192 results about "Transforming growth factor beta" patented technology

Previous methods for culturing human embryonic stem cells have required either fibroblast feeder cells or a medium which has been exposed to fibroblast feeder cells in order to maintain the stem cells in an undifferentiated state. It has now been found that if high levels of fibroblast growth factor, gamma amino butyric acid, pipecholic acid, lithium and transforming growth factor beta are added to the medium in which the stem cells are cultured, the stem cells will remain undifferentiated indefinitely through multiple passages, even without feeder cells or conditioned medium.

The present invention relates to antibody molecules, in particular antibody molecules that bind Transforming Growth Factor beta (TGFβ), and uses thereof. More particularly, the invention relates to antibody molecules that bind and preferably neutralise TGFβ1, TGFβ2 and TGFβ3, so-called “pan-specific” antibody molecules, and uses of such antibody molecules. Preferred embodiments within the present invention are antibody molecules, whether whole antibody (e.g. IgG, such as IgG1 or IgG4) or antibody fragments (e.g. scFv, Fab, dAb).

The present invention is based on the seminal discovery that targeted immunomodulatory antibodies and fusion proteins can counter act or reverse immune tolerance of cancer cells. Cancer cells are able to escape elimination by chemotherapeutic agents or tumor-targeted antibodies via specific immunosuppressive mechanisms in the tumor microenvironment and such ability of cancer cells is recognized as immune tolerance. Such immune suppressive mechanisms include immunosuppressive cytokines (for example, Transforming growth factor beta (TGF-β) and regulatory T cells and / or immunosuppressive myeloid dendritic cells (DCs). By counteracting tumor-induced immune tolerance, the present invention provides effective compositions and methods for cancer treatment, optional in combination with another existing cancer treatment. The present invention provides strategies to counteract tumor-induced immune tolerance and enhance the antitumor efficacy of chemotherapy by activating and leveraging T cell-mediated adaptive antitumor immunity against resistant or disseminated cancer cells.

Treating or preventing the early stages of degeneration of articular cartilage or subchondral bone in the affected joint of a mammal is accomplished by administering a chondroprotective compound of Formula (I):where A is hydroxy, (C1-C4)alkoxy, amino, hydroxy-amino, mono-(C1-C2)alkylamino, di-(C1-C2)alkylamino; X and Y are independently H or (C1-C2)alkyl; and n is 1 or 2; R6 is halogen, (C1-C3)alkyl, trifluoromethyl, or nitro; R9 is H; (C1-C2)alkyl; phenyl or phenyl-(C1-C2)alkyl, where phenyl is optionally mono-substituted by fluoro or chloro; -C(=O)-R, where R is (C1-C2)alkyl or phenyl, optionally mono-substituted by fluoro or chloro; or -C(=O)-O-R', where R1 is (C1-C2)alkyl.This treatment ameliorates, diminishes, actively treats, reverses or prevents any injury, damage or loss of articular cartilage or subchondral bone subsequent to said early stage of said degeneration. Whether or not a mammal needs such treatment is determined by whether or not it exhibits a statistically significant deviation from normal standard values in synovial fluid or membrane from the affected joint, with respect to at least five of the following substances: increased interleukin-1 beta (IL-1beta); increased tumor necrosis factor alpha (TNFalpha); increased ratio of IL-1beta to IL-1 receptor antagonist protein (IRAP); increased expression of p55 TNF receptors (p55 TNF-R); increased interleukin-6 (IL-6); increased leukemia inhibitory factor (LIF); decreased insulin-like growth factor-1 (IGF-1); decreased transforming growth factor beta (TGFbeta); decreased platelet-derived growth factor (PDGF); decreased basic fibroblast growth factor (b-FGF); increased keratan sulfate; increased stromelysin; increased ratio of stromelysin to tissue inhibitor of metalloproteases (TIMP); increased osteocalcin; increased alkaline phosphatase; increased cAMP responsive to hormone challenge; increased urokinase plasminogen activator (uPA); increased cartilage oligomeric matrix protein; and increased collagenase.

Methods and devices are described for the regulation of Transforming Growth actor (TGF)-β1, β2, and / or β3 protein gene expression in bone cells and other tissues via the capacitive coupling or inductive coupling of specific and selective electric fields to the bone cells or other tissues, where the specific and selective electric fields are generated by application of specific and selective electric and electromagnetic signals to electrodes or one or more coils or other field generating device disposed with respect to the bone cells or other tissues so as to facilitate the treatment of diseased or injured bone and other tissues. By gene expression is meant the up-regulation or down-regulation of the process whereby specific portions (genes) of the human genome (DNA) are transcribed into mRNA and subsequently translated into protein. Methods and devices are provided for the targeted treatment of injured or diseased bone and other tissue that include generating specific and selective electric and electromagnetic signals that generate fields in the target tissue optimized for increase of TGF-β1, β2, and / or β3 protein gene expression and exposing bone and other tissue to the fields generated by specific and selective signals so as to regulate TGF-β1, β2, and / or β3 protein gene expression in such tissue. The resulting methods and devices are useful for the targeted treatment of bone fractures, fractures at risk, delayed unions, nonunion of fractures, bone defects, spine fusions, osteonecrosis or avascular necrosis, as an adjunct to other therapies in the treatment of one or all of the above, in the treatment of osteoporosis, and in other conditions in which TGF-β1, β2, and / or β3 protein may be implicated.

