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Use of IL-23 and IL-17 antagonists to treat autoimmune ocular inflammatory disease

Inactive Publication Date: 2008-08-21
NAT INST OF HEALTH OFFICE OF TECHNILOGY TRANSFER +1
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Benefits of technology

[0020]In still other embodiments, the specified treatment regimen also comprises administering a therapeutic agent that does not antagonize IL-17 or IL-23 activity but is capable of alleviating at least one symptom of the AOID or at least one side effect of the IL-17 or IL-23 antagonists during any or al

Problems solved by technology

OIDs cause pain, irritation, and watering, and may result in loss of visual function.
However, a number of uveitis cases are not responsive to or become refractory to these drugs (see, e.g., Kulkarni, P.
Also, these drugs are associated with serious side effects such as cataracts, glaucoma, delayed wound healing, altered prostaglandin production, corneal complications, increased ocular pressure, superinfections, and reduced immunity to infection (see, e.g., Id., at 181; Guidera, A. C., et al.
Because the existing therapies for AOID have less than optimal efficacy or undesirable side effects, new treatment regimens are needed.

Method used

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Examples

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examples

[0100]The present invention is based upon studies in IL-23p19 knockout (KO) mice and administration of anti-IL-23p19 and anti-IL-17 antibodies to murine models of autoimmune uveitis. These experiments were performed according to the Materials and Methods described in Section II below.[0101]I. Results and Discussion

[0102]In the experiments involving IL-23p19 KO mice, the EAU susceptibility of IL-23p19 KO (IL-23 deficient) mice were compared to the EAU susceptibility of IL-12p35 KO (IL-12 deficient) and IL-12p40 KO (IL-12 and IL-23 deficient) mice. All mice were on the C57BL / 6 background and the EAU induction and scoring was as described in General Methods below. It was found that IL-12p35 is not required for generation of IRBP-specific eye tissue destruction. In contrast, IL-23p19 is essential for development of EAU (Table 1). Cytokine analysis of lymph node cell cultures derived from IRBP-immunized mice showed that the EAU susceptible IL-12 deficient mice (IL-12p35KO) had elevated l...

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Abstract

Novel methods and drug products for treating autoimmune ocular inflammatory disease are disclosed, which involve administration of agents that antagonize one or both of IL-17 and IL-23 activity.

Description

[0001]This application claims the benefit of U.S. Provisional Patent Application No. 60 / 837312, filed Aug. 11, 2006 and the benefit of 60 / 713792, filed Sep. 1, 2005, each of which is incorporated by reference.STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH AND DEVELOPMENT[0002]This invention was made in part with Government support under Cooperative Research and Development Agreement (CRADA) Number M-01969-04, and amendments thereto, executed between Schering-Plough Biopharma and the National Eye Institute, National Institutes of Health. The Government of the United States of America has certain rights in this invention.FIELD OF THE INVENTION[0003]The present invention relates generally to the modulation of immune responses in the eye. More specifically, the invention relates to the use of antagonists of interleukin-23 (IL-23) and interleukin-17 (IL-17) to treat autoimmune ocular inflammatory disease.BACKGROUND OF THE INVENTION[0004]Ocular inflammatory disease (OID) is a general te...

Claims

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Application Information

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IPC IPC(8): A61K39/395A61P29/00
CPCA61K2039/505A61K39/3955C07K2316/96C07K16/244C07K2317/76A61P1/02A61P19/02A61P27/00A61P27/02A61P29/00A61P31/06A61P37/00A61P37/06A61P43/00
Inventor CUA, DANIEL J.KASTELEIN, ROBERT A.TSAI, VAN T.CASPI, RACHELSILVER, PHYLLISLUGER, DROR
Owner NAT INST OF HEALTH OFFICE OF TECHNILOGY TRANSFER
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