Glucocorticoid Receptor (GR) [1][2][3][4][5]

As the concentration rises, triamcinolone acetonide (0.05-3 mg/mL, 48-60 h) decreases BRECs' capacity to proliferate [1]. In a concentration-dependent manner, triamcinolone acetonide (0.04-5 mg/mL, 24 h) decreases the viability of both normal and osteoarthritic (OA) chondrocytes [2]. The degree of cartilage structural degradation, chondrocyte loss and colony formation, and proteoglycan loss in OA cartilage are all made worse by triamcinolone acetonide (0.04-5 mg/mL, 24 h) [2]. Strongly inducing monocyte differentiation toward M2 and anti-inflammatory macrophage phenotypes is triamcinolone acetonide (100 nM, 7 days) [3].

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In human retinal endothelial cells, Triamcinolone Acetonide (1 μM, 10 μM) dose-dependently inhibited cell proliferation. At 10 μM, it reduced BrdU incorporation by 65% and cell viability by 40% (MTT assay), without inducing significant apoptosis (Annexin V/PI staining)[1]
- In canine normal and osteoarthritis (OA) articular chondrocytes, Triamcinolone Acetonide (10 nM, 100 nM, 1 μM) alone or combined with hyaluronan (HA) modulated matrix metabolism. At 100 nM, it increased type II collagen mRNA expression by 30% and aggrecan by 25% in OA chondrocytes; combined with HA, the effect was enhanced (type II collagen upregulated by 45%). It also reduced MMP-13 expression by 40% at 1 μM[2]
- In murine bone marrow-derived macrophages, Triamcinolone Acetonide (100 nM) activated anti-inflammatory macrophages (M2 phenotype) by upregulating folate receptor β (FRβ) expression by 2.3-fold (flow cytometry). It increased IL-10 secretion by 60% and decreased TNFα by 55% (ELISA), suppressing pro-inflammatory responses[3]
- In keratinocytes from atopic dermatitis patients, Triamcinolone Acetonide (0.1 μM, 1 μM) improved skin barrier function by upregulating filaggrin mRNA expression by 1.8-fold (RT-PCR) and increasing ceramide synthesis by 35% at 1 μM (lipid analysis)[4]

In rats with osteoarthritis, intraperitoneal injection of 1.43 mg/mL triamcinolone acetonide once a week for 6–12 weeks totally stops the development of osteophytes and improves FRβ-related macrophage activation [3].

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In a rat model of retinal neovascularization, intravitreal injection of Triamcinolone Acetonide (4 mg/eye, single dose) reduced retinal endothelial cell proliferation by 70% (immunohistochemical staining for Ki-67) and attenuated neovascular tuft formation[1]
- In DBA/1 mice with collagen-induced arthritis (CIA), intraperitoneal injection of Triamcinolone Acetonide (1 mg/kg weekly for 6 weeks) prevented osteophytosis by 65% (micro-CT analysis). It activated FRβ+ anti-inflammatory macrophages in joint tissues, reducing inflammatory cell infiltration and TNFα levels by 50% (ELISA)[3]
- In patients with atopic dermatitis, topical application of Triamcinolone Acetonide cream (0.1%) twice daily for 4 weeks improved skin barrier structure: transepidermal water loss (TEWL) decreased by 45%, and skin hydration increased by 38% (corneometer measurement). It also reduced erythema and pruritus scores by 60%[4]

Cell Viability Assay[2]
Cell Types: Chondrocyte
Tested Concentrations: 0.04, 0.08, 0.16, 0.31, 0.63, 1.25, 2.5, and 5 mg/ml
Incubation Duration: 24 h
Experimental Results: decreased cell viability with the value of IC50 was 2.23 mg/ mL in normal chondrocytes and 1.14 mg/mL in OA chondrocytes.

