25 results about "Double stranded rna" patented technology

Embodiments of the invention include a method of purifying circular RNA (circRNA) from a solution. The method an include steps of (a) incubating the solution at about 55°C, (b) cellulose chromatography, (c) desalting and purifying RNA reactions with magnetic carboxylic acid beads, (d) ethanol precipitation to remove double stranded RNA byproducts and concentrated RNA, (e) poly-A polymerase treatment, (f) desalting and purifying RNA reactions with magnetic carboxylic acid beads to remove poly A reaction components, (g) RNase R treatment, and (h) desalting and purifying the solution to yield purified circRNA. In aspects, the method removes, among other contaminates, in vitro transcribed circular RNA from linear and doubled stranded RNA.

The present disclosure relates to double stranded RNA agents targeting the hepatitis B virus (HBV) genome, and methods of using such agents to inhibit expression of one or more HBV genes and methods of treating subjects having an HBV infection or HBV-associated disorder, e.g., chronic hepatitis B infection.

One aspect of this disclosure is directed to a method for treating a cancer in a subject in need thereof by administering to the subject at least a first compound and a second compound in any order together or separately. The first compound is an effective amount of a checkpoint inhibitor optionally with at least one pharmaceutically acceptable carrier. The second compound is an effective amount of an Therapeutic Double Stranded RNA (tdsRNA) optionally with at least one pharmaceutically acceptable carrier. The compounds can be administered together or separately. Compositions for the practice of the method are also described.

The technology described herein relates to 5 '-modified nucleosides, nucleotides, oligonucleotides and double stranded RNAs, such as siRNAs, as well as kits comprising them and their use for inhibition of target genes.

The present invention provides a double-stranded RNA having a nucleotide analogue. The double stranded RNAs of the present invention exhibit reduced off-target toxicity.

The present disclosure relates to methods of treating, preventing, or modulating cardiovascular disease in a patient in need thereof using a double stranded RNA agent that reduces expression of Angiotensin (AGT).

The present invention relates to RNAi agents, e.g., double stranded RNA (dsRNA) agents, targeting the AGT gene. The invention also relates to methods of using such RNAi agents to inhibit expression of an AGT gene and to methods of preventing and treating an AGT-associated disorder, e.g., high blood pressure.

Compounds of Formula (I), or pharmaceutically acceptable salts, tautomers, or stereoisomers thereof, are provided. The compounds of formula (I) are contained inside oligonucleotides, or at the 5 '-and / or 3'-terminus, for delivery of double-stranded RNA to extrahepatic tissue, such as the eye. The invention also relates to oligonucleotides, double-stranded RNAs, vectors, cells, pharmaceutical compositions and kits comprising the compounds of formula (I).

The invention discloses a nasal delivery double-chain RNA / Mn < 2 + > nano-drug as well as a preparation method and application thereof in immunotherapy. And adding the polymer into a solution containing double-stranded RNA and manganese salt, and self-assembling to form the nasal delivery double-stranded RNA / Mn < 2 + > nano-drug. The invention provides a new technical scheme for the barrier of the BBB. The nano delivery system has the advantages in the aspects of overcoming the BBB and improving the in-vivo biological distribution of the drug, and the surface of the nano carrier is modified with a ligand targeted to an endothelial cell overexpression receptor, such as ApoE peptide and the like, so that the drug can be delivered to penetrate through the BBB; a non-invasive nasal-brain delivery strategy becomes a new scheme for improving drug availability and reducing toxic and side effects, the drug can bypass BBB and rapidly enter brain parenchyma through olfactory bulb and trigeminal nerve conduction pathways, and an immune drug delivered by the nasal cavity can rapidly enter nasopharynx-related lymphatic tissue (NALT) and is transferred to CLN through a lymphatic network around the nasal cavity, so that the immune drug can be rapidly delivered to the nasopharynx-related lymphatic tissue (NALT). Further, a potent local immune response aiming at the in-situ GBM is induced.

Described herein are synthetic methods for producing sequence-specific RNA oligonucleotides that eliminate impurities produced in prior art methods. In one aspect, a first amplification primer includes one or more deoxyuridine residues, wherein at least one of the one or more deoxyuridine residues is at position −1, −2, −3, −4 or −5 of the promoter region for the single-subunit, DNA-dependent RNA polymerase. The deoxyuridines are excised to provide an amplified functional template DNA which is then used to synthesize RNA which has reduced immunogenic double stranded RNA compared to controls.

