Darn doesn't sound to promising, but some people have had some
positive results with Kineret. This is from the John Hopkins website
(editorial comments are from John Hopkins)
http://www.hopkins-arthritis.som.jhmi.edu/edu/eular2004/ra-treatments-il1.html

OP0108 TREATMENT OF MODERATE TO SEVERE RHEUMATOID ARTHRITIS WITH
IL1-TRAP
C.O. Bingham III, M. Genovese, L. Moreland, J. Papadopoulos, M.V.
Parsey; United States

Kineret® is currently the only approved therapy aimed at the
inhibition of IL-1, a cytokine involved in the pathogenesis of
rheumatoid arthritis (RA). Its efficacy is modest, however, perhaps
due to its short half-life. In this study, Bingham et al investigate
the efficacy and safety of a new IL-1 inhibitor, IL-1 Trap. IL-1 Trap
is a specific, high affinity inhibitor of IL-1 consisting of the Fc
portion of human IgG1 and the extracellular domains of both IL-1
receptor components (the Type I receptor and receptor accessory
protein) administered subcutaneously once weekly.

Methods: 201 patients with moderate to severe RA (>10 swollen and
tender joints) were randomized to one of four treatment groups: 25mg,
50mg, or 100mg weekly subcutaneous injections of IL-1 Trap, or
placebo. Patients had to have failed at least one prior DMARD and were
allowed to continue current therapy at stable doses, including
prednisone, methotrexate, and NSAIDS. No other biologic therapy, such
anti-TNF inhibitors, was permitted. ACR 20 at 12 weeks was as the
primary endpoint.

Results: The majority of patients in all groups were on background
DMARDs (60-68%). The mean baseline DAS28 scores ranged from 5.47-5.77.
The ACR 20 scores at week 12 using a LOCF analysis were 46.0%, 20.8%,
34.8%, and 30.9% in the 100mg, 50mg, 25mg, and placebo groups,
respectively (pNS).

ESR and CRP decreased in a dose-dependent fashion with statistical
significance reached at 12 weeks for the 100 mg dose compared to
placebo: CRP (mean change -1.3 mg/dL vs. -0.1 mg/dL, p<0.001) and ESR
(LS mean change –7.8 vs. –1.0, p=0.044). The AUC for DAS28 of the
100mg dose was significantly different compared to placebo for the
active treatment period (p = 0.008, ANOVA). Also, the change in DAS 28
at the 100mg dose was significantly different from placebo at nearly
all time points tested.

Injection site reactions (burning) were the most common adverse event
and occurred with similar frequency (34%) in both the 100mg IL-1 Trap
and placebo groups. No increased incidence of infections was found.
Antibodies to IL-1 occurred in <5% of patients treated with IL-1 Trap
and the occurrence was not dose-related.

Conclusion: Although the ACR 20 response to IL-1 Trap treatment was
not significantly higher compared to placebo, the 100mg dose showed
some clinical and biological efficacy as evidenced by the
significantly enhanced reduction in ESR and CRP levels, as well as the
significant reduction in DAS28 score. Given the apparent safety at
these doses of IL-1 Trap and trends towards efficacy, further study at
higher doses is warranted.

Editorial Comments: IL-1 exhibits potent pro-inflammatory properties
and is believed to be an important mediator of bone and joint
destruction in RA. The failure of anakinra to have a profound effect
in RA has called the role of IL-1 in RA somewhat into question. But
the short half-life and relatively low potency of anakinra makes it a
less than ideal agent for a definitive proof-of-concept study of IL-1
in RA.

IL-Trap, an IL-1 inhibitor with high (picomolar) affinity and long
duration of action, was a hopeful new agent for this long awaited
proof-of-concept study. The current results are disappointing. Despite
its high potency and affinity, the clinical response to this agent was
dismal, although it is true that a high enough dose may not have been
employed in this Phase II study. We may have to finally accept the
fact that TNF, but not IL-1, drives the inflammatory processes in the
rheumatoid joint.

 

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