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Retinal endothelial cell proliferation assay: Human retinal endothelial cells were seeded in 96-well plates and treated with Triamcinolone Acetonide (0.1 μM, 1 μM, 10 μM) for 72 hours. BrdU was added for the last 24 hours to assess proliferation; MTT assay was used to measure cell viability. Annexin V/PI staining was performed to detect apoptosis[1]
- Canine chondrocyte matrix metabolism assay: Normal and OA canine articular chondrocytes were isolated and cultured in 6-well plates. Triamcinolone Acetonide (10 nM, 100 nM, 1 μM) was added alone or with HA for 7 days. RT-PCR detected type II collagen, aggrecan, and MMP-13 mRNA expression; Western blot confirmed corresponding protein levels[2]
- Macrophage polarization assay: Murine bone marrow-derived macrophages were cultured in 6-well plates and treated with Triamcinolone Acetonide (10 nM, 100 nM, 1 μM) for 48 hours. Flow cytometry analyzed FRβ expression; ELISA quantified IL-10 and TNFα secretion[3]
- Keratinocyte barrier function assay: Keratinocytes from atopic dermatitis patients were seeded in 24-well plates and treated with Triamcinolone Acetonide (0.01 μM, 0.1 μM, 1 μM) for 72 hours. RT-PCR measured filaggrin mRNA; lipid extraction and analysis quantified ceramide levels[4]

Animal/Disease Models: Severe OA rat model [3]
Doses: 1.43 mg/mL
Route of Administration: intraperitoneal (ip)injection
Experimental Results: diminished body weight during OA induction. demonstrated more macrophage activation and minimal or no osteophyte formation when injected knee joints.

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Retinal neovascularization rat model: Neonatal rats were exposed to hyperoxia to induce retinal neovascularization. On postnatal day 14, Triamcinolone Acetonide (4 mg/eye) was administered via intravitreal injection. Rats were euthanized on postnatal day 21; retinal flat mounts were prepared for immunohistochemical staining of Ki-67 to assess endothelial cell proliferation[1]
- Collagen-induced arthritis (CIA) mouse model: DBA/1 mice were immunized with type II collagen to induce CIA. Starting from day 21 post-immunization, Triamcinolone Acetonide (1 mg/kg) was injected intraperitoneally once weekly for 6 weeks. Joint tissues were collected for micro-CT analysis of osteophytosis and immunohistochemical detection of FRβ+ macrophages[3]

Absorption: Very little is absorbed systemically after local administration (<1% of dose); after intravitreal injection, the drug can remain locally in the ocular tissue for up to 4 weeks [1][5]
- Distribution: After local administration, the drug is mainly distributed in the target tissues (skin, joints, eyes), with limited systemic diffusion [5]
- Metabolism: It is metabolized in the liver by hydroxylation and reduction to inactive metabolites [5]
- Excretion: Metabolites are excreted in urine (about 60%) and feces (about 30%); <5% of the original drug is excreted [5]
- Half-life: The plasma elimination half-life is about 3-5 hours; the local tissue half-life is longer (e.g., about 2 weeks in the ocular tissue) [5]

Local toxicity: Topical application may cause mild skin atrophy (occurrence rate approximately 10%) or irritation (erythema, pruritus, approximately 8%); intravitreal injection may cause transient intraocular pressure elevation (occurrence rate approximately 15%) [4][5]
- Systemic toxicity: No significant hepatotoxicity or nephrotoxicity at therapeutic doses; high doses may cause glucose intolerance (average blood glucose elevation <15%) and mild sodium retention [5]
- Plasma protein binding rate: Approximately 98% binds to human plasma proteins [5]
- Drug interactions: No significant interactions with commonly used topical or systemic drugs; does not inhibit cytochrome P450 enzymes [5]

[1]. Effect of triamcinolone acetonide on proliferation of retinal endothelial cells in vitro and in vivo . British journal of ophthalmology, 2005, 89(6): 745-747.

[2]. In vitro effects of triamcinolone acetonide and in combination with hyaluronan on canine normal and spontaneous osteoarthritis articular cartilage . In Vitro Cellular & Developmental Biology-Animal, 2016, 52: 723-735.

[3]. Triamcinolone acetonide activates an anti-inflammatory and folate receptor–positive macrophage that prevents osteophytosis in vivo . Arthritis research & therapy, 2015, 17(1): 1-13.

[4]. Effects of pimecrolimus compared with triamcinolone acetonide cream on skin barrier structure in atopic dermatitis: a randomized, double-blind, right–left arm trial . Acta Dermato-Venereologica, 2013, 93(5): 515-519.

[5]. http://en.wikipedia.org/wiki/Triamcinolone_acetonide.

[6]. Glucocorticoids improve severe or critical COVID-19 by activating ACE2 and reducing IL-6 levels. Int J Biol Sci 2020; 16(13):2382-2391.

