Thursday, July 31, 2014
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Asthma; multiple sclerosis
necrosis factor receptor superfamily member 9 (TNFRSF9; 4-1BB; CD137)
Mouse and in vitro
studies suggest LGALS9 is required for the efficacy of anti-4-1BB antibodies
in inflammatory and autoimmune disease. In a mouse experimental autoimmune
encephalomyelitis (EAE) model of MS and a mouse model of allergic asthma,
anti-4-1BB antibodies caused near-complete suppression of disease development
in wild-type mice but failed to protect Lgals9-deficient mice. In
vitro assays showed that human LGALS9 bound to 4-1BB at a
carbohydrate-recognition domain and that binding is prevented when the site
is deglycosylated. Researchers did not disclose next steps, which could
include identifying LGALS9 agonists.
Pfizer Inc. has the
anti-TNFRSF9 mAb PF-05082566 in Phase I
testing to treat cancer and non-Hodgkin's lymphoma.
Bristol-Myers Squibb Co.
has the TNFRSF9-targeting mAb urelumab (BMS-663513) in Phase I
testing to treat solid tumors.
Published online July 31, 2014
Patent application filed;
available for licensing
Madireddi, S. et al. J.
Exp. Med.; published online June 23, 2014;
Contact: Michael Croft, La Jolla Institute for Allergy &
La Jolla, Calif.
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