2-(4-(3-methyl-2-thienyl)phenyl)propionic-acid has been researched along with Arthritis--Rheumatoid* in 2 studies
1 trial(s) available for 2-(4-(3-methyl-2-thienyl)phenyl)propionic-acid and Arthritis--Rheumatoid
| Article | Year |
|---|---|
[Late phase II clinical study of M-5011C on rheumatoid arthritis--a multi-institutional double-blind, three group comparative, dose finding study].
Topics: Activities of Daily Living; Aged; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Double-Blind Method; Drug Administration Schedule; Female; Humans; Male; Middle Aged; Phenylpropionates | 1997 |
1 other study(ies) available for 2-(4-(3-methyl-2-thienyl)phenyl)propionic-acid and Arthritis--Rheumatoid
| Article | Year |
|---|---|
The effects of a newly developed nonsteroidal anti-inflammatory drug (M-5011) on arachidonic acid metabolism in rheumatoid synovial fibroblasts.
M-5011 (d-2-[4-(3-methyl-2-thienyl)phenyl]propionic acid) is a newly developed nonsteroidal anti-inflammatory drug (NSAID) that displays potent anti-inflammatory and analgesic properties with low ulcerogenic activities in animal models. In this study, the effects of M-5011 on arachidonic acid (AA) metabolism in synovial fibroblasts from patients with rheumatoid arthritis were evaluated and compared with those of other NSAIDs in vitro. Either M-5011 or ketoprofen potently inhibited prostaglandin (PG) E2 production by cyclooxygenase (COX)-2 from exogenous AA in interleukin-1beta (IL-1beta)-stimulated cells. The IC50 values of M-5011 and ketoprofen were 4.4 x 10(-7) and 5.9 x 10(-7) M, respectively. However, diclofenac and indomethacin were one order less potent. Although the latter two drugs exhibited time-dependent and irreversible inhibition on COX-2 in IL-1beta-stimulated cells, the inhibitory effects of M-5011 and ketoprofen were reversible. PGE2 production by COX-1 from exogenous AA in non-stimulated cells was also inhibited by M-5011 with a potency less than that of ketoprofen. In addition, M-5011 inhibited [14C]AA release from prelabeled synovial cells stimulated with bradykinin. However, ketoprofen hardly affected the [14C]AA release. It is likely that the effects of M-5011 on AA metabolism are, in part, responsible for its in vivo efficacy and safety profile. Topics: Anti-Inflammatory Agents, Non-Steroidal; Arachidonic Acid; Arthritis, Rheumatoid; Bradykinin; Carbon Radioisotopes; Cells, Cultured; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprostone; Dose-Response Relationship, Drug; Female; Fibroblasts; Humans; Indomethacin; Interleukin-1; Isoenzymes; Ketoprofen; Membrane Proteins; Middle Aged; Phenylpropionates; Prostaglandin-Endoperoxide Synthases; Synovial Membrane | 1997 |