Abstract: Methods for treating bladder cancer and solid tumors are disclosed. The methods include administering to a patient a compound of formula 1 Pharmaceutical compositions of compound 1 are also disclosed.

Abstract: Methods for treating bladder cancer and solid tumors are disclosed. The methods include administering to a patient a compound of formula 1 Pharmaceutical compositions of compound 1 are also disclosed.

Abstract: Methods for treating bladder cancer and solid tumors are disclosed. The methods include administering to a patient a compound of formula 1 Pharmaceutical compositions of compound 1 are also disclosed.

Abstract: The present invention relates to an isolated naturally-occurring soluble truncated IL-23R? protein, which is a translated protein resulting from a mRNA splice variant of IL-23R?. The soluble IL-23R? proteins (e.g., ?9 and ?8,9) represents a novel soluble IL-23R? protein, which is lacking a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end (due to frame-shift). ELISA reveals that ?9 is present in blood and can serve as a diagnostic tool for auto-immune diseases including Crohn's disease. There is also provided a method of recombinant production for this soluble truncated form of IL-23R? protein. More importantly, the present invention provides an utility application of the ?9 and ?8,9 protein in inhibit IL-23R-mediated cell signaling. More particularly, ?9 and ?8,9 blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of ?9 and ?8,9 in treating a human patient inflicted with Crohn's disease.

Abstract: The present invention provides a method of specifically detecting IFN-?2 mRNA or IFN-?3 mRNA. There is provided a qRT-PCR method specifically detecting, discriminating and quantifying IFN-?2 and IFN-?3 mRNA in a biological sample obtained from a human. There is provided qRT-PCR methods and primers and probes that specifically detect IFN-?2 mRNA but not IFN-?3 mRNA and vice versa in humans in order to detect, quantify and discriminate IFN-?2 mRNA and IFN-?3 mRNA.

Abstract: The present invention relates to anti-sense oligonucleotides (AONs) used to induce exon 9 skipping in IL-23R? gene. Exon 9 skipping of the IL23R? gene ultimately causes specific induction of a novel soluble truncated IL-23R? (?9) protein, characterized by a lack in a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end as a result of frame-shift. The present invention provides a utility application of the use of AONs to induce production of a ?9 protein which inhibits IL-23R-mediated cell signaling. More particularly, ?9 protein blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of AONs in treating a mammal such as a human patient inflicted with Crohn's disease.

Abstract: The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-?1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-?1 (i.e., increases the production of IFN-?1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-?1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-?1 protein that promotes an anti-viral response as well as treats asthma diseases and colon diseases.

Abstract: The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-?1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-?1 (i.e., increases the production of IFN-?1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-?1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-?1 protein that promotes an anti-viral response as well as treats asthma diseases and colon diseases.

Abstract: The present invention relates to novel linear and cyclic polypeptides that bind to IL-23 receptor and inhibit the binding of IL-23 to its corresponding receptor and cell signaling thereof. The novel polypeptides of the present invention has a core structure of WX1X2X3W, where W is tryptophan, and X1, X2 and X3 are amino acids, with the proviso that when one of X1, X2 or X3 is W, the remaining two of X1, X2 or X3 cannot be W. Preferred core structures include WVDYW or WQDYW. The present invention relates a composition containing the novel polypeptides (linear or cyclic), and use of same in inhibiting cell functions including production of IL-22 and IL-17F from immune cells as well as in treating IL-23 associated human diseases including, for example, inflammatory bowel diseases, psoriasis and Crohn's disease, ulcerative colitis and multiple sclerosis.

Abstract: A naturally-occurring soluble truncated IL-23R? protein (i.e., ?9 IL-23R?) is shown to be present in a biological sample and can serve as a diagnostic tool for autoimmune diseases. There is provided an enzyme-linked immunosorbent assay (ELISA) and test kit for the serological detection of the soluble truncated form of IL-23R? protein. More particularly, antibody-sandwich ELISA method and kits for ?9 IL-23R? as an antigen were developed to detect ?9 IL-23R? levels in biological samples from a mammal and a human patient and are used as a diagnostic index. The present disclosed ELISA has utility as a diagnostic tool to detect Crohn's disease in patients using EDTA-plasma.

Abstract: The present invention provides a method of specifically detecting IFN-?2 mRNA or IFN-?3 mRNA. There is provided a qRT-PCR method specifically detecting, discriminating and quantifying IFN-?2 and IFN-?3 mRNA in a biological sample obtained from a human. There is provided qRT-PCR methods and primers and probes that specifically detect IFN-?2 mRNA but not IFN-?3 mRNA and vice versa in humans in order to detect, quantify and discriminate IFN-?2 mRNA and IFN-?3 mRNA.

