| Stereochemistry | RACEMIC |
| Molecular Formula | C16H18O3 |
| Molecular Weight | 258.3123 |
| Optical Activity | ( + / - ) |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 1 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(C(O)=O)C1=CC=C(\C=C2/CCCCC2=O)C=C1
InChI
InChIKey=AUZUGWXLBGZUPP-GXDHUFHOSA-N
InChI=1S/C16H18O3/c1-11(16(18)19)13-8-6-12(7-9-13)10-14-4-2-3-5-15(14)17/h6-11H,2-5H2,1H3,(H,18,19)/b14-10+
| Molecular Formula | C16H18O3 |
| Molecular Weight | 258.3123 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | RACEMIC |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 1 |
| Optical Activity | ( + / - ) |
Pelubiprofen, 2-[4-(Oxocyclohexylidene methyl)phenyl]propionic acid, is one of the 2-arylpropionic acid class of non-steroidal anti-inflammatory drugs (NSAIDs). It has wide variety of indications proposed: osteoarthritis, rheumatoid arthritis, musculoskeletal pain, post-operative trauma, backache, neck-shoulder syndrome and dental pain. Pelubiprofen is a prodrug of 2-arylpropionic acid with relatively selective effects on cyclooxygenase-2 activity. Antiinflammatory properties of pelubiprofen are due to its ability to both decrease prostaglandin synthesis by inhibiting the activities of cyclooxygenases (COXs) and IkB kinase-b (IKK-b). Pelubiprofen was found to have an anti-edema effect in the carrageenan-induced paw edema model in rats, one of the well-established acute inflammatory models in vivo. Pelubiprofen was well tolerated in single doses up to 120mg and at a dosage of 180 mg/day. No drug accumulation was evident, suggesting that it may be useful for long term treatment.
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RAW 264.7 mouse macrophage cell line. Pelubiprofen potently diminished PGE2 productions through inhibition of COX enzyme activity (IC50 values for COX-1 and COX-2 are 10.66 +/-0.99 and 2.88 +/-1.01 uM, respectively), but also reduced the expressions of COX-2, inducible nitric oxide (iNOS), tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), and IL-6 at transcriptional level in LPS-induced RAW 264.7 cells. Pelubiprofen attenuated the LPS-induced transcription activity and the DNA binding activity of NF-kB, which was accompanied by a parallel reduction of degradation and phosphorylation of inhibitory kappa B-a (IkB-a) and consequently by decreased nuclear translocation of NF-kB. Pelubipofen inhibited the LPS-induced phosphorylation of IKK-b and transforming growth factor-b activated kinase-1 (TAK1).
