Patents by Inventor Peter L. Sazani
Peter L. Sazani has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
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Publication number: 20210363222Abstract: The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.Type: ApplicationFiled: December 28, 2020Publication date: November 25, 2021Inventors: Henrik Orum, Peter L. Sazani
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Publication number: 20200283776Abstract: Methods and compositions are disclosed for controlling expression of TNF receptors (TNFR1 and TNFR2) and of other receptors in the TNFR superfamily using compounds that modulate splicing of pre-mRNA encoding these receptors. More specifically these compounds cause the removal of the transmembrane domains of these receptors and produce soluble forms of the receptor which act as an antagonist to reduce TNF-? activity or activity of the relevant ligand. Reducing TNF-? activity provides a method of treating or ameliorating inflammatory diseases or conditions associated with TNF-? activity. Similarly, diseases associated with other ligands can be treated in like manner. In particular, the compounds of the invention are splice-splice switching oligomers (SSOs) which are small molecules that are stable in vivo, hybridize to the RNA in a sequence specific manner and, in conjunction with their target, are not degraded by RNAse H.Type: ApplicationFiled: October 22, 2019Publication date: September 10, 2020Inventors: Peter L. Sazani, Ryszard Kole, Henrik Orum
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Publication number: 20190359986Abstract: The present invention relates to compositions and methods for preparing splice variants of TNFalpha receptor (TNFR) in vivo or in vitro, and the resulting TNFR protein variants. Such variants may be prepared by controlling the splicing of pre-mRNA molecules and regulating protein expression with splice switching oligonucleotides or splice switching oligomers (SSOs) The preferred SSOs according to the invention target exon 7 or 8 of TNFR1 (TNFRSF1A) or TNFR2 (TNFRSF1A) pre-MRNA, typically resulting in the production of TNFR variants which comprise a deletion in part or the entire exon 7 or 8 respectfully. SSOs targeting exon 7 are found to result in a soluble form of the TNFR, which has therapeutic benefit for treatment of inflammatory diseases. The SSO's are characterised in that they are substantially incapable or incapable of recruiting RNaseH.Type: ApplicationFiled: March 21, 2019Publication date: November 28, 2019Applicant: Roche Innovation Center Copenhagen A/SInventors: Henrik Orum, Peter L. Sazani
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Publication number: 20190309047Abstract: The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.Type: ApplicationFiled: May 13, 2019Publication date: October 10, 2019Inventors: Henrik Orum, Peter L. Sazani
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Publication number: 20190017052Abstract: Methods and compositions are disclosed for controlling expression of TNF receptors (TNFR1 and TNFR2) and of other receptors in the TNFR superfamily using compounds that modulate splicing of pre-mRNA encoding these receptors. More specifically these compounds cause the removal of the transmembrane domains of these receptors and produce soluble forms of the receptor which act as an antagonist to reduce TNF-? activity or activity of the relevant ligand. Reducing TNF-? activity provides a method of treating or ameliorating inflammatory diseases or conditions associated with TNF-? activity. Similarly, diseases associated with other ligands can be treated in like manner. In particular, the compounds of the invention are splice-splice switching oligomers (SSOs) which are small molecules that are stable in vivo, hybridize to the RNA in a sequence specific manner and, in conjunction with their target, are not degraded by RNAse H.Type: ApplicationFiled: July 19, 2018Publication date: January 17, 2019Inventors: Peter L. Sazani, Ryszard Kole, Henrik Orum
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Publication number: 20180051290Abstract: Methods and compositions are disclosed for controlling expression of TNF receptors (TNFR1 and TNFR2) and of other receptors in the TNFR superfamily using compounds that modulate splicing of pre-mRNA encoding these receptors. More specifically these compounds cause the removal of the transmembrane domains of these receptors and produce soluble forms of the receptor which act as an antagonist to reduce TNF-? activity or activity of the relevant ligand. Reducing TNF-? activity provides a method of treating or ameliorating inflammatory diseases or conditions associated with TNF-? activity. Similarly, diseases associated with other ligands can be treated in like manner. In particular, the compounds of the invention are splice-splice switching oligomers (SSOs) which are small molecules that are stable in vivo, hybridize to the RNA in a sequence specific manner and, in conjunction with their target, are not degraded by RNAse H.Type: ApplicationFiled: November 3, 2017Publication date: February 22, 2018Inventors: Peter L. Sazani, Ryszard Kole, Henrik Orum
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Publication number: 20170198024Abstract: The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.Type: ApplicationFiled: March 15, 2017Publication date: July 13, 2017Inventors: Henrik Orum, Peter L. Sazani
