Fluocinonide targets the glucocorticoid receptor. It binds to the cytosolic glucocorticoid receptor. The newly formed receptor-ligand complex translocates into the cell nucleus, where it binds to glucocorticoid response elements in the promoter region of target genes. This modulates gene expression, leading to anti-inflammatory, antipruritic, and vasoconstrictive effects. It inhibits phospholipase A2 and suppresses cytokine release. It is a potent glucocorticoid steroid.

Fluocinonide cream has a lower potential to produce atrophic changes of the skin than either clobetasol cream or clobetasol propionate foam. Fluocinonide (Vanos) is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders. Target: Glucocorticoid Receptor Fluocinonide is a potent glucocorticoid steroid used topically as an anti-inflammatory agent for the treatment of skin disorders such as eczema and seborrhoeic dermatitis. Fluocinonide ranks as a high-potency topical corticosteroid. Minimal amounts should be used for a minimal length of time to avoid the occurrence of adverse effects. Fluocinonide should not be used if infection is present. Fluocinonide is used in veterinary medicine. It is a treatment for allergies in dogs. Natural systemic cortisol concentrations can be suppressed for weeks after one week of topical exposure.
In vitro, Fluocinonide prevents inflammation and epidermal cell proliferation induced by TPA. It binds to the glucocorticoid receptor and has anti-inflammatory properties. It inhibits the expression of pro-inflammatory cytokines and enzymes, such as phospholipase A2. These in vitro studies confirm its mechanism as a glucocorticoid receptor agonist and its anti-inflammatory effects. It is a potent topical corticosteroid.

Fluocinonide causes prompt and sustains pituitary-adrenocortical suppression in healthy dogs. Fluocinonide results in significant reduction of plasma cortisol and iACTH concentrations by day 2 of treatment in healthy dog, and the lower concentrations continued to day 5. One week after the last application of Fluocinonide, plasma iACTH concentrations in the corticosteroid-treated dogs has returned to the range of values for the control dogs; however, pre- and post-ACTH cortisol concentrations remains suppressed in Fluocinonide treated dogs. Two weeks after the last treatment, the pre-ACTH plasma cortisol concentrations of corticosteroid-treated dogs returns to those of the control dogs, but the post-ACTH plasma cortisol concentrations remains suppressed.

Non-cellular receptor binding assays for Fluocinonide typically involve measuring its affinity for the glucocorticoid receptor. These assays use purified receptor or cytosolic preparations and measure the displacement of a labeled ligand. Its binding affinity and potency as a glucocorticoid receptor agonist can be characterized. These experiments are essential for characterizing its receptor binding properties.

In vitro cell-based assays for Fluocinonide are conducted using cells expressing the glucocorticoid receptor to assess its effects on gene expression and inflammation. Cells are treated with the compound, and the expression of glucocorticoid-responsive genes is measured by qPCR or reporter gene assays. Its effects on inflammatory cytokine production and phospholipase A2 activity can also be assessed. These experiments are crucial for confirming its mechanism of action.

In vivo animal studies for Fluocinonide are typically conducted in animal models of skin inflammation to evaluate its topical efficacy. The compound is applied topically to the affected skin area, and its effects on inflammation, redness, and epidermal proliferation are assessed. Its systemic absorption and safety are also evaluated. These studies are essential for validating its in vivo efficacy as a topical corticosteroid.

Absorption, Distribution and Excretion
The extent of transdermal absorption of topical corticosteroids depends on several factors, including the excipients, the integrity of the epidermal barrier, and whether an occlusive dressing is used. Generally, transdermal absorption is minimal. Corticosteroids are primarily metabolized in the liver and then excreted via the kidneys.
Fluocinonide has a molecular weight of 494.53 g/mol. It is a potent fluorinated corticosteroid. It is applied topically, and its systemic absorption is minimal. Its pharmacokinetic properties are characterized by low systemic bioavailability. It is a prescription drug for the treatment of various skin disorders.

Effects During Pregnancy and Lactation
◉ Overview of Medication Use During Lactation
No studies have been conducted on fluocinolone acetonide during lactation. Since only large-area application of potent corticosteroids is likely to have systemic effects on the mother, short-term topical application of corticosteroids is unlikely to pose a risk to the nursing infant through breast milk. However, it is advisable to use the least potent medication on the smallest possible area of skin. It is especially important to ensure that the infant's skin does not come into direct contact with the treated area. Only low-potency corticosteroids should be used on the nipple or areola, where the infant may ingest the medication directly through the skin; fluocinolone acetonide should be avoided on the nipples. Only water-soluble creams or gels should be applied to the breasts, as ointments may expose the infant to high concentrations of mineral oil through licking. If topical corticosteroids are applied to the breast or nipple area, they should be thoroughly wiped off before breastfeeding.
◉ Effects on Breastfed Infants
A mother applied a topical corticosteroid (isofluprednisolone acetate) with high mineralocorticoid activity to her nipples, resulting in QT interval prolongation, Cushing's syndrome-like symptoms, severe hypertension, growth retardation, and electrolyte imbalance in her 2-month-old breastfed infant. The mother had been using the cream due to nipple pain since the infant's birth.
◉ Effects on Lactation and Breast Milk
As of the revision date, no relevant published information was found.
Fluocinonide has an established safety profile from its clinical use. It is generally well-tolerated when used topically. Common side effects include local skin reactions, such as burning, itching, or dryness. Prolonged use may cause skin atrophy or other corticosteroid-related side effects. Comprehensive toxicological data are available from its clinical use. Fluocinonide is an approved topical corticosteroid.

J Drugs Dermatol.2008 Jan;7(1):28-32;J Drugs Dermatol.2008 Jan;7(1):28-32.

