please respect their individual licenses regarding proper use and redistribution.
    https://pharos.nih.gov/about
  41. Springer Nature
  42. The Cambridge Structural Database
  43. Thieme Chemistry
    LICENSE
    The Thieme Chemistry contribution within PubChem is provided under a CC-BY-NC-ND 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc-nd/4.0/
  44. Wikidata
  45. Wikipedia
  46. Medical Subject Headings (MeSH)
    LICENSE
    Works produced by the U.S. government are not subject to copyright protection in the United States. Any such works found on National Library of Medicine (NLM) Web sites may be freely used or reproduced without permission in the U.S.
    https://www.nlm.nih.gov/copyright.html
  47. PubChem
  48. GHS Classification (UNECE)
  49. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  50. PATENTSCOPE (WIPO)
  51. NCBI
CONTENTS