Diflorasone acts as a corticosteroid hormone receptor agonist. It enters cells by diffusion across the cell membrane and binds to the glucocorticoid receptor (GR) in the cytoplasm. The receptor complex subsequently translocates to the nucleus and activates or represses genes by interacting with glucocorticoid response elements (GREs). Gene activation leads to anti-inflammatory effects, while gene repression inhibits production of pro-inflammatory cytokines.

In vitro, diflorasone demonstrates corticosteroid hormone receptor agonist activity with anti-inflammatory and immunosuppressive properties. It is used in research applications to study glucocorticoid receptor signaling and inflammation pathways. The compound shows potent anti-inflammatory activity in various in vitro models of skin inflammation.

In vivo, diflorasone is used topically for the treatment of inflammatory skin conditions such as eczema and psoriasis. It exhibits anti-inflammatory, antipruritic, and vasoconstrictive properties. Treatment should be limited to 2 consecutive weeks and discontinued when adequate results have been achieved. It should not be used with occlusive dressings.

In vitro receptor binding assays for diflorasone typically use membrane preparations or cytosolic fractions from cells expressing glucocorticoid receptors. Radiolabeled dexamethasone or other glucocorticoid ligands are displaced by increasing concentrations of diflorasone to determine binding affinity (Ki). Non-specific binding is determined in the presence of excess unlabeled glucocorticoid. Bound radioactivity is measured by scintillation counting.

Cell-based functional assays for diflorasone involve treating various cell lines with the compound and measuring glucocorticoid receptor-mediated transcriptional activity. Cells transfected with a glucocorticoid-responsive reporter gene (e.g., luciferase under a GRE) are treated with varying concentrations of diflorasone. Reporter gene activity is measured after 24-48 hours. EC50 values are calculated from dose-response curves. Anti-inflammatory effects are assessed by measuring cytokine production in stimulated cells.

In vivo animal studies for diflorasone typically involve topical application to animal models of skin inflammation, such as croton oil-induced ear edema in mice or oxazolone-induced contact hypersensitivity. The compound's ability to reduce inflammation, erythema, and pruritus is assessed. Efficacy is measured by ear thickness, histological evaluation, and inflammatory cytokine levels. Duration of treatment and withdrawal effects are also evaluated.

Absorption, Distribution and Excretion
Topical corticosteroids can be absorbed through intact, healthy skin. The extent of transdermal absorption of topical corticosteroids depends on a variety of factors, including excipients and the integrity of the epidermal barrier. Skin blockage, inflammation, and/or other disease processes may also increase transdermal absorption. Metabolism/Metabolites Primarily metabolized in the liver and then excreted via the kidneys.
Following topical application, diflorasone is absorbed through the skin and handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Once absorbed, it is metabolized in the liver and excreted primarily through renal pathways. The compound has a molecular weight of 410.45 g/mol and a molecular formula of C22H28F2O5. Systemic absorption is minimal with proper use.

Effects During Pregnancy and Lactation
◉ Overview of Medication Use During Lactation
The use of topical diflubenzuron during lactation has not been studied. 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 a precautionary practice 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; diflubenzuron 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 any 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 birth.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.

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Protein binding
The degree of binding to plasma proteins varies.
Diflorasone is a potent topical corticosteroid with a favorable safety profile when used as directed. Common local side effects include burning, stinging, itching, and dryness at the application site. Prolonged use or application to large areas may lead to systemic corticosteroid side effects, including adrenal suppression. The compound is contraindicated in patients with known hypersensitivity to corticosteroids.

Diflurapone is a 16β-analyte of flumethasone. It is used as a topical anti-inflammatory and antipruritic agent in the form of 17,21-diacetate to treat various skin conditions. It has anti-inflammatory effects. It is an 11β-hydroxysteroid, 20-oxosteroid, 17α-hydroxysteroid, fluorinated steroid, glucocorticoid, 21-hydroxysteroid, 3-oxo-Δ1,Δ4-steroid, primary α-hydroxy ketone, and tertiary α-hydroxy ketone. It is derived from the hydrogenation of pregnane. Diflurapone is a topical corticosteroid used to treat skin itching and inflammation. Diflurapone is a corticosteroid. The mechanism of action of diflurapone is as a corticosteroid hormone receptor agonist. Diflurapone is a synthetic glucocorticoid with anti-inflammatory and immunosuppressive effects. Like other glucocorticoids, diflurapone enters cells by diffusion across the cell membrane and binds to glucocorticoid receptors (GR) in the cytoplasm. Subsequently, the receptor complex translocates to the cell nucleus and activates or inhibits the gene by interacting with a short palindromic DNA sequence called a glucocorticoid response element (GRE). Gene activation produces anti-inflammatory effects, such as upregulation of IκB, while gene inhibition suppresses the production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2, and IL-6, thereby preventing the activation of cytotoxic T lymphocytes.
See also: Diflurazepam diacetate (active ingredient).
Indications
For relief of inflammatory and pruritus symptoms in corticosteroid-sensitive dermatitis.
FDA Label
Mechanism of Action
The anti-inflammatory mechanism of topical steroid treatment for corticosteroid-sensitive dermatitis is not fully understood. However, it is believed that the mechanism of action of corticosteroids is through induction of phospholipase A2 inhibitory proteins (collectively known as lipocortin). It is speculated that these proteins control the biosynthesis of potent inflammatory mediators such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.

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Pharmacodynamics
Like other topical corticosteroids, diflubenzuron has anti-inflammatory, antipruritic, and vasoconstrictive effects. The pharmacokinetic pathway of topical corticosteroids after absorption through the skin is similar to that of systemically administered corticosteroids. Diflubenzuron is a potent topical corticosteroid and should not be used with occlusive dressings. It is recommended that the course of treatment not exceed two consecutive weeks and that treatment be discontinued after achieving the desired therapeutic effect.
D如果真的flor as one (also known as Apexicon, Florone, and Psorcon) is a synthetic glucocorticoid used for the relief of inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. It is a potent topical corticosteroid that should be used with caution and not with occlusive dressings. The precise mechanism of anti-inflammatory activity of topical steroids is thought to involve the induction of phospholipase A2 inhibitory proteins (lipocortins), which control the biosynthesis of prostaglandins and leukotrienes.

C22H28F2O5

410.4578

410.19

2557-49-5

71415

White to off-white solid powder

1.4±0.1 g/cm3

569.8±50.0 °C at 760 mmHg

228-239ºC

298.4±30.1 °C

0.0±3.6 mmHg at 25°C

1.579

1.61

3

7

2

29

839

9

C[C@@]12[C@](C(CO)=O)(O)[C@@H](C)C[C@@]1([H])[C@]3([H])C[C@H](F)C4=CC(C=C[C@]4(C)[C@@]3(F)[C@@H](O)C2)=O

WXURHACBFYSXBI-XHIJKXOTSA-N

InChI=1S/C22H28F2O5/c1-11-6-13-14-8-16(23)15-7-12(26)4-5-19(15,2)21(14,24)17(27)9-20(13,3)22(11,29)18(28)10-25/h4-5,7,11,13-14,16-17,25,27,29H,6,8-10H2,1-3H3/t11-,13-,14-,16-,17-,19-,20-,21-,22-/m0/s1

(6S,8S,9R,10S,11S,13S,14S,16S,17R)-6,9-difluoro-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13,16-trimethyl-6,7,8,11,12,14,15,16-octahydrocyclopenta[a]phenanthren-3-one

U 34865; Diflorasone

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 : ~130 mg/mL (~316.73 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.09 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.09 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.09 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.)