Fluocinolone is an organic molecular entity. It is a topical glucocorticoid used to treat eczema. Fluocinolone is a corticosteroid. Its mechanism of action is as a corticosteroid receptor agonist. Fluocinolone is a synthetic glucocorticoid, a derivative of fluocinolone acetone, with anti-inflammatory and antipruritic activities. Fluocinolone binds to glucocorticoid receptors, and the ligand-receptor complex translocates to the nucleus, activating the transcription of genes containing glucocorticoid response elements. Lipocorticin-1 is one of the factors induced by fluocinolone; it interacts with and inhibits the activity of cytoplasmic phospholipase 2α, thereby preventing the translocation of phospholipase to the perinuclear membrane, which in turn prevents the release of arachidonic acid and its conversion into inflammatory prostaglandins. Furthermore, MAPK phosphatase 1 is induced, thereby preventing the triggering of the MAPK cascade, which in turn inhibits Jun N-terminal kinase and c-Jun-mediated pro-inflammatory effects. Finally, fluocinolone directly binds to and inhibits nuclear factor κB, thereby inhibiting the transcription of cyclooxygenase 2 and subsequent prostaglandin synthesis.
A topical corticosteroid used to treat eczema.
See also: Fluocinolone; Sodium Hyaluronate (ingredient).
Drug Indications

A topical anti-inflammatory product used to relieve inflammation and itching symptoms in skin conditions sensitive to corticosteroids.
FDA Label
Mechanism of Action

Fluocinolone is a potent topical corticosteroid used to treat skin conditions such as eczema. Fluocinolone binds to cytoplasmic glucocorticoid receptors. Upon binding to the receptor, the newly formed receptor-ligand complex translocates to the cell nucleus and binds to multiple glucocorticoid response elements (GREs) in the promoter regions of target genes. Subsequently, the DNA-bound receptor interacts with basal transcription factors, leading to increased expression of specific target genes. The anti-inflammatory effects of corticosteroids are thought to be related to lipocortin, a phospholipase A2 inhibitory protein that controls the biosynthesis of prostaglandins and leukotrienes by inhibiting arachidonic acid. Specifically, glucocorticoids induce the synthesis of lipocortin-1 (annexin-1), which then binds to the cell membrane, preventing phospholipase A2 from contacting its substrate arachidonic acid. This leads to a reduction in the production of arachidonic acid. The expression of cyclooxygenases (COX-1 and COX-2) is also inhibited, thereby enhancing the effects of glucocorticoids. In other words, the two major products of inflammation—prostaglandins and leukotrienes—are inhibited by glucocorticoids. Glucocorticoids can also stimulate lipocortin-1 to escape into the extracellular space. Lipocortictin-1 binds to leukocyte membrane receptors, inhibiting various inflammatory responses, including epithelial cell adhesion, migration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mast cells. Furthermore, corticosteroids suppress the immune system through mechanisms including decreased lymphatic function, reduced immunoglobulin and complement concentrations, lymphopenia, and interference with antigen-antibody binding. Similar to other glucocorticoids, fluocinolone acetonide exerts its physiological antagonistic effect on insulin by reducing glycogen production (glycogen formation). It also promotes the breakdown of lipids (lipolysis) and proteins, thereby mobilizing extrahepatic amino acids and ketone bodies. This leads to an increase in blood glucose levels. Simultaneously, glycogen production in the liver is reduced.

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Pharmacodynamics
Fluocinolone acetonide is a potent glucocorticoid used topically as an anti-inflammatory agent to treat skin conditions such as eczema. It relieves itching, redness, dryness, crusting, scaling, inflammation, and discomfort caused by inflammatory skin conditions.
Fluocinonide (Vanos) is a potent synthetic fluorinated corticosteroid used topically for its anti-inflammatory properties. It binds to the glucocorticoid receptor and modulates gene expression. It is used for the treatment of skin disorders such as eczema and seborrhoeic dermatitis. Fluocinonide is an approved drug with a well-established clinical profile.

C26H32F2O7

494.52

494.211

356-12-7

9642

White to off-white solid powder

1.3±0.1 g/cm3

591.1±50.0 °C at 760 mmHg

309ºC

311.3±30.1 °C

0.0±3.8 mmHg at 25°C

1.560

3.36

1

9

4

35

1070

9

CC(=O)OCC(=O)[C@@]12[C@@H](C[C@@H]3[C@@]1(C[C@@H]([C@]4([C@H]3C[C@@H](C5=CC(=O)C=C[C@@]54C)F)F)O)C)OC(O2)(C)C

WJOHZNCJWYWUJD-IUGZLZTKSA-N

InChI=1S/C26H32F2O7/c1-13(29)33-12-20(32)26-21(34-22(2,3)35-26)10-15-16-9-18(27)17-8-14(30)6-7-23(17,4)25(16,28)19(31)11-24(15,26)5/h6-8,15-16,18-19,21,31H,9-12H2,1-5H3/t15-,16-,18-,19-,21+,23-,24-,25-,26+/m0/s1

2-((2S,6aS,6bR,7S,8aS,8bS,11aR,12aS,12bS)-2,6b-difluoro-7-hydroxy-6a,8a,10,10-tetramethyl-4-oxo-2,4,6a,6b,7,8,8a,8b,11a,12,12a,12b-dodecahydro-1H-naphtho[2,1:4,5]indeno[1,2-d][1,3]dioxol-8b-yl)-2-oxoethyl acetate

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)

DMSO: 99 mg/mL (200.2 mM)
Water: 1 mg/mL (Insoluble)
Ethanol: N/A

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.06 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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