Abstract: A naturally-occurring soluble truncated IL-23R? protein (i.e., ?9 IL-23R?) is shown to be present in a biological sample and can serve as a diagnostic tool for autoimmune diseases. There is provided an enzyme-linked immunosorbent assay (ELISA) and test kit for the serological detection of the soluble truncated form of IL-23R? protein. More particularly, antibody-sandwich ELISA method and kits for ?9 IL-23R? as an antigen were developed to detect ?9 IL-23R? levels in biological samples from a mammal and a human patient and are used as a diagnostic index. The present disclosed ELISA has utility as a diagnostic tool to detect Crohn's disease in patients using EDTA-plasma.

Abstract: The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-?1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-?1 (i.e., increases the production of IFN-?1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-?1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-?1 protein that promotes an anti-viral response as well as treats asthma diseases and colon diseases.

Abstract: The present invention provides a method of specifically detecting IFN-?2 mRNA or IFN-?3 mRNA. There is provided a qRT-PCR method specifically detecting, discriminating and quantifying IFN-?2 and IFN-?3 mRNA in a biological sample obtained from a human. There is provided qRT-PCR methods and primers and probes that specifically detect IFN-?2 mRNA but not IFN-?3 mRNA and vice versa in humans in order to detect, quantify and discriminate IFN-?2 mRNA and IFN-?3 mRNA.

Abstract: The present invention relates to anti-sense oligonucleotides (AONs) used to induce exon 9 skipping in IL-23R? gene. Exon 9 skipping of the IL23R? gene ultimately causes specific induction of a novel soluble truncated IL-23R? (?9) protein, characterized by a lack in a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end as a result of frame-shift. The present invention provides a utility application of the use of AONs to induce production of a ?9 protein which inhibits IL-23R-mediated cell signaling. More particularly, ?9 protein blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of AONs in treating a mammal such as a human patient inflicted with Crohn's disease.

Abstract: The present invention relates to novel linear and cyclic polypeptides that bind to IL-23 receptor and inhibit the binding of IL-23 to its corresponding receptor and cell signaling thereof. The novel polypeptides of the present invention has a core structure of WX1X2X3W, where W is tryptophan, and X1, X2 and X3 are amino acids, with the proviso that when one of X1, X2 or X3 is W, the remaining two of X1, X2 or X3 cannot be W. Preferred core structures include WVDYW or WQDYW. The present invention relates a composition containing the novel polypeptides (linear or cyclic), and use of same in inhibiting cell functions including production of IL-22 and IL-17F from immune cells as well as in treating IL-23 associated human diseases including, for example, inflammatory bowel diseases, psoriasis and Crohn's disease, ulcerative colitis and multiple sclerosis.

Abstract: The present invention relates to anti-sense oligonucleotides (AONs) used to induce exon 9 skipping in IL-23R? gene. Exon 9 skipping of the IL23R? gene ultimately causes specific induction of a novel soluble truncated IL-23R? (?9) protein, characterized by a lack in a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end as a result of frame-shift. The present invention provides a utility application of the use of AONs to induce production of a ?9 protein which inhibits IL-23R-mediated cell signaling. More particularly, ?9 protein blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of AONs in treating a mammal such as a human patient inflicted with Crohn's disease.

Abstract: The present invention relates to novel polypeptides that bind to IL-23 receptor and inhibit the binding of IL-23 to its corresponding receptor and cell signaling thereof. The novel polypeptides of the present invention has a core structure of WX1X2X3W, where W is tryptophan, and X1, X2 and X3 are amino acids, with the proviso that when one of X1, X2 or X3 is W, the remaining two of X1, X2 or X3 cannot be W. Preferred core structures include WVDYW or WQDYW. The present invention relates a composition containing the novel polypeptides, and use of same in treating IL-23 associated human diseases including, for example, inflammatory bowel diseases, psoriasis and Crohn's disease.

Abstract: The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-?1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-?1 (i.e., increases the production of IFN-?1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-?1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-?1 protein that promotes an anti-viral response as well as treats asthma diseases.

Abstract: The present invention relates to novel linear and cyclic polypeptides that bind to IL-23 receptor and inhibit the binding of IL-23 to its corresponding receptor and cell signaling thereof. The novel polypeptides of the present invention has a core structure of WX1X2X3W, where W is tryptophan, and X1, X2 and X3 are amino acids, with the proviso that when one of X1, X2 or X3 is W, the remaining two of X1, X2 or X3 cannot be W. Preferred core structures include WVDYW or WQDYW. The present invention relates a composition containing the novel polypeptides (linear or cyclic), and use of same in inhibiting cell functions including production of IL-22 and IL-17F from immune cells as well as in treating IL-23 associated human diseases including, for example, inflammatory bowel diseases, psoriasis and Crohn's disease, ulcerative colitis and multiple sclerosis.