The present invention provides methods and systems to identify and quantify double-stranded RNA (dsRNA) in a sample. A capture molecule can be immobilized to a solid surface. The solid surface can then be contacted with a sample including the dsRNA, wherein the capture molecule immobilized on the solid surface specifically binds to the dsRNA. The binding response of the dsRNA to the solid surface can then be measured by biolayer interferometry to detect the dsRNA in the sample. The measured binding response can be compared to a standard curve relating binding response to concentration to determine a concentration of the dsRNA in the sample.

The present invention relates to a novel affinity separation matrix that comprises novel binding ligands for double stranded RNA (dsRNA) and the use of said affinity separation matrix for purifying ribonucleic acid preparations. The present invention further relates to a method of purifying ribonucleic acid preparations and a kit for use in a method of purifying ribonucleic acid preparations, implementing the novel affinity separation matrix. The present disclosure also relates to a method of production of a single-stranded RNA (ssRNA) preparation.

The present invention relates to new double stranded RNA (dsRNA) structures and their use in gene silencing.

Compounds of Formula (I), or pharmaceutically acceptable salts, tautomers, or stereoisomers thereof, are provided. The compound of formula (I) is contained inside the nucleotide, or at the 5 '-and / or 3'-terminus, for delivery of the double-stranded RNA to extrahepatic tissue, such as the central nervous system or the eye. Oligonucleotides, double-stranded RNAs, vectors, cells, pharmaceutical compositions and kits comprising the compounds of Formula (I) are also provided.

Provided herein double stranded RNA (dsRNA) mi29b mimics and methods of treating fibrotic diseases or disorders with the same.

The present disclosure provides a double-stranded nucleic acid, compositions, and methods relating thereto. The present disclosure encompasses the recognition that structural elements of double stranded nucleic acid, such as stereochemistry of backbone chiral centers (chiral internucleonic linkages), and / or patterns thereof, specially, double-stranded nucleic acid having one or more chirally enriched phosphorothioate internucleotide linkages can have significant impact on oligonucleotide properties and activities, e.g., RNA interference (RNAi) activity, stability, delivery, etc. The present disclosure also provides methods for treatment of diseases using provided double stranded nucleic acid compositions, for example, in RNA interference.

Provided are TrkA RNAi agents for reducing expression of TrkA, which comprise a sense strand and an antisense strand forming a double stranded RNA (dsRNA), compositions comprising these RNAi agents and methods of their use.

The present invention relates to double-stranded RNA molecules having A to G substitutions, precursor RNA molecules thereof, and their use in modifying cells such as for gene silencing.

The present invention relates to RNAi agents, e.g., double stranded RNA (dsRNA) agents, targeting the Angiopoietin-like 3 (ANGPTL3) gene. The invention also relates to methods of using such RNAi agents to inhibit expression of an ANGPTL3 gene and to methods of preventing and treating an ANGPTL3-associated disorder, e.g., a disorder of lipid metabolism, such as hyperlipidemia or hypertriglyceridemia.

The present invention relates to RNAi agents, e.g., double stranded RNA (dsRNA) agents, targeting the apolipoprotein C3 gene (APOC3). The invention also relates to methods of using such RNAi agents to inhibit expression of an APOC3 gene and to methods of preventing and treating an APOC3-associated disorder, e.g., hypertriglyceridemia, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, polycystic ovary syndrome, kidney disease, obesity, type 2 diabetes mellitus (insulin resistance), hypertension, artherosclerosis and pancreatitis.

The present invention relates to double-stranded RNA molecules having A to G substitutions, precursor RNA molecules thereof, and their use in modifying cells such as for gene silencing.

Disclosed herein is a double stranded RNA (dsRM A) molecule for RNA interference. A method for inhibiting the expression of complement factor B (CFB) and a method for treating a complement-related disease are also provided.

Provided are compositions, systems and methods for removal of double stranded RNA from a mixture utilizing affinity agents having high binding affinity and selectivity for double stranded RNA over single stranded RNA.

The present invention relates to the production of RNA, in particular to in vitro transcription. Specifically, the present invention relates to methods for decreasing the content of double stranded RNA (dsRNA) during RNA in vitro transcription (IVT).

The present invention relates to RNAi agents, e.g., double stranded RNA (dsRNA) agents, targeting the complement component C3 gene (C3). The invention also relates to methods of using such RNAi agents to inhibit expression of a C3 gene and to methods of preventing and treating a C3-associated disorder, e.g., cold agglutinin disease (CAD), warm autoimmune hemolytic anemia, and paroxysmal nocturnal hemoglobinuria (PNH), lupis nephritis (LN), bullous pemphigoid, pemphigus, e.g., pemphigus vulgaris (PV) and pemphigus foliaceus (PF), and C3 glomerulopathy.