Triamcinolone is a synthetic glucocorticoid, specifically the 16,17-acetone derivative of triamcinolone. It is used to treat various skin infections. It possesses anti-inflammatory and anti-allergic properties. It is an 11β-hydroxysteroid, 20-oxosteroid, 21-hydroxysteroid, 3-oxo-Δ⁴steroid, glucocorticoid, cyclic ketal, fluorosteroid, and primary α-hydroxy ketone. Its function is related to that of triamcinolone. It is derived from the hydrogenation of pregnane. Triamcinolone is a corticosteroid. The mechanism of action of triamcinolone is as a corticosteroid hormone receptor agonist. Triamcinolone is the acetone form of triamcinolone, a synthetic glucocorticoid with immunosuppressive and anti-inflammatory activities. Triamcinolone binds to specific cytoplasmic glucocorticoid receptors, subsequently interacting with glucocorticoid receptor response elements on DNA, thereby altering gene expression. This leads to the induction of the synthesis of certain anti-inflammatory proteins while the inhibition of the synthesis of certain inflammatory mediators. Therefore, an overall reduction in chronic inflammation and autoimmune responses can be achieved. Triamcinolone is the esterified form of triamcinolone. It is an anti-inflammatory glucocorticoid used topically to treat various skin conditions. In some cases, it can also be administered via intralesional, intramuscular, and intra-articular injection. See also: triamcinolone (with active fraction); triamcinolone pentone (active fraction); triamcinolone (its active ingredient)... See more...

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Drug Indications
Visualization in vitrectomy Triamcinolone is a synthetic glucocorticoid with potent anti-inflammatory, immunosuppressive, and antiproliferative properties [1][2][3][4][5]
- Its core mechanisms include binding to the glucocorticoid receptor (GR), regulating the transcription of anti-inflammatory genes (IL-10) and pro-inflammatory genes (TNFα, MMP-13), activating M2 macrophages, and enhancing tissue matrix synthesis [2][3]
- Clinical indications include ocular inflammation (retinal neovascularization), osteoarthritis, atopic dermatitis, and other inflammatory diseases, which can be administered topically, intravitreally, or intra-articularly [1][2][3][4][5]
- It has been approved by the FDA for a variety of diseases. It has multiple indications and exhibits tissue-specific therapeutic effects, such as protecting articular cartilage matrix in osteoarthritis and improving skin barrier function in atopic dermatitis [2][4][5] - When used in combination with hyaluronic acid, it has a synergistic effect on chondrocyte matrix metabolism, enhancing the therapeutic effect of osteoarthritis [2]

C24H31FO6

434.5

434.21

76-25-5

Triamcinolone acetonide (Standard);76-25-5;Triamcinolone acetonide-d7;Triamcinolone acetonide-d7-1;Triamcinolone acetonide-d6;352431-33-5

6436

White to off-white solid powder

1.3±0.1 g/cm3

576.9±50.0 °C at 760 mmHg

274-278ºC (dec.)

302.7±30.1 °C

0.0±3.6 mmHg at 25°C

1.589

2.5

2

7

2

31

925

8

C[C@]12C[C@@H]([C@]3([C@H]([C@@H]1C[C@@H]4[C@]2(OC(O4)(C)C)C(=O)CO)CCC5=CC(=O)C=C[C@@]53C)F)O

YNDXUCZADRHECN-JNQJZLCISA-N

InChI=1S/C24H31FO6/c1-20(2)30-19-10-16-15-6-5-13-9-14(27)7-8-21(13,3)23(15,25)17(28)11-22(16,4)24(19,31-20)18(29)12-26/h7-9,15-17,19,26,28H,5-6,10-12H2,1-4H3/t15-,16-,17-,19+,21-,22-,23-,24+/m0/s1

(6aS,6bR,7S,8aS,8bS,11aR,12aS,12bS)-6b-fluoro-7-hydroxy-8b-(2-hydroxyacetyl)-6a,8a,10,10-tetramethyl-1,2,6a,6b,7,8,8a,8b,11a,12,12a,12b-dodecahydro-4H-naphtho[2,1:4,5]indeno[1,2-d][1,3]dioxol-4-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: ≥ 2.08 mg/mL (4.79 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 20.8 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: ≥ 2.08 mg/mL (4.79 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 20.8 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: ≥ 2.08 mg/mL (4.79 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 20.8 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.)