title: Reduction of acute-phase proteins with tenidap sodium, a cytokine-modulating anti-rheumatic drug.
abstract: Four independent studies have investigated and compared the effects of tenidap sodium, naproxen and placebo on CRP in patients with active RA. One of these studies also investigated the effects of tenidap and naproxen on serum amyloid A (SAA) concentrations and ESR. The duration of the four studies ranged between 2 weeks and 24 weeks, and depending on the study, tenidap sodium was administered orally in doses of 40-120 mg/day and naproxen in doses of 1000 mg/day. In all four studies serum CRP concentrations in tenidap-treated patients had decreased significantly from baseline at the time of final assessment. The decrease in CRP concentration in tenidap-treated patients was observed as early as 1 week after initiation of therapy and was sustained for up to 6 months, the last assessment timepoint. CRP concentrations in naproxen-treated and placebo patients were essentially unchanged. The decreases from baseline observed in tenidap-treated patients were significantly greater than the changes observed in naproxen-treated or placebo patients. After 24 weeks of tenidap treatment the decrease in CRP was paralleled by significant decreases in SAA concentration and ESR. The finding that tenidap sodium rapidly, consistently and significantly lowered CRP serum concentrations differentiates tenidap sodium from the NSAID, naproxen. This could possibly have important therapeutic implications given that other long-term investigations have shown that reducing serum CRP and SAA concentrations correlates with a reduction in radiographically-assessed disease progression.
authors.affiliation: Central Research Division, Pfizer Inc, Groton, CT 06340.
authors.forename: L D
authors.initials: LD
authors.lastname: Loose
authors.forename: J D
authors.initials: JD
authors.lastname: Sipe
authors.forename: D S
authors.initials: DS
authors.lastname: Kirby
authors.forename: A R
authors.initials: AR
authors.lastname: Kraska
authors.forename: E S
authors.initials: ES
authors.lastname: Weiner
authors.forename: W R
authors.initials: WR
authors.lastname: Shanahan
authors.forename: M R
authors.initials: MR
authors.lastname: Leeming
authors.forename: P
authors.initials: P
authors.lastname: Farrow
authors.forename: C B
authors.initials: CB
authors.lastname: Stack
authors.forename: N
authors.initials: N
authors.lastname: Ting
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D002097:C-Reactive Protein / Q000032:analysis; D016207:Cytokines / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D007211:Indoles / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009288:Naproxen / Q000008:administration & dosage / Q000627:therapeutic use; D000078183:Oxindoles; D000685:Serum Amyloid A Protein / Q000032:analysis
chemical_list: D000209:Acute-Phase Proteins; D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D007211:Indoles; D000078183:Oxindoles; D000685:Serum Amyloid A Protein; D009288:Naproxen; D002097:C-Reactive Protein; C062866:tenidap