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Technology: IFN-beta

Interferon beta (IFN-) was shown to counteract interferon gamma (IFN-y) effects in multiple tissues:


IFN- inhibits Th1 cytokines, including IFN-y, in multiple sclerosis, whereas Th2 cytokines are induced. The therapeutic effect of IFN- in multiple sclerosis is most likely related to the antagonistic effects on IFN-y.


IFN- suppresses mitogen-induced release of pro-inflammatory cytokines such as IFN-y by peripheral blood mononuclear cells.


IFN- antagonises IFN-y-induced expression of specific antigens by human and murine macrophages.


IFN-beta inhibits IFN-y-expression by T-cells and natural killer cells.

TIGO concluded that one approach to develop a causal treatment of alopecia areata would be the re-positioning of IFN- and showing its effect in a clinical proof-of-concept trial in this new indication.

TIGO is currently planning in cooperation with partners from academia and clinical dermatology a clinical study programme for the clinical validation of the use of IFN- in alopecia areata.

IFN- containing pharmaceutical products are marketed for other indications than alopecia areata. Hence extensive data concerning safety on systemic use in humans is available and well documented.

Not taking into account the innovative aspects of the project, time-to-market authorisation for the proposed therapeutic concept, i.e. repurposing of IFN- containing pharmaceutical products, will be considerably shorter and associated with less risk as compared to the development of new pharmaceuticals for this indication.

An European patent is pending.

on the right:
Ribbon diagram of IFN- backbone with side chains of residues known to be important for activity.

Interferon beta

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