Abstract: A method of inhibiting the function of myostatin is provided. An antisense oligonucleotide of 15-30 bases or a salt or a solvate thereof, wherein the antisense oligonucleotide has a nucleotide sequence complementary to a target sequence in exon 3 of the myostatin gene and is capable of allowing the expression of a splicing variant of myostatin. A pharmaceutical drug, a food, a feed, an agent for promoting myocyte proliferation and/or hypertrophy, an agent for increasing muscle mass and/or suppressing muscle weakness, an agent for switching the splicing of the myostatin gene from production of myostatin to production of a splicing variant thereof, an agent for decreasing myostatin signaling, and an anticancer agent, each of which comprises the above antisense oligonucleotide or a salt or a solvate thereof.

Abstract: The present invention establishes a molecular therapy for glycogen storage disease type Ia. The present invention provides an oligonucleotide of 15-30 bases comprising a nucleotide sequence complementary to die cDNA of G6PC gene with c.648G>T mutation, wherein the oligonucleotide comprises a sequence complementary to a region comprising any site between the 82nd to the 92nd nucleotide from the 5? end of exon 5 of the G6PC gene with c.648C>T mutation, a pharmacologically acceptable salt or solvate thereof. Also provided is a pharmaceutical drug comprising the oligonucleotide, a pharmacologically acceptable salt or solvate thereof (e.g., therapeutic drug for glycogen storage disease type Ia).

Abstract: An antisense oligonucleotide is provided which induces exon skipping in ACE2 gene. An antisense oligonucleotide of 15-30 bases or a salt or a solvate thereof, wherein the antisense oligonucleotide has a nucleotide sequence complementary to a target site in exon 18 of angiotensin-converting enzyme 2 gene and is capable of inducing exon skipping in angiotensin-converting enzyme 2 gene. A pharmaceutical drug comprising the antisense oligonucleotide or a salt or a solvate thereof; and an agent for inhibiting the expression of angiotensin-converting enzyme 2 protein and/or for enhancing the expression of soluble angiotensin-converting enzyme 2.

Abstract: A novel method of myostatin inhibition is provided. An antisense oligonucleotide of 15-30 bases or a salt or a solvate thereof, wherein the antisense oligonucleotide has a nucleotide sequence complementary to a target site in exon 1 of the myostatin gene and is capable of inhibiting the production of the mRNA of the myostatin gene. A pharmaceutical drug, a food, a feed, an agent for promoting myocyte proliferation and/or hypertrophy, an agent for increasing muscle mass and/or inhibiting muscle weakness, an agent for inhibiting production of the mRNA of the myostatin gene, and an inhibitor of the function of myostatin, each of which comprises the above antisense oligonucleotide or a salt or a solvate thereof.

Abstract: A method of inhibiting myostatin signaling via a myostatin splice variant-derived protein is provided. The protein and an expression system thereof are applicable to therapy for diseases in which myostatin is involved.

Abstract: The present invention establishes a method for treating cardiac dysfunction. An oligonucleotide of 15-30 bp comprising a nucleotide sequence complementary to a part of the intron 55 region of a dystrophin gene, which comprises the sequence of 5?-TGTCTTCCT-3? or 5?-CAGCTTGAACCGGGC-3? (SEQ ID NO: 64) (wherein “T” may be “U” in either sequence), a pharmacologically acceptable salt thereof, or a solvate thereof. A prophylactic and/or a therapeutic for cardiac dysfunction, comprising the above-described oligonucleotide, a pharmacologically acceptable salt thereof, or a solvate thereof. A suppressor of Dp116 expression, comprising the above-described oligonucleotide, a pharmacologically acceptable salt thereof, or a solvate thereof.

Abstract: The present invention establishes a molecular therapy for glycogen storage disease type Ia. The present invention provides an oligonucleotide of 15-30 bases comprising a nucleotide sequence complementary to the cDNA of G6PC gene with c.648G>T mutation, wherein the oligonucleotide comprises a sequence complementary to a region comprising any site between the 82nd to the 92nd nucleotide from the 5? end of exon 5 of the G6PC gene with c.648G>T mutation, a pharmacologically acceptable salt or solvate thereof. Also provided is a pharmaceutical drug comprising the oligonucleotide, a pharmacologically acceptable salt or solvate thereof (e.g., therapeutic drug for glycogen storage disease type Ia).

Abstract: Insertion of variant exons of CD44 gene of cancer stem cells into its mRNA is inhibited whereupon the cancer stem cells lose their properties so that they are rendered sensitive to anticancer agents and radiation, possibly leading to cancer treatment. A drug for cancer treatment, comprising an antisense oligonucleotide capable of inducing skipping of variant exon(s) of CD44 gene to thereby increase expression of normal CD44 mRNA, a pharmaceutically acceptable salt thereof, a solvate thereof or a prodrug thereof. An oligonucleotide of 20-23 bp having the entirety or a part of any one of the nucleotide sequences as shown in SEQ ID NOS: 1 to 19, a pharmaceutically acceptable salt thereof, a solvate thereof or a prodrug thereof. A drug for inducing skipping of at least one variant exon selected from the group consisting of variant exons 8, 9 and 10 of CD44 gene, comprising the above-described oligonucleotide, a pharmaceutically acceptable salt thereof, a solvate thereof or a prodrug thereof.