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Publication number: 20170191067Abstract: Methods and compositions are disclosed for controlling expression of TNF receptors (TNFR1 and TNFR2) and of other receptors in the TNFR superfamily using compounds that modulate splicing of pre-mRNA encoding these receptors. More specifically these compounds cause the removal of the transmembrane domains of these receptors and produce soluble forms of the receptor which act as an antagonist to reduce TNF-? activity or activity of the relevant ligand. Reducing TNF-? activity provides a method of treating or ameliorating inflammatory diseases or conditions associated with TNF-? activity. Similarly, diseases associated with other ligands can be treated in like manner. In particular, the compounds of the invention are splice-splice switching oligomers (SSOs) which are small molecules that are stable in vivo, hybridize to the RNA in a sequence specific manner and, in conjunction with their target, are not degraded by RNAse H.Type: ApplicationFiled: January 17, 2017Publication date: July 6, 2017Inventors: Peter L. Sazani, Ryszard Kole, Henrik Orum
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Publication number: 20170015697Abstract: The present invention relates to compositions and methods for preparing splice variants of TNFalpha receptor (TNFR) in vivo or in vitro, and the resulting TNFR protein variants. Such variants may be prepared by controlling the splicing of pre-mRNA molecules and regulating protein expression with splice switching oligonucleotides or splice switching oligomers (SSOs). The preferred SSOs according to the invention target exon 7 or 8 of TNFR1 (TNFRSF1A) or TNFR2 (TNFRSF1A) pre-mRNA, typically resulting in the production of TNFR variants which comprise a deletion in part or the entire exon 7 or 8 respectfully. SSOs targeting exon 7 are found to result in a soluble form of the TNFR, which has therapeutic benefit for treatment of inflammatory diseases. The SSO's are characterized in that they are substantially incapable or incapable of recruiting RNaseH.Type: ApplicationFiled: June 22, 2015Publication date: January 19, 2017Inventors: Henrik Orum, Peter L. Sazani
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Publication number: 20150252371Abstract: Methods and compositions are disclosed for controlling expression of TNF receptors (TNFR1 and TNFR2) and of other receptors in the TNFR superfamily using compounds that modulate splicing of pre-mRNA encoding these receptors. More specifically these compounds cause the removal of the transmembrane domains of these receptors and produce soluble forms of the receptor which act as an antagonist to reduce TNF-? activity or activity of the relevant ligand. Reducing TNF-? activity provides a method of treating or ameliorating inflammatory diseases or conditions associated with TNF-? activity. Similarly, diseases associated with other ligands can be treated in like manner. In particular, the compounds of the invention are splice-splice switching oligomers (SSOs) which are small molecules that are stable in vivo, hybridize to the RNA in a sequence specific manner and, in conjunction with their target, are not degraded by RNAse H.Type: ApplicationFiled: March 12, 2015Publication date: September 10, 2015Inventors: Peter L. Sazani, Ryszard Kole, Henrik Orum
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Publication number: 20150166634Abstract: The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.Type: ApplicationFiled: March 2, 2015Publication date: June 18, 2015Inventors: Henrik Orum, Peter L. Sazani
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Publication number: 20140357849Abstract: The present invention relates to compositions and methods for preparing splice variants of TNFalpha receptor (TNFR) in vivo or in vitro, and the resulting TNFR protein variants. Such variants may be prepared by controlling the splicing of pre-mRNA molecules and regulating protein expression with splice switching oligonucleotides or splice switching oligomers (SSOs). The preferred SSOs according to the invention target exon 7 or 8 of TNFR1 (TNFRSF1A) or TNFR2 (TNFRSF1A) pre-mRNA, typically resulting in the production of TNFR variants which comprise a deletion in part or the entire exon 7 or 8 respectfully. SSOs targeting exon 7 are found to result in a soluble form of the TNFR, which has therapeutic benefit for treatment of inflammatory diseases. The SSO's are characterized in that they are substantially incapable or incapable of recruiting RNaseH.Type: ApplicationFiled: October 18, 2013Publication date: December 4, 2014Applicant: SANTARIS PHARMA A/SInventors: Henrik Orum, Peter L. Sazani
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Publication number: 20140057968Abstract: Methods and compositions are disclosed for controlling expression of TNF receptors (TNFR1 and TNFR2) and of other receptors in the TNFR superfamily using compounds that modulate splicing of pre-mRNA encoding these receptors. More specifically these compounds cause the removal of the transmembrane domains of these receptors and produce soluble forms of the receptor which act as an antagonist to reduce TNF-? activity or activity of the relevant ligand. Reducing TNF-? activity provides a method of treating or ameliorating inflammatory diseases or conditions associated with TNF-? activity. Similarly, diseases associated with other ligands can be treated in like manner. In particular, the compounds of the invention are splice-splice switching oligomers (SSOs) which are small molecules that are stable in vivo, hybridize to the RNA in a sequence specific manner and, in conjunction with their target, are not degraded by RNAse H.Type: ApplicationFiled: March 11, 2013Publication date: February 27, 2014Inventors: Peter L. Sazani, Ryszard Kole, Henrik Orum
