Absorption, Distribution and Excretion
Topical corticosteroids can be absorbed from intact healthy skin. The extent of percutaneous absorption of topical corticosteroids is determined by many factors, including the vehicle and the integrity of the epidermal barrier. Occlusion, inflammation and/or other disease processes in the skin may also increase percutaneous absorption.

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Metabolism / Metabolites
Metabolized, primarily in the liver, and then excreted by the kidneys.

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Topical diflorasone 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. Only the lower potency corticosteroids should be used on the nipple or areola where the infant could directly ingest the drugs from the skin; diflorasone should be avoided on the nipple. 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. Any topical corticosteroid should be wiped off thoroughly prior to nursing if it is being applied to the breast or nipple area.
◉ 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.

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Protein Binding
Bound to plasma proteins in varying degrees.

Diflorasone is the 16beta-analogue of flumethasone. It is used as the 17,21-diacetate as a topical anti-inflammatory and antipruritic in the treatment of various skin disorders. It has a role as an anti-inflammatory drug. It is an 11beta-hydroxy steroid, a 20-oxo steroid, a 17alpha-hydroxy steroid, a fluorinated steroid, a glucocorticoid, a 21-hydroxy steroid, a 3-oxo-Delta(1),Delta(4)-steroid, a primary alpha-hydroxy ketone and a tertiary alpha-hydroxy ketone. It derives from a hydride of a pregnane.
Diflorasone is a topical corticosteroid used to treat itching and inflammation of the skin.
Diflorasone is a Corticosteroid. The mechanism of action of diflorasone is as a Corticosteroid Hormone Receptor Agonist.
Diflorasone is a synthetic glucocorticoid with anti-inflammatory and immunosuppressive properties. Like other glucocorticoids, diflorasone enters the cell 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 short, palindromic DNA sequences called glucocorticoid response element (GRE). Gene activation leads to the exertion of anti-inflammatory effects, e.g. upregulation of IkappaB, while gene repression inhibits production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2 and IL-6, thereby preventing activation of cytotoxic T-lymphocytes.
See also: Diflorasone Diacetate (active moiety of).

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Drug Indication
For relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatoses.
FDA Label

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Mechanism of Action
The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A₂ inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation 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, diflorasone has anti-inflammatory, antipruritic, and vasoconstrictive properties. Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Diflorasone is a potent topical corticosteroid that should not be used with occlusive dressings. It is recommended that treatment should be limited to 2 consecutive weeks and therapy should be discontinued when adequate results have been achieved.

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.)