170 results about "Cell adhesion molecule" patented technology

An artificial antigen presenting system is presented. The herein presented microspheres combine negative regulators individually or at varying combinations along with MCH molecules and can induce antigen specific tolerance. The herein described methods provide for the construction of artificial biodegradable microsomes containing MHC: peptide complexes, accessory molecules, co-stimulatory molecules, adhesion molecules, and other molecules relevant to T cell binding or modulation. Additionally, the present invention is directed to compositions and methods for treating conditions which would benefit from modulation of T cell response, for example, autoimmune disorders, allergies, cancers, viral infections, and graft rejection.

The present invention relates to a monoclonal antibody that specifically binds to vascular cell adhesion molecule-1 (VCAM-1 or CD106). Specifically, the present invention relates to an antibody that specifically binds to both human and mouse vascular cell adhesion molecule-1 (VCAM-1), a method for producing the same, a composition for diagnosis or treatment comprising them and a method for diagnosis or treatment using them. The monoclonal antibody of the present invention is the first recombinant monoclonal antibodies that is specific to human and mouse VCAM-1. In addition, the monoclonal antibody of the present invention shows a strong affinity to VCAM-1 expressed in rat skeletal muscle and porcine endothelial cells as well as human and mouse endothelial cells and is found to strongly inhibit the interaction between leukocytes and activated endothelial cells. Accordingly, the monoclonal antibody of the present invention can inhibit a VCAM-1 mediated adhesion of leukocytes to endothelial cells and potently treat VCAM-1 mediated disease, especially inflammatory disease or cancer.

A method for the inhibition of the binding of .alpha..sub.4.beta..sub.1 integrin to its receptors, for example VCAM-1 (vascular cell adhesion molecule-1) and fibronectin; compounds that inhibit this binding; pharmaceutically active compositions comprising such compounds; and the use of such compounds either as above, or in formulations for the control or prevention of diseases states in which .alpha..sub.4.beta..sub.1 is involved.

A method is provided for treating mammals, including humans, with advanced or large-tumour burdens. The method involves administering an immunotherapeautic agent in conjunction with a tumour growth restricting agent, in amounts effective to eradicate any advanced or large tumours present. In preferred embodiments, the immunotherapeautic agent comprises a T-cell co-stimulatory cell adhesion molecule (CAM) or a mammalian expression vector containing DNA which encodes a T-cell co-stimulatory CAM, such as B7.1, and the tumour growth restricting agent is flavone acetic acid, 5,6-dimenthyl-xanthenone-4-acetic acid, or an agent which disrupts the expression or activity of hypoxia-inducible factor-1 (HIF-1).

The present invention relates to a monoclonal antibody that specifically binds to vascular cell adhesion molecule-1 (VCAM-1 or CD106). Specifically, the present invention relates to an antibody that specifically binds to both human and mouse vascular cell adhesion molecule-1 (VCAM-1), a method for producing the same, a composition for diagnosis or treatment comprising them and a method for diagnosis or treatment using them. The monoclonal antibody of the present invention is the first recombinant monoclonal antibodies that is specific to human and mouse VCAM-1. In addition, the monoclonal antibody of the present invention shows a strong affinity to VCAM-1 expressed in rat skeletal muscle and porcine endothelial cells as well as human and mouse endothelial cells and is found to strongly inhibit the interaction between leukocytes and activated endothelial cells. Accordingly, the monoclonal antibody of the present invention can inhibit a VCAM-1 mediated adhesion of leukocytes to endothelial cells and potently treat VCAM-1 mediated disease, especially inflammatory disease or cancer.

The invention relates to disulfide-rich dimer molecules which inhibit binding of α4β7 to the mucosal addressin cell adhesion molecule (MAdCAM) in vivo, and show high selectivity against α4β1 binding.

The invention relates to peptide dimer compounds and peptide monomer compounds that potently inhibit binding of α4β7 to the mucosal addressin cell adhesion molecule (MAdCAM) in vivo, possess high selectivity against α4β1 binding, and have high stability under gastrointestinal conditions.

Disclosed are methods, compositions, devices, and kits for the isolation of brain-specific exosomes. Specifically, methods, compositions, devices, and Unbound kits comprising an isolated brain-specific extracellular vesicle or exosome joined to a first binding agent that is specific for tau, β-amyloid, SlOO β, neuron-specific enolase, glycoprotein A2B5, CD133, NQ01, synaptophysin, neuronal nuclei, MAB 1569, polysialic acid-neural cell adhesion molecule (PSA-NCAM), or neurogenic differentiation 1 (NeuroD or Beta2), or glycosylated or phosphorylated forms of these molecules, are provided.