Abstract: Oligonucleotides having a nucleotide sequence complementary to nucleotide numbers such as 2571-2607, 2578-2592, 2571-2592, 2573-2592, 2578-2596, 2578-2601 or 2575-2592 of the dystrophin cDNA (Gene Bank accession No. NM_004006.1) and therapeutic agents for muscular dystrophy comprising such oligonucleotides.

Abstract: Oligonucleotides having a nucleotide sequence complementary to nucleotide numbers such as 2571-2607, 2578-2592, 2571-2592, 2573-2592, 2578-2596, 2578-2601 or 2575-2592 of the dystrophin cDNA (Gene Bank accession No. NM_004006.1) and therapeutic agents for muscular dystrophy comprising such oligonucleotides.

Abstract: Insertion of variant exons of CD44 gene of cancer stem cells into its mRNA is inhibited whereupon the cancer stem cells lose their properties so that they are rendered sensitive to anticancer agents and radiation, possibly leading to cancer treatment. A drug for cancer treatment, comprising an antisense oligonucleotide capable of inducing skipping of variant exon(s) of CD44 gene to thereby increase expression of normal CD44 mRNA, a pharmaceutically acceptable salt thereof, a solvate thereof or a prodrug thereof. An oligonucleotide of 20-23 bp having the entirety or a part of any one of the nucleotide sequences as shown in SEQ ID NOS: 1 to 19, a pharmaceutically acceptable salt thereof, a solvate thereof or a prodrug thereof. A drug for inducing skipping of at least one variant exon selected from the group consisting of variant exons 8, 9 and 10 of CD44 gene, comprising the above-described oligonucleotide, a pharmaceutically acceptable salt thereof, a solvate thereof or a prodrug thereof.

Abstract: A readthrough inducing agent for inducing readthrough of a premature stop codon generated by nonsense mutations, the readthrough inducing agent comprising a compound having a structure expressed by the following Structural Formula (A), and a drug for treating a genetic disease caused by nonsense mutations, the drug comprising the readthrough inducing agent.

Abstract: An object of the present invention is to provide a prophylactic or ameliorating agent for a genetic disease that is caused by a mutation in an exon of a gene and is capable of forming a functional truncated protein by skipping of the exon comprising the mutation. The prophylactic or ameliorating agent used in the present invention is a prophylactic or ameliorating agent for a genetic disease that is caused by a mutation in an exon of a gene and is capable of forming a functional truncated protein by skipping of the exon comprising the mutation, wherein the prophylactic or ameliorating agent contains a compound having a molecular weight of 1500 or lower.

Abstract: Oligonucleotides having a nucleotide sequence complementary to nucleotide numbers such as 2571-2607, 2578-2592, 2571-2592, 2573-2592, 2578-2596, 2578-2601 or 2575-2592 of the dystrophin cDNA (Gene Bank accession No. NM_004006.1) and therapeutic agents for muscular dystrophy comprising such oligonucleotides.

Abstract: Oligonucleotides having a nucleotide sequence complementary to nucleotide numbers such as 2571-2607, 2578-2592, 2571-2592, 2573-2592, 2578-2596, 2578-2601 or 2575-2592 of the dystrophin cDNA (Gene Bank accession No. NM_004006.1) and therapeutic agents for muscular dystrophy comprising such oligonucleotides.

Abstract: A readthrough inducing agent for inducing readthrough of a premature stop codon generated by nonsense mutations, the readthrough inducing agent comprising a compound having a structure expressed by the following Structural Formula (A), and a drug for treating a genetic disease caused by nonsense mutations, the drug comprising the readthrough inducing agent.

Abstract: Oligonucleotides having a nucleotide sequence complementary to nucleotide numbers such as 2571-2607, 2578-2592, 2571-2592, 2573-2592, 2578-2596, 2578-2601 or 2575-2592 of the dystrophin cDNA (Gene Bank accession No. NM_004006.1) and therapeutic agents for muscular dystrophy comprising such oligonucleotides.

Abstract: Provided are a self-diagnosis system and a test circuit determination method that are capable of determining normality of a test circuit which diagnoses a test target circuit. A self-diagnosis system according to an aspect of the present invention includes a test circuit including first and second diagnosis controllers which determine normality of a test target circuit by using an execution result of a test pattern in the test target circuit; and a test circuit determination unit which determines normality of the test circuit by comparing a normality determination result of the test target circuit output from the first diagnosis controller with a normal determination result of the test target circuit output from the second diagnosis controller.

Abstract: Oligonucleotides having a nucleotide sequence complementary to nucleotide numbers such as 2571-2607, 2578-2592, 2571-2592, 2573-2592, 2578-2596, 2578-2601 or 2575-2592 of the dystrophin cDNA (Gene Bank accession No. NM_004006.1) and therapeutic agents for muscular dystrophy comprising such oligonucleotides.

Abstract: An object of the present invention is to provide a prophylactic or ameliorating agent for a genetic disease that is caused by a mutation in an exon of a gene and is capable of forming a functional truncated protein by skipping of the exon comprising the mutation. The prophylactic or ameliorating agent used in the present invention is a prophylactic or ameliorating agent for a genetic disease that is caused by a mutation in an exon of a gene and is capable of forming a functional truncated protein by skipping of the exon comprising the mutation, wherein the prophylactic or ameliorating agent contains a compound having a molecular weight of 1500 or lower.