Compositions for mucosal and oral administration comprising hcg fragments

Abstract

The invention relates to the field of immunology, more specifically to the field of immune-mediated disorders such as allergies, auto-immune disease, transplantation-related disease and other inflammatory diseases. The invention in particular relates to the systemic treatment of inflammatory disease by oral or mucosal administration of a pharmaceutical composition with a gene-regulatory peptide. The invention provides a pharmaceutical composition in a form for mucosal application for the treatment of a subject suffering from disease, the pharmaceutical composition comprising a pharmacologically effective amount of a gene-regulatory peptide or a functional analogue thereof together with a pharmaceutically acceptable diluent.

Description

CROSS-REFERENCE TO RELATED APPLICATIONS[0001]This application is a divisional of co-pending U.S. patent application Ser. No. 11 / 243,438, filed Oct. 4, 2005, U.S. Pat. No. 7,517,529 (Apr. 14, 2009), which is a continuation of PCT International Patent Appl'n No. PCT / EP2004 / 003747, filed on Apr. 8, 2004, designating the United States of America, and published, in English, as PCT International Publication No. WO 2004 / 093897 on Nov. 4, 2004, which International Application itself claims priority to EP 03076028.4, filed Apr. 8, 2003 with the European Patent Office (EPO), EP 03076029.2, filed Apr. 8, 2003 with the EPO, of EP 03076027.6, filed Apr. 8, 2003, with the EPO, of EP 03076026.8, filed Apr. 8, 2003 with the EPO, of EP 03076022.7 filed Apr. 8, 2003 with the EPO, of U.S. Ser. No. 10 / 409,671, filed Apr. 8, 2003, of EP 03076021.9, filed Apr. 8, 2003 with the EPO, of EP 03076025.0, filed Apr. 8, 2003 with the EPO, of EP 03076024.3, filed Apr. 8, 2003 with the EPO, of EP 03076030.0, file...

AI Technical Summary

Benefits of technology

[0032]Consequently, a novel therapeutic inroad is provided, using the pharmaceutical potential of gene-regulatory peptides and derivatives thereof. Indeed, evidence of specific up- or down-regulation of NFκB driven pro- or anti-inflammatory cytokine cascades that are each, and in concert, directing the body's immune response was found in silico in gene-arrays by expression profiling studies, in vitro after treatment of immune cells and in vivo in experimental animals treated with gene-regulatory peptides. Also, considering that NFκB is a primary effector of disease (A. S. Baldwin, J. Clin. Invest., 2001, 107:3-6), using the hCG-derived gene-regulatory peptides offer significant potential for the treatment of a variety of human and animal diseases, thereby tapping the pharmaceutical potential of the exact substances that help balance the mother's immune system such that her pregnancy is safely maintained.

Problems solved by technology

In most cases, this complex defense network successfully restores normal homeostasis, but at other times the immunological or inflammatory mediators may actually prove deleterious to the host.

These immunological mediators are generally seen to cause the life-threatening systemic disease seen with sepsis / SIRS.

These immunological mediators are, on the one hand, required locally, for example, as effective antibacterial response, but are, in contrast, potentially toxic when secreted into the circulation.

When secreted into the circulation, these mediators can cause, in an upward spiral of cause and effect, the further systemic release of these mediators, in the end leading to severe disease, such as multiple organ failure and death.

During the diabetic phase, the inflammatory responses in the mice (and humans suffering from established diabetes) are much more diverse, due to the vascular damage caused by the high glucose levels tissue damage results throughout the body, again inflammatory mediators get released and secondary inflammations flourish, resulting in inflammation throughout whole body, however, with much more serious consequences to the patient than the earlier phase at first sight seems to cause.

Moreover, upon co-transfer, Th2 T-cells could not ameliorate the Th1-induced diabetes, even when Th2 cells were co-transferred in ten-fold excess.

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