Faron Pharmaceuticals Oy

Other

Biotie Therapies Corporation

Marko Salmi

Sirpa Jalkanen

Markku Jalkanen

Mikael Maksimow

Heikki Irjala

The invention relates to a novel cell derived from the human body, where said cell comprises a Clever-1 receptor; to a method for affecting the immune system of an individual and for treatment of diseases or conditions related to the function of the immune system and to methods for screening of cancer patients that may respond to an anti-Clever-1 therapy or for diagnosing of a pregnancy complication or for estimating the risk of such complication in a pregnant woman.

Cell and therapeutical and diagnostical methods based thereon

This invention concerns methods for monitoring the development of and for treatment of ARDS in a patient. The method for monitoring the development of ARDS is based on comparing the level or activity of the biomarkers obtained in a sample drawn at a later point of time to the levels or activities of the same biomarkers in a sample drawn at a previous point of time. A favorable change in the level or activity of a certain biomarker represents a regression of the disease (recovery of the patient), and, conversely, an adverse change in the level or activity of a certain biomarker represents a worsening of the disease. If, for example, the level or activity for one or more of the biomarkers monitored discontinues to show a favorable change or starts to show an unfavorable change, the treatment of the patient is enhanced by administering a therapeutically active agent useful in the treatment of ARDS. The invention concerns further a method for simultaneous determination of a multiple of biomarkers in a sample from a patient, wherein said biomarkers are related to ARDS. The level or the activity of the biomarkers is determined. The invention also concerns a diagnostic kit useful for carrying out the method, particularly a kit comprising a chip, such as a microarray suitable for use in biochip technology.

Method for determining acute respiratory distress syndrome (ARDS) related biomarkers, a method to monitor the development and treatment of ARDS in a patient

The invention concerns a method for monitoring the development of a disease in a patient, and for assessing the efficacy of a therapy influencing on the CD73 level or activity in the patient, in particular a cytokine therapy or a statin therapy. CD73 in a tissue fluid drawn from the patient is used as a biomarker. The invention concerns also methods for determining of CD73 protein in a sample drawn from an individual's tissue fluid.

Biomarker for monitoring development of diseases and assessing the efficacy of therapies

This invention relates to a method for treatment or prevention of metabolic syndrome and diseases or conditions resulting therefrom in an individual, wherein an effective amount of an amine oxidase enzyme inhibitor is administered to said individual. In addition, the invention relates to a method for inhibiting an amine oxidase enzyme or for treatment or prevention of diseases or conditions benefiting from inhibition of an amine oxidase enzyme in an individual, wherein a vitamin B1, its derivative, its precursor or metabolite is administered to said individual. Finally, the invention relates to a food product comprising an amine oxidase enzyme inhibitor in combination with a foodstuff, a food additive comprising an amine oxidase enzyme inhibitor in combination with a liquid, solid or semisolid carrier.

Compositions useful especially for treatment or prevention of metabolic syndrome

A novel protein Common Lymphatic Endothelial and Vascular Endothelial Receptor-1 (CLEVER-1) is described. CLEVER-1 mediates leukocyte and malignant cell binding to vascular and lymphoid endothelial cells. CLEVER-1 is the first protein that has been reported to mediate both influx into and efflux from the lymph nodes. Also provided are methods of treating inflammation and preventing metastasis of malignant cells by providing an inhibitor of CLEVER-1 binding.

Common lymphatic endothelial and vascular endothelial receptor-1 (CLEVER-1) and uses thereof

A novel endothelial cell molecule, VAP-1, is described that mediates lymphocyte binding in man. Further described are anti-VAP-1 monoclonal antibodies and methods for the diagnosis and treatment of inflammatory and autoimmune diseases by the administration of VAP-1 binding compounds, such as anti-VAP-1 antibodies.

Method for antagonizing vascular adhesion protein-1 (VAP-1)-mediated

CD44 is a family of glycoproteins involved in cell-cell and cell-matrix interactions. In addition to the major 90 kD form present on most hematopoietic cells, larger forms are found on keratinocytes and carcinoma cell lines. These bigger isoforms of CD44 arise by alternative splicing that results in insertion of one or more of the 'variant' exons into the extracellular part of the 90 kD constant form of the molecule. Antibodies were raised against a synthetic peptide containing a sequence encoded by the human exon 6A mAb thus obtained (designated Var3.1) strongly reacted with the plasma membranes of squamous cells in upper layers of skin and tonsil surface epithelia. Weaker staining was seen in germinal centers, vascular endothelia and enterocytes. CD44v6 was absent from tissue leukocytes and connective tissue components. In comparison, Hermes-3 epitope (on the constant part) containing forms of CD44 were preferentially localized in basal layers of epithelia, present on the surface of most leukocytes and connective tissue cells, and undetectable on the luminal surface of high endothelial venules. In benign neoplasms, epithelial cells stained with mAb Var3.1 like in normal tissues. In contrast, immunostaining of 30 squamous carcinoma specimens (both primary and metastatic lesions) revealed that malignant transformation resulted in down-regulation or disappearance of Var3.1 epitope, but in majority of cases, not in diminished expression of the Hermes-3 epitope. An examination of serum samples from normal individuals and from patients with inflammatory diseases indicated that CD44v6 was increased in samples from patients with rheumatoid arthritis or inflammatory bowel disease.

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Turku, Finland

Marko Salmi