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Vol. 284, Issue 2, 687-692, February 1998
From the Departments of Immunopharmacology (J.R.J., B.B., L.H.,
D.E.G., J.D.W.),
Cellular Biochemistry (S.K.) and
Medicinal Chemistry
(J.A.), SmithKline Beecham Pharmaceuticals, King of Prussia,
Pennsylvania
Chronic inflammatory diseases often are accompanied by intense
angiogenesis, supporting the destructive proliferation of inflammatory tissues. A model of inflammatory angiogenesis is the murine air pouch
granuloma, which has a hyperangiogenic component. In this model, we
explored the regulation of inflammatory angiogenesis using SB 220025, a
specific inhibitor of human p38 mitogen-activated protein (MAP) kinase,
with an IC50 value of 60 nM and 50- to 1000-fold selectivity vs. other kinases tested. In
vivo, this compound reduced the lipopolysaccharide-induced
production of tumor necrosis factor at an ED50 value of 7.5 mg/kg. In the inflammatory angiogenesis model, over the course of
granuloma development, we observed elevated levels of interleukin-1
and tumor necrosis factor-
during the chronic inflammatory phase
when intense angiogenesis occurs. SB 220025 at 30 mg/kg b.i.d. p.o. was
able to greatly reduce the expression of these cytokines and inhibit
angiogenesis by 
40%. To further study the effects of p38/CSBP MAP
kinase inhibition in angiogenesis-dependent chronic inflammatory
disease, SB 220025 was tested in murine collagen-induced arthritis. In
this model, SB 220025 was able to prevent the progression of
established arthritis. Thus, this p38/CSBP MAP kinase inhibitor, which
can reduce inflammatory cytokine production and inhibit angiogenesis,
is an effective treatment for chronic proliferative inflammatory
disease.
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