Abcam, ab141281, Fluticasone propionate, Glucocorticoid agonist

Size: 10mg / 50mg
MW 500.6 Da, Purity >99%. Potent, selective glucocorticoid agonist (EC 50 = 3.7 nM). Higher affinity for the glucocorticoid receptor compared to beclomethasone (K d = 0.5 nM). Lipophilic anti-inflammatory agent. Biological effects include eosinophil apoptosis, reduction in mast cell production and inhibition of TNF-α induced endothelial cell adhesion. Active in vivo .
Key facts
CAS number:80474-14-2,
Purity:>99%,
Form:SolidSee storage information,
Molecular weight:500.6 Da,
Molecular formula:C25H31F3O5S,
PubChem:444036,
Nature:Synthetic,
Solubility:Soluble in DMSO to 100 mM,
Biochemical name:Fluticasone propionate,
Biological description:Potent, selective glucocorticoid agonist (EC50 = 3.7 nM). Higher affinity for the glucocorticoid receptor compared to beclomethasone (Kd = 0.5 nM). Lipophilic anti-inflammatory agent. Biological effects include eosinophil apoptosis, reduction in mast cell production and inhibition of TNF-α induced endothelial cell adhesion. Active in vivo.,
Canonical smiles:CCC(=O)OC1(C(CC2C1(CC(C3(C2CC(C4=CC(=O)C=CC43C)F)F)O)C)C)C(=O)SCF,
Isomeric smiles:CCC(=O)O[C@@]1([C@@H](C[C@@H]2[C@@]1(C[C@@H]([C@]3([C@H]2C[C@@H](C4=CC(=O)C=C[C@@]43C)F)F)O)C)C)C(=O)SCF,
InChi:InChI=1S/C25H31F3O5S/c1-5-20(31)33-25(21(32)34-12-26)13(2)8-15-16-10-18(27)17-9-14(29)6-7-22(17,3)24(16,28)19(30)11-23(15,25)4/h6-7,9,13,15-16,18-19,30H,5,8,10-12H2,1-4H3/t13-,15+,16+,18+,19+,22+,23+,24+,25+/m1/s1,
InChiKey:WMWTYOKRWGGJOA-CENSZEJFSA-N,
IUPAC Name:[(6S,8S,9R,10S,11S,13S,14S,16R,17R)-6,9-difluoro-17-(fluoromethylsulfanylcarbonyl)-11-hydroxy-10,13,16-trimethyl-3-oxo-6,7,8,11,12,14,15,16-octahydrocyclopenta[a]phenanthren-17-yl] propanoate

Properties and Storage Information:
Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions-Ambient, Appropriate long-term storage conditions-Ambient, Storage information-The product can be stored for up to 12 months

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
The Glucocorticoid Receptor (GR) Progesterone Receptor (PR) and Mineralocorticoid Receptor (MR) are important members of the nuclear receptor superfamily. These receptors function as transcription factors and regulate the expression of specific genes in response to their respective ligands. Mechanically when ligands bind to these receptors they induce a conformational change allowing receptor dimerization and nuclear localization. They weigh approximately 94-99 kDa and get expressed in various tissues such as the liver kidney brain and reproductive organs. The Glucocorticoid Receptor is also known as NR3C1 while the Progesterone Receptor is called NR3C3 and the Mineralocorticoid Receptor is referred to as NR3C2.
Biological function summary
These receptors play critical roles in maintaining homeostasis and regulating various physiological processes. The Glucocorticoid Receptor modulates the immune response and metabolic processes while the Progesterone Receptor is important for reproductive functions and pregnancy maintenance. The Mineralocorticoid Receptor regulates electrolyte and fluid balance. These receptors can form complexes with co-regulators and other transcription factors to achieve precise control over gene expression.
Pathways
These receptors participate in the glucocorticoid and mineralocorticoid signaling pathways. The Glucocorticoid Receptor is involved in the HPA axis (hypothalamic-pituitary-adrenal axis) influencing stress response and metabolic control. The Progesterone Receptor plays a role in the regulation of the menstrual cycle and pregnancy-related processes. The Mineralocorticoid Receptor is key in the renin-angiotensin-aldosterone system (RAAS) affecting blood pressure regulation. These receptors interact with other proteins like heat shock proteins for stability and functionality within these pathways.
Disruptions in receptor functions often link to conditions such as Cushing's syndrome and congenital adrenal hyperplasia. The Glucocorticoid Receptor's malfunction can contribute to the development of Cushing's syndrome due to excessive cortisol levels. Meanwhile aberrations in Mineralocorticoid Receptor activity can lead to hypertension and electrolyte imbalance in patients with congenital adrenal hyperplasia. Interaction with proteins like the angiotensin II receptor further emphasizes their involvement in these disorders.