Dexamethasone fluorescein
Dexamethasone fluorescein is a fluorescently labeled steroid conjugate that binds to glucocorticoid receptors. Dexamethasone fluorescein binds to glucocorticoid receptors. Dexamethasone fluorescein serves as a marker for evaluating the delivery of drugs via subconjunctival injection and intratympanic administration. Sustained transscleral diffusion is achieved when Dexamethasone fluorescein is delivered via fibrin sealant. Dexamethasone fluorescein can be used to investigate the binding and localization of glucocorticoid receptors.
For research use only. We do not sell to patients.
- CAS No.: 216854-76-1
- Formula: C45H45FN2O9S2
- Molecular Weight:840.98
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Dexamethasone fluorescein (10-4 M; 6 h) exhibits a steady-state permeability constant (Ktrans) of 1.64 × 10-6 cm/sec in human scleral sections, which is significantly lower than the permeability of more hydrophilic compounds fluorescein and methotrexate-fluorescein[1].
Dexamethasone fluorescein (100 μM; 10 hr) exhibits steady, gradual release from a fibrin sealant depot over 10 hours, with 4.0% of the initial amount released by the end of the period[3].
Dexamethasone fluorescein (100 μM; 24 hr) delivered via fibrin sealant shows sustained transscleral diffusion across excised human scleral sections over 24 hours, with 1% of the initial amount diffused, an apparent scleral permeability of 1.58×10-7 cm/s, and minimal tissue uptake of 3%[3].
Dexamethasone fluorescein (1.0×10-4 M; 24 hr) delivered in balanced salt solution (BSS) shows rapid transscleral diffusion across excised human scleral sections over 24 hours, with 18% of the initial amount diffused, an apparent scleral permeability of 2.57×10-6 cm2/s, and substantial tissue uptake of 23%[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 216854-76-1
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Molecular Weight 840.98
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Formula C45H45FN2O9S2
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SMILES
O=C1OC2(C3=CC=C(O)C=C3OC4=CC(O)=CC=C42)C5=CC=C(NC(NCCSCC([C@@]6([C@@]7([C@@]([C@@]8([H])[C@]([C@H](C7)O)([C@@]9(C(CC8)=CC(C=C9)=O)C)F)([H])C[C@H]6C)C)O)=O)=S)C=C51
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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How to Select the Route of Administration for Mammals
Route-of-administration selection in mammals is a pharmacokinetic, pharmacodynamic, formulation, animal-welfare, and translational decision, not a default technical choice. The selected route should match the study goal: intravenous dosing is most useful when complete systemic exposure and rapid onset are required, oral dosing is most translational for orally intended medicines but is affected by absorption and first-pass metabolism, subcutaneous or intramuscular dosing can provide slower systemic exposure, and intraperitoneal dosing can be useful in rodent proof-of-concept studies but may have limited clinical translation. Published route-comparison studies show that the same compound can produce different exposure, onset, bioavailability, tissue distribution, and tolerability depending on route; therefore, route choice should be supported by pilot pharmacokinetic or pharmacodynamic evidence when the literature is insufficient. Unresolved questions include how to standardize route sel
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Purity & Documentation
References
[1]. Cruysberg LP, et al. In vitro human scleral permeability of fluorescein, dexamethasone-fluorescein, methotrexate-fluorescein and rhodamine 6G and the use of a coated coil as a new drug delivery system. J Ocul Pharmacol Ther. 2002 Dec;18(6):559-69. [Content Brief]
[2]. Li W, et al. Permeation Enhancers for Intratympanically-applied Drugs Studied Using Fluorescent Dexamethasone as a Marker. Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology. 2018 Jun;39(5):639-647. [Content Brief]
[3]. Cruysberg LP, et al. In vitro sustained human transscleral drug delivery of fluorescein-labeled dexamethasone and methotrexate with fibrin sealant. Current eye research. 2005 Aug;30(8):653-60. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)