Methods and compositions are disclosed for inhibiting proliferation of human colon adenocarcinoma cells, reducing pro-inflammatory molecules, adhesion molecules, and vascular smooth muscle cell proliferation, and for increasing NO production. The present invention describes the use of phenolic compositions, purified from oats or synthetically produced, to decrease the effective amount of pro-inflammatory molecules and / or cell adhesion molecules. Alternatively, an alcoholic extract or concentrate from oats can be used. The methods of the present invention can be used as a treatment or prophylaxis of a wide variety of disorders associated with inflammatory states and / or with a lack of or need for nitric oxide (NO), such as inflammatory conditions, pain, free radical associated disorders, cardiovascular diseases, autoimmune disorders, pathological platelet aggregation, pathological vasoconstriction, vascular effects of diabetes, stroke, atherosclerosis, hypertension, abnormal vasospasm, and restenosis after angioplasty.

A composition, method and kit comprising a compound for the inhibition of the binding of α4β1 integrin to its receptors, for example VCAM-1 (vascular cell adhesion molecule-1) and fibronectin and other therapeutic compounds for the control or prevention of diseases states in which α4β1 is involved.

The invention relates to disulfide-rich peptide molecules which inhibit binding of α4β7 to the mucosal addressin cell adhesion molecule (MAdCAM) in vivo, and show high selectivity against α4β1 binding.

The invention relates to disulfide-rich dimer molecules which inhibit binding of α4β7 to the mucosal addressin cell adhesion molecule (MAdCAM) in vivo, and show high selectivity against α4β1 binding.

The invention relates to disulfide-rich dimer molecules which inhibit binding of α4β7 to the mucosal addressin cell adhesion molecule (MAdCAM) in vivo, and show high selectivity against α4β1 binding.

The invention relates to thioether monomer and dimer peptide molecules which inhibit binding of α4β7 to the mucosal addressing cell adhesion molecule (MAdCAM) in vivo.

The invention relates to thioether monomer and dimer peptide molecules which inhibit binding of α4β7 to the mucosal addressing cell adhesion molecule (MAdCAM) in vivo.

A method for the inhibition of the binding of α4β1 integrin to its receptors, for example VCAM-1 (vascular cell adhesion molecule-1) and fibronectin; compounds that inhibit this binding; pharmaceutically active compositions comprising such compounds; and to the use of such compounds either a above, or in formulations for the control or prevention of diseases states in which α4β1 is involved.

The invention provides a novel herbal composition containing the extracts of the leaves and / or stem of <italic>Argemone mexicana < / highlight>plant, optionally containing the extracts of the fruits of <italic>Cuminum cyminum< / highlight>, which exhibits useful in vitro, in vivo and interesting immunological and pharmacological activities; a process for preparation thereof; and a method of treatment of psoriasis and related immunological and biological disorders by administration of the said novel herbal composition. The useful in vitro, in vivo and interesting immunological and pharmacological activities exhibited by the extracts and fractions of the leaves and / or stem of <italic>Argemone mexicana < / highlight>plant include immunosuppression, lymphoproliferation inhibition, cytokine modulation such as IL-2 inhibition, IFNgamma inhibition, IL-10 induction, keratinocyte proliferation inhibition, keratolytic activity, endothelial cell proliferation inhibition, inhibition of cell adhesion molecule expression such as ICAM-1, MEST inhibition, and enzymes inhibition such as p60src Tyrosine kinase, which are known to be involved in anti-psoriatic activity. The novel herbal composition(s) is useful in the treatment of various disorders, such as psoriasis including plaque psoriasis, gutatte psoriasis, pustular psoriasis and psoriasis of the nails; dermatitis and scleroderma; eczema; inflammatory disorders and other autoimmune diseases like psoriatic arthritis, rheumatoid arthritis, Crohn's disease, multiple sclerosis, irritable bowel disease, ankylosing spondilitis, systemic lupus erythremetosus and Sjogren's syndrome; allergies like asthma and chronic obstructive pulmonary disease and is safe, well-tolerated, non-toxic, with minimal and reversible adverse reactions or side effects, and most importantly, with minimal relapse or recurrence of the disease following completion of a treatment regimen. The invention also describes the presence of phosphodiesterase (III, IV and V) inhibition and 5-Lipoxygenase inhibition in the aqueous, ethanolic or aqueous-ethanolic extracts of fruits of <italic>Cuminum cyminum < / highlight>plant.

The current invention relates to methods of producing a surface with enhanced cell-adhesive properties comprising treating a pre-formed surface such that at least one intermediate reactive group is exposed on the surface. The exposed intermediate reactive group is then reacted to create a self-assembled monolayer, comprising at least one reactive group. The self-assembled monolayer is created non-mechanically. The reactive group is then coupled to at least one cell-adhesive molecule. The current invention also relates to cell culture devices comprising at least one oxygen-sensing compound and a cell-adhesive molecule.

Methods, uses, agents and compositions useful for the diagnosis, prevention and / or treatment of inflammatory conditions, such as neuroinflammatory conditions such as multiple sclerosis, and for the identification and selection of inflammatory cytokine-secreting T cell or a precursor thereof, based on the expression and / or modulation of melanoma cell adhesion molecule (MCAM) are disclosed.