The invention provides an artificial lentis, which contains anti-transforming growth factor beta 2 antibody membrane on the surface and can inhibit intercurrent post-cataract after cataract surgery, and also provides a the production method thereof. The production method includes the steps that: the artificial lentis is charged with positive electricity or negative electricity after the artificial lentis is cleaned, dried, and pretreated on the surface; the artificial lentis is soaked in a polyelectrolyte solution the charge of which is opposite to the surface charge of the artificial lentis for adsorbing, and rinsing the artificial lentis by deionized water, and drying the artificial lentis by nitrogen gas; the artificial lentis is soaked in a phosphate buffering solution of anti-transforming growth factor beta 2 antibody, the pH value of which is 4-10, and the carried charge of which is opposite to that of the polyelectrolyte, for adsorption; finally, the artificial lentis is rinsed by phosphate buffering solution, and the artificial lentis is dried by nitrogen gas; the alternating assembly steps are repeated. The artificial lentis of the invention can inhibit the transformation and differentiation as well as cyst membrane shrinkage of the lentis epithelial cells in a target way, and then interdicts the occurrence of the post-cataract, and has excellent biocompatibility. The production method of the invention is scientific and simple, and can ensure the activity under a dry state and the safety and reliability during medical transplantation of the anti-transforming growth factor beta 2.

Anti-cancer agents and / or transforming growth factor beta (TGF-beta or TGFβ) antagonists are disclosed, where the agents and / or antagonists include a therapeutically effective amount of a combination of therapeutically active portions of sRII and therapeutically active portions of sRIII or a fusion polypeptide or protein comprising therapeutically active portions of sRII and therapeutically active portions of sRIII. Methods for preventing, treating and / or ameliorating the symptoms of cancer are also disclosed based on administering an effective amount of a composition of this invention.

Specific binding members, particularly antibodies and fragments thereof, which bind to transforming growth factor beta 1 (TGF-β1) are provided, particularly recognizing human and mouse TGF-β1 and not recognizing or binding TGF-β2 or TGF-β3. Particular antibodies are provided which specifically recognize and neutralize TGF-β1. These antibodies are useful in the diagnosis and treatment of conditions associated with activated or elevated TGF-β1, including cancer, and for modulating immune cells and immune response, including immune response to cancer or cancer antigens. The anti-TGF-β1 antibodies, variable regions or CDR domain sequences thereof, and fragments thereof may also be used in therapy in combination with chemotherapeutics, immune modulators, or anti-cancer agents and / or with other antibodies or fragments thereof. Antibodies of this type are exemplified by the novel antibodies hereof, including antibody 13A1, whose sequences are provided herein.

The present invention provides a method for treating or arresting the progress of pathologies characterized by an accumulation of extracellular matrix components by providing an agent to suppress the activity of transforming growth factor beta (TGF-beta) a peptide growth factor which is anabolic and leads to fibrosis and angiogenesis. In one embodiment, such agent is anti-TGF-beta antibody. Pathologies which can be so treated include, but are not limited to, glomerulonephritis, adult respiratory distress syndrome and cirrhosis of the liver. The invention further provides a method for the diagnosis of pathologies, or incipient pathologies, which are characterized by the accumulation of extracellular matrix components in tissues by determining the levels of TGF-beta in the tissues, a high level being indicative of such pathologies.

The invention provides methods, compositions, and kits for treating a variety of conditions using substances that display one or more activities of transforming growth factor-β (TGF-β mimics). Conditions include skin conditions, wounds, and the need for soft tissue augmentation. Compositions that may be used to treat such conditions contain a TGF-β mimic. Kits that may be used to treat such conditions contain a TGF-β mimic.

The invention concerns TGF-beta in a crystalline form which shows no adsorption or less adsorption to the walls of vials than the soluted TGF-beta and which is more stable towards oxidative agents than the soluted form. TGF-beta crystals of the invention can be used for structure determination and for drug design and for the production of a slow release pharmaceutical preparation.

The invention discloses the application of resveratrol and naringenin, particularly the application of the resveratrol and the naringenin in restraining the level increasing of the transforming growth factor Beta 1 in the human body and preparing medicines used for preventing or treating diabetes and nephropathy.