32 results about "Antiangiogenesis Therapy" patented technology

The present invention provides methods for direct killing of cancer cells using anti-α5β1 antibodies. Generally, the method comprises contacting a cancer cell that expresses α5β1 on its surface with an anti-α5β1 antibody, and thereby inducing the death of the cancer cell. The methods of the invention may be employed at an early stage of cancer development in a patient to prevent tumor establishment. In addition, the methods may be used to treat previously formed tumors especially in cancer that have not proven susceptible to anti-angiogenesis therapy. The methods may be employed as a combination therapy of anti-α5β1 antibodies together with cancer chemotherapeutic agents or other molecular-based cancer therapeutic agents.

Methods for determining whether a patient in at particular risk of hypertension associated with anti-VEGF treatment or has a greater likelihood of benefiting from anti-VEGF therapy by screening a sample isolated from the patient for specific genomic polymorphisms.

Methods for selecting whether to administer an anti-angiogenic therapeutic agent to a subject include steps of measuring the expression levels of one or more biomarkers selected from Table 2 or Table 3 in a sample from the subject; assessing from the expression levels of the one or more biomarkers whether the sample from the subject is positive or negative for a biomarker signature, wherein if the sample is positive for the biomarker signature an anti-angiogenic therapeutic agent is contraindicated. Related prognostic methods and treatment methods are also provided. The invention is particularly applicable in ovarian and colorectal cancers.

The present invention is based on the identification of novel biomarkers predictive of responsiveness to a combination of anti-immune checkpoint and anti-angiogenesis therapies.

Anti-angiogenic treatments, treatments of hyperpermeability disorders, treatments of neuropathic and neurodegenerative disorders, pain treatments, methods of reducing the risk of pre-eclampsia and compounds for use in such methods are described.

Methods for treating angiogenesis-mediated diseases are disclosed. More particularly, the present disclosure relates to methods of inhibiting ferrochelatase as an antiangiogenic therapy.

Anti-angiogenic treatments, treatments of hyperpermeability disorders, treatments of neuropathic and neurodegenerative disorders, pain treatments, methods of reducing the risk of pre-eclampsia and compounds for use in such methods are described.

Methods for determining whether a patient in at particular risk of hypertension associated with anti-VEGF treatment or has a greater likelihood of benefiting from anti-VEGF therapy by screening a sample isolated from the patient for specific genomic polymorphisms.

The invention relates to the technical field of recombinant human endostatin preparation prepared molecular targeting developers, and concretely provides a novel positron-emitting radionuclide or gadolinium labeled recombinant human endostatin developer and its application in the evaluation and the predication of the curative effective of the antiangiogenetic therapy through the noninvasive and dynamic observation of the conditions of new vessels of a plurality of tumors. The invention also provides a preparation method of the developer. The positron-emitting radionuclide or gadolinium can be combined with human endostatin through a bifunctional chelating agent.

The present invention is directed to methods for developing novel anti-angiogenic therapies. This invention discovers secretogranin III (Scg3) not only as a novel disease-selective angiogenic factor but also as a target for anti-angiogenic therapy of vascular diseases. Inhibitors against Scg3 can treat diabetic retinopathy, wet age-related macular degeneration, retinopathy of prematurity, retinal vein occlusion, neovascular glaucoma, corneal neovascularization, and cancers.

The present invention offers a solution to the lack of an effective alternative method to those already known to treat angiogenesis. In particular, the present invention is the first to show that a substantially pure population of exosomes derived from MenSCs have capacity to reduce tumor angiogenesis in diseases such as prostate cancer, breast cancer and pancreatic cancer. In this sense, the present invention shows that a substantially pure population of MenSCs-derived exosomes reduce the endogenous levels of reactive oxygen species (ROS) in cancer cells and the expression of pro-angiogenic factors such as VEGF, NF-KB, FGF and HIFα in the treated tumors. Overall, the invention offers a promising alternative method to treat angiogenesis. Since it is principally composed of exosomes produced by the Stem cells present in menstrual fluid, the invention provides an ease access and repeated sampling in a non-invasive manner. Such attributes allow the rapid production of the treatment.

The invention provides a vaccine based on an epitope simulating human vascular endothelial growth factor VEGF, as well as a preparation method thereof. A VEGF mimic epitope which is specifically affinitive with human-mouse chimeric monoclonal antibody Avastin is screened out by use of a phage random presentation technique, and the amino acid sequence of the mimic epitope is Asp-His-Thr-Leu-Tyr-Thr-Pro-Tyr-His-Thr-His-Pro; the mimic epitope has no homology with the protein sequence of VEGF. A vaccine which can induce a polypeptide epitope aiming at VEGF molecular autoantibody in vivo is constructed on the basis of the mimic epitope. The invention provides a strategy for developing and designing the tumor therapeutic vaccine, which is targeted at the VEGF. The VEGF is one of molecules whichhas the strongest effect of promoting vascular growth, and is an ideal target for resisting angiogenesis and treating tumors. Therefore, the vaccine replaces or replenishes monoclonal antibody passive immunotherapy with an active immunity mode, so as to lay foundations for overcoming the defects of monoclonal antibody therapy.

The invention relates to a K237 peptide modified invisible nano particle loaded with an anti-tumor angiogenesis drug. The invisible nano particle consists of the anti-tumor angiogenesis drug, K237 peptide and an invisible nano particle. The invention further provides a preparation method and application of the K237 peptide modified invisible nano particle loaded with the anti-tumor angiogenesis drug. The invention selectively targets the newly generated tumor blood vessels, greatly improves the concentration of the anti-tumor angiogenesis drug (such as the concentration of paclitaxel) in the chrotoplast in the blood vessels, maximumly reduces the concentration of the anti-tumor angiogenesis drug in the normal organs, and overcomes the side-effects caused by the distribution of the drug throughout the body. Since the therapeutic target is the chrotoplast in the tumor blood vessels, drug resistance can not be developed, and the nano particle is potentially effective to the tumor which is already in existence and is resistant to multiple anti-tumor angiogenesis drugs (such as paclitaxel). The invention aims to realize anti-angiogenic tumor therapy and the invisible nano particle can also restrain the metastasis and recrudescence of tumors.

The present application describes therapy with angiogenesis antagonists such as anti-VEGF antibodies. In particular, the application describes the use of such antagonists to treat autoimmune disease in a patient who has failed prior treatment such as treatment with DMARDs or TNFα-inhibitors.