This invention relates to the suppression of graft rejection, particularly to the suppression of xenograft rejection. In particular, the invention relates to biological tissues that contain endothelial cells that may be induced to generate a compound which down-regulates the expression of a cell adhesion molecule in these cells.

The present invention provides targeted delivery systems to deliver pharmaceuticals to irradiated tissue comprising a biomolecule carrier, a targeting moiety to cellular adhesion molecules and a pharmaceutical. The present invention also provides methods of selectively targeting endothelial tissue for delivery of a pharmaceutical thereto and of treating a pathophysiological state in an individual using the targeted delivery systems disclosed herein. Further provided is a method of optimizing an immunoliposome for specific targeting of a pharmaceutical encapsulated therein to irradiated tissue by selecting a liposome that has a greater rate of adhesion to the irradiated tissue than a rate of uptake by the reticuloendothelial system.

A composition is provided for modulating or attenuating the cytokine induced cell surface expression of cell adhesion molecules, comprising an antibody that binds digoxin. There is also provided a method of modulating or attenuating the cytokine induced cell surface expression of a cell adhesion molecule in a patient by administering to a digoxin antibody composition to a patient in need of such treatment.

The invention relates to disulfide-rich dimer molecules which inhibit binding of α4β7 to the mucosal addressin cell adhesion molecule (MAdCAM) in vivo, and show high selectivity against α4β1 binding.

Methods, uses, agents and compositions useful for the diagnosis, prevention and / or treatment of inflammatory conditions, such as neuroinflammatory conditions such as multiple sclerosis, and for the identification and selection of inflammatory cytokine-secreting T cell or a precursor thereof, based on the expression and / or modulation of melanoma cell adhesion molecule (MCAM) are disclosed.

A method is provided for treating mammals, including humans, with advanced or large-tumour burdens. The method involves administering an immunotherapeautic agent in conjunction with a tumour growth restricting agent, in amounts effective to eradicate any advanced or large tumours present. In preferred embodiments, the immunotherapeautic agent comprises a T-cell co-stimulatory cell adhesion molecule (CAM) or a mammalian expression vector containing DNA which encodes a T-cell co-stimulatory CAM, such as B7.1, and the tumour growth restricting agent is flavone acetic acid, 5,6-dimenthyl-xanthenone-4-acetic acid, or an agent which disrupts the expression or activity of hypoxia-inducible factor-1 (HIF-1).

Methods and compositions are disclosed for reducing pro-inflammatory molecules, adhesion molecules, and vascular smooth muscle cell proliferation, and for increasing NO production. The present invention describes the use of phenolic compositions, purified from oats or synthetically produced, to decrease the effective amount of pro-inflammatory molecules and / or cell adhesion molecules. Alternatively, an alcoholic extract or concentrate from oats can be used. The methods of the present invention can be used as a treatment or prophylaxis of a wide variety of disorders associated with inflammatory states and / or with a lack of or need for nitric oxide (NO), such as inflammatory conditions, pain, free radical associated disorders, cardiovascular diseases, autoimmune disorders, pathological platelet aggregation, pathological vasoconstriction, vascular effects of diabetes, stroke, atherosclerosis, hypertension, abnormal vasospasm, and restenosis after angioplasty.

The invention relates to a nucleic acid, in particular to a nucleic acid aptamer of the epithelial cell adhesion molecule and a preparation method thereof. The invention provides a high-specificity and high-affinity nucleic acid aptamer of the epithelial cell adhesion molecule EpCAM and a preparation method and applications thereof. The nucleic acid aptamer of the epithelial cell adhesion molecule EpCAM is of the G-quadruplex structure or the stem-loop structure. The preparation method comprises the following steps: designing and synthetizing a single-stranded DNA (deoxyribonucleic acid) random oligonucleotide library, screening the target oligonucleotide sequence, and identifying the binding specificity and affinity of the sequence to the target protein through the flow cytometry. The screened nucleic acid aptamer is non-toxic, has small molecular weight and good permeability, is easy in synthesis and marking and can only perform specific identification to the EpCAM protein and perform specific identification and specific expression to the cell line of the EpCAM protein; and the nucleic acid aptamer can not identify the cell line which does not express the protein.

The present invention relates to methods and compositions for monitoring, diagnosis, prognosis, and determination of treatment regimens in subjects suffering from or suspected of having a renal injury. In particular, the invention relates to using assays that detect one or more biomarkers selected from the group consisting of Tumor necrosis factor receptor superfamily member 1OB, Cadherin-16, Caspase-9, Bcl2 antagonist of cell death, Caspase-1, Cadherin-1, Poly [ADP-ribose] polymerase 1, Cyclin-dependent kinase inhibitor 1, Cadherin-5, Myoglobin, Apolipoprotein A-II, Mucin-16, Carcinoembryonic antigen-related cell adhesion molecule 5, and Cellular tumor antigen p53 as diagnostic and prognostic biomarker assays in renal injuries.