| Stereochemistry | ABSOLUTE |
| Molecular Formula | C33H43FO7 |
| Molecular Weight | 570.6887 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 8 / 8 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@]4(C)[C@@]3(F)[C@@H](O)C[C@]2(C)[C@@]1(OC(=O)C5CC5)C(=O)COC(=O)C6CCCCC6
InChI
InChIKey=JPTKVJWWVFLEJL-GVPGRCOTSA-N
InChI=1S/C33H43FO7/c1-19-15-25-24-12-11-22-16-23(35)13-14-30(22,2)32(24,34)26(36)17-31(25,3)33(19,41-29(39)21-9-10-21)27(37)18-40-28(38)20-7-5-4-6-8-20/h13-14,16,19-21,24-26,36H,4-12,15,17-18H2,1-3H3/t19-,24+,25+,26+,30+,31+,32+,33+/m1/s1
Dexamethasone is an anti-inflammatory agent that is FDA approved for the treatment of many conditions, including rheumatic problems, a number of skin diseases, severe allergies, asthma, chronic obstructive lung disease, croup, brain swelling and others. Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. Adverse reactions are: Glaucoma with optic nerve damage, visual acuity and field defects; cataract formation; secondary ocular infection following suppression of host response; and perforation of the globe may occur; muscle weakness; osteoporosis and others. Aminoglutethimide may diminish adrenal suppression by corticosteroids. Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance.
CNS Activity
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Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
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Drug as victim
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PubMed
Patents
Sample Use Guides
The dose and administration frequency varies with the therapeutic protocol and the associated treatment(s). The usual posology of NEOFORDEX® is 40 mg once per day of administration.
Route of Administration:
Oral
The effects on apoptosis and related signaling pathways in the t(4;14)+ multiple myeloma (MM) subset, applying drug combinations including a FGFR3 tyrosine kinase inhibitor (RTKI), the proteasome inhibitor bortezomib, and dexamethasone were tested. RTKI, bortezomib, and dexamethasone were active as single agents in t(4;14)+ MM. RTK inhibition triggered complementary proapoptotic pathways (e.g., decrease of antiapoptotic Mcl-1 protein, down-regulation of p44/42 mitogen-activated protein kinase, and activation of proapoptotic stress-activated protein/c-Jun NH(2)-terminal kinases). Synergistic or additive effects were found by combinations of RTKI with dexamethasone or bortezomib. In t(4;14)+, N-ras-mutated NCI-H929 cells, resistance to RTKI was overcome by addition of dexamethasone. Notably, the combination of RTKI and dexamethasone showed additive proapoptotic effects in bortezomib-insensitive t(4;14)+ MM.
ACTIVE MOIETY
SUBSTANCE RECORD