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Publication number: 20130123479Abstract: The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.Type: ApplicationFiled: December 31, 2012Publication date: May 16, 2013Inventors: Peter L. Sazani, Henrik Orum
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Publication number: 20120142759Abstract: The present invention relates to splice switching oligonucleotides or splice switching oligomers (SSOs). The preferred SSOs according to the invention target exon 7 of TNFR1 (TNFRSF1A) or TNFR2 (TNFRSF1A) pre-mRNA, typically resulting in the production of TNFR variants which comprise a deletion in part or the entire exon 7 respectfully. SSOs targeting exon 7 are found to result in a soluble form of the TNFR, which has thereputic benefit for treatment of inflammatory diseases. The SSO's are characterized in that they are substantially incapable or incapable of recruiting RNaseH.Type: ApplicationFiled: October 19, 2007Publication date: June 7, 2012Inventors: Peter L. Sazani, Maria Graziewicz, Ryszard Kole
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Publication number: 20120040917Abstract: The present invention relates to compositions and methods for preparing splice variants of TNFalpha receptor (TNFR) in vivo or in vitro, and the resulting TNFR protein variants. Such variants may be prepared by controlling the splicing of pre-mRNA molecules and regulating protein expression with splice switching oligonucleotides or splice switching oligomers (SSOs). The preferred SSOs according to the invention target exon 7 or 8 of TNFR1 (TNFRSF1A) or TNFR2 (TNFRSF1A) pre-mRNA, typically resulting in the production of TNFR variants which comprise a deletion in part or the entire exon 7 or 8 respectfully. SSOs targeting exon 7 are found to result in a soluble form of the TNFR, which has therapeutic benefit for treatment of inflammatory diseases. The SSO's are characterized in that they are substantially incapable or incapable of recruiting RNaseH.Type: ApplicationFiled: December 3, 2010Publication date: February 16, 2012Inventors: HENRIK ØRUM, PETER L. SAZANI
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Publication number: 20110237521Abstract: Methods and compositions are disclosed for controlling expression of TNF receptors (TNFR1 and TNFR2) and of other receptors in the TNFR superfamily using compounds that modulate splicing of pre-mRNA encoding these receptors. More specifically these compounds cause the removal of the transmembrane domains of these receptors and produce soluble forms of the receptor which act as an antagonist to reduce TNF-? activity or activity of the relevant ligand. Reducing TNF-? activity provides a method of treating or ameliorating inflammatory diseases or conditions associated with TNF-? activity. Similarly, diseases associated with other ligands can be treated in like manner. In particular, the compounds of the invention are splice-splice switching oligomers (SSOs) which are small molecules that are stable in vivo, hybridize to the RNA in a sequence specific manner and, in conjunction with their target, are not degraded by RNAse H.Type: ApplicationFiled: November 24, 2010Publication date: September 29, 2011Inventors: Peter L. Sazani, Ryszard Kole, Henrik Orum
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Publication number: 20110105740Abstract: The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.Type: ApplicationFiled: August 30, 2010Publication date: May 5, 2011Inventor: PETER L. SAZANI
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Patent number: 7785834Abstract: The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.Type: GrantFiled: May 1, 2007Date of Patent: August 31, 2010Assignees: Ercole Biotech, Inc., University of North Carolina at Chapel Hill, Santaris Pharma A/SInventors: Peter L. Sazani, Maria Graziewicz, Ryszard Kole, Henrik Ørum
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Publication number: 20090264353Abstract: The present invention relates to compositions and methods for preparing splice variants of TNFalpha receptor (TNFR) in vivo or in vitro, and the resulting TNFR protein variants. Such variants may be prepared by controlling the splicing of pre-mRNA molecules and regulating protein expression with splice switching oligonucleotides or splice switching oligomers (SSOs). The preferred SSOs according to the invention target exon 7 or 8 of TNFR1 (TNFRSF1A) or TNFR2 (TNFRSF1A) pre-mRNA, typically resulting in the production of TNFR variants which comprise a deletion in part or the entire exon 7 or 8 respectfully. SSOs targeting exon 7 are found to result in a soluble form of the TNFR, which has therapeutic benefit for treatment of inflammatory diseases. The SSO's are characterized in that they are substantially incapable or incapable of recruiting RNaseH.Type: ApplicationFiled: October 19, 2007Publication date: October 22, 2009Inventors: Henrik Orum, Peter L. Sazani