Title: Therapeutic Polypeptides, Nucleic Acids Encoding the Same, and Methods of Use. Number: 20040229779. Filed: Aug. 8, 2003. Lead Inventor: Ramesh Kekuda, CuraGen.
The patent application, its abstract states, covers “nucleic acid sequences that encode novel polypeptides. Also [covered] are polypeptides encoded by these nucleic acid sequences, and antibodies that immunospecifically bind to the polypeptide, as well as derivatives, variants, mutants, or fragments of the novel polypeptide, polynucleotide, or antibody specific to the polypeptide.”
According to the abstract, the invention further comprises “therapeutic, diagnostic, and research methods for diagnosis, treatment, and prevention of disorders involving any one of these novel human nucleic acids and proteins.”
Title: Inhibition of Gene Expression by Delivery of Small-Interfering RNA to Post-Embryonic Animal Cells In Vivo. Number: 20040229358. Filed: Nov. 7, 2001. Lead Inventor: David Lewis, Mirus.
The patent application, its abstract states, covers “a process ... to deliver small interfering RNA to cells in vivo for the purpose of inhibiting gene expression in that cell.
“The small interfering RNA is less than 50 base-pairs in length,” the abstract notes. “This process is practiced on post-embryonic animals. Inhibition is sequence-specific and relies on sequence identity of the small interfering RNA and the target nucleic acid molecule.”
Title: RNA Interference-Mediating Small RNA Molecules. Number: 20040229266. Filed: Nov. 18, 2004. Lead Inventor: Thomas Tuschl, Max Planck Institute.
According to the patent application’s abstract, the invention comprises “double-stranded RNA [that induce] sequence-specific post-transcriptional gene silencing in many organisms by a process known as RNA interference.”
The abstract notes that “using a Drosophila in vitro system, we demonstrate that 19-23 [nucleotide] short RNA fragments are the sequence-specific mediators of RNAi. The short interfering RNAs are generated by an RNase III-like processing reaction from long dsRNA,” it adds. “Chemically synthesized siRNA duplexes with overhanging 3’ ends mediate efficient target RNA cleavage in the lysate, and the cleavage site is located near the center of the region spanned by the guiding siRNA.
“Furthermore, we provide evidence that the direction of dsRNA processing determines whether sense or antisense target RNA can be cleaved by the produced siRNP complex,” the abstract states.
Title: Efficient Gene Silencing in Plants Using Short-dsRNA Sequences. Number: 20040231016. Filed: Feb. 19, 2004. Lead Inventor: Ming Bo Wang, Commonwealth Scientific and Industrial Research Organization.
“Methods and means are provided to increase the efficiency of gene silencing when using dsRNA sequences which have a stem length shorter than about 200 base pairs by providing chimeric genes encoding such dsRNA sequences with a promoter recognized by DNA dependent RNA polymerase III comprising all cis-acting promoter elements which interact with DNA dependent RNA polymerase III,” the patent application’s abstract states.
Title: Animal Model Exhibiting Pathological Conditions of Alzheimer’s Disease. Number: 20040226055. Filed: Jan. 22, 2004. Inventor: Tadeusz Wieloch, Lund University.
The invention, the patent application’s abstract states, “provides an animal model that exhibits a pathological condition characteristic of Alzheimer’s disease.
This invention also provides various methods of using this animal model for the development of modulators of Alzheimer’s disease-associated genes or polypeptides.”
Additionally, the abstract notes, the invention comprises “a method of developing a modulator of pathogenesis of Alzheimer’s disease. The compositions and methods of the present invention are particularly useful in Alzheimer’s disease research and drug development.”
The patent application specifically claims “a method of developing a modulator of pathogenesis of Alzheimer’s disease [by] administering a candidate modulator … [such as] an antisense oligonucleotide [or] ... a small interfering RNA … to a test animal model.” The model is generated by inducing ... forebrain ischemia in the animal; allowing the animal to recover so that a pathological condition of Alzheimer's disease is exhibited; and detecting a change in the pathological condition in the test animal model relative to a control, the application notes.