34 results about "Antagomir" patented technology

Methods are provided for treating fibrosis of a tissue, including fibrosis of the liver, using combinations of antagomirs and / or locked nucleic acids. Compositions therefor are also provided.

The present application discloses roles for miR-93 in treating hypoxia and ischemia. Endothelial cells (HUVEC) and myocytes (C2C12) expressed miR-93 and up-regulated miR-93 in response to hypoxia and serum starvation. Over-expression of miR-93 in HUVECs promoted cell proliferation, prevented hypoxia-induced apoptosis, and enhanced endothelial cell tube formation. miR-93 knockdown in HUVECs resulted in increased hypoxia-induced apoptosis and decreased tube formation. Over-expression or knockdown of miR-93 in myocytes resulted in reduced or increased hypoxia-induced apoptosis, respectively. Down-regulation of miR-93 in C57BL / 6 mice with antagomiR resulted in attenuated perfusion recovery (% non-ischemic leg at day-21: Scramble 85.22.9 vs. AntagomiR-93 67.96). Over-expression of miR-93 in BALB / C mice improved perfusion recovery (% non-ischemic leg at day 21: PremiR-93 757.5 vs. Scramble 59.62.5). The present invention encompasses the use of miR-93 and regulation of miR-93 to treat and prevent hypoxia, ischemia, and other injuries, diseases, disorders, and conditions associated with ischemia.

The miRNA miR-33 is shown to inhibit the expression of carnitine O-octaniltransferase (CROT), Carnitine palmitoyltransferase 1A (CPT1a) and hydroxyacyl-CoA-dehydrogenase (HADHB), reduce fatty acid oxidation in hepatic cells, and target the insulin receptor substrate 2 (IRS-2) independent of its ability to elevating plasma high density lipoprotein (HDL) levels. MiR-33 inhibitors are also shown to increase cholesterol efflux from peripheral cells, such as cholesterol-laden macrophages present in atherosclerotic plaques. Compositions and methods are therefore provided for treating or preventing metabolic syndrome and atherosclerosis using miR-33 inhibitors. The miR-33 inhibitors are preferably antagomirs having a single-stranded nucleic acid sequence that is complementary to at least 12 contiguous nucleotides in miR-33 and therefore forms a duplex with miR-33 under physiological conditions.

The invention discloses an anti-skin squamous cell carcinoma medicament, i.e., antagomir-365-2. The antagomir-365-2 is a chemically-modified antisense oligonucleotide of which the nucleotide sequence is shown as SEQIDNO:1 in which two continuous basic groups at a 5' end and four continuous basic groups at a 3' end are modified with thiophosphoric acid, the 3' tail end is marked with cholesterol, and all basic groups are modified through methylation. The anti-skin squamous cell carcinoma medicament, i.e., antagomir-365-2 disclosed by the invention can be enriched on a target cell by overcomingthe obstacles of cell membranes, tissues and the like, can directly enter cells cultured in vitro and in-vivo tumorigenesis tissues, is an ideal medicament for performing in-vitro and in-vivo skin squamous cell carcinoma treatment experiments, and can be used for effectively inhibiting invasion and transfer of tumor cells in vitro and effectively inhibiting growth of tumors and eliminating tumorsin vivo. The antagomir-365-2 disclosed by the invention has a remarkable resisting effect on skin squamous cell carcinoma, and is a target gene medicament for treating skin cancers.

The invention relates to negative functional modulators of erythropoietin (EPO) for use in the treatment of cancers, in the therapy of autoimmune -based and non-autoimmune based chronic inflammatory diseases, and in the treatment of patients under-going organ or tissue transplant, or for the treatment of hemophilic arthropathy, hemophilia A and B, von Willebrand disease, angiodysplasia, proliferative disorders and neurological diseases characterized in their pathogenesis by primary neuroinflammation and / or neuroinflammation secondary to other causes. Such modulators are anti-EPO antibodies and their derivatives: anti-EPO receptor antibodies (EPOR), antisense oligonucleotides, decoy DNA, decoy RNA, ribozyme, antagomir, shRNA, LNA and / or siRNAs that inhibit the expression of the gene encoding EPO or EPOR.

The invention relates to the diagnostic and therapeutic uses of a miRNA molecule, an equivalent or a source thereof in a neuronal deficiency or a disease and condition associated with neuronal deficiency.

The present invention relates to microRNAs (miRNAs) which are associated with cancer, particularly including hematologic malignancies, and particularly T-cell acute lymphoblastic leukemia (T-ALL), and to the assessment and modulation thereof in the treatment and management of cancer. The present invention is directed to methods and compositions for diagnosing and treating cancer, particularly T-ALL, by modulating miRNAs, and the use of miRNAs and antagonists thereof, particularly antagomirs, for predicting and assessing response to treatment, in assays for isolating and selecting antagonists, and as compositions for the treatment and management of cancer. Methods and compositions are provided for treatment or alleviation of cancer, particularly T-ALL, with antagonists / antagomirs of miRNAs, particularly one or more of miR-19b, miR-20a, miR26, miR92, miR148 and miR223.

The inhibition of miRNA miR-33 is shown to promote the polarization of macrophages from an M1 to an M2 phenotype. MiR-33 inhibitors are therefore useful for treating inflammation in subjects. Endogenous microRNAs can be silenced using antagomirs. The miR-33 inhibitor is preferably an antagomir having a single-stranded nucleic acid sequence that is complementary to at least 12 contiguous nucleotides in miR-33 and therefore forms a duplex with miR-33 under physiological conditions.

The invention relates to a miRNA molecule. The miRNA molecule is of a two-strand structure containing a sense strand and an antisense strand, wherein the nucleotide sequence of the sense strand is shown as SEQ ID NO: 1 in a sequence table, and the nucleotide sequence of the antisense strand is shown as SEQ ID NO: 2 in the sequence table; or the miRNA molecule is of a single-strand structure of which the nucleotide sequence is shown as SEQ ID NO: 3 in the sequence table. According to the artificially designed and synthesized miRNA avi-miR-184-3p agomir and miRNA avi-miR-184-3p antagomir have lethality for aphid, a novel effective product is provided to prevent and control aphid; the target gene under the action of the product can be used as an ideal candidate gene resource for developing RNAi-mediated novel pest resisting crops. Therefore, a novel research ideal on pest prevention and control is provided; the miRNA molecule is high in research value and has a good application prospect.

The invention discloses a drug for treating neovascularization diseases. The drug uses miRNA-132 and miRNA-155 as targets, and uses two specific antagonistic oligonucleotides antagomir-132 and antagomir-155 as the basic components of the drug. Knocking down the above two micronucleic acids in the lesion at the same time can inhibit the excessive proliferation of new blood vessels and achieve the therapeutic effect. In order to ensure the effective use of the drug, the present invention adopts in vivo import carriers, such as histidine-lysine polypeptide polymer HKP, and ligand-targeted import nanoparticle system RGD-PEG-HKP, to enhance drug import into blood vessel proliferation Site (ocular or tumor site) specificity and efficiency.