Patents by Inventor Steven Idell
Steven Idell 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: 20240059736Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: ApplicationFiled: August 15, 2023Publication date: February 22, 2024Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Sreerama SHETTY, Steven IDELL
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Patent number: 11780879Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: GrantFiled: October 12, 2021Date of Patent: October 10, 2023Assignee: Board of Regents, the University of Texas SystemInventors: Sreerama Shetty, Steven Idell
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Publication number: 20230100467Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: ApplicationFiled: December 2, 2022Publication date: March 30, 2023Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Sreerama SHETTY, Steven IDELL
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Publication number: 20220098239Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: ApplicationFiled: October 12, 2021Publication date: March 31, 2022Inventors: Sreerama SHETTY, Steven IDELL
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Patent number: 11161875Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: GrantFiled: December 3, 2019Date of Patent: November 2, 2021Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Sreerama Shetty, Steven Idell
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Publication number: 20210330741Abstract: Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).Type: ApplicationFiled: July 5, 2021Publication date: October 28, 2021Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Robert O. WILLIAMS, III, Steven IDELL, Sreerama SHETTY
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Publication number: 20210212988Abstract: Pharmaceutical compositions and methods are described which rely upon glycogen synthase kinase 3 (form ?; GSK 3?) inhibitors, most preferably 9-ING-41, to inhibit fibrotic pulmonary remodeling in vivo including proliferation and differentiation of myofibroblasts to fibrotic fibroblasts in several mouse models. Therapeutic targeting of GSK-3? with the clinically useful specific inhibitor, 9-ING-41, mitigates fibrotic pulmonary remodeling in vivo and provides a mode of therapy of human IPF by specific GSK-3? inhibition with 9-ING-41.Type: ApplicationFiled: May 16, 2019Publication date: July 15, 2021Inventors: Torry A. TUCKER, Steven IDELL
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Patent number: 11033611Abstract: Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).Type: GrantFiled: January 28, 2019Date of Patent: June 15, 2021Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Robert O. Williams, III, Steven Idell
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Publication number: 20200165298Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: ApplicationFiled: December 3, 2019Publication date: May 28, 2020Inventors: Sreerama SHETTY, Steven IDELL
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Publication number: 20200164028Abstract: Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).Type: ApplicationFiled: November 27, 2019Publication date: May 28, 2020Inventors: Robert O. WILLIAMS, III, Steven IDELL, Sreerama SHETTY
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Publication number: 20190255157Abstract: Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).Type: ApplicationFiled: January 28, 2019Publication date: August 22, 2019Inventors: Robert O. WILLIAMS, III, Steven IDELL
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Patent number: 10377796Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: GrantFiled: March 10, 2017Date of Patent: August 13, 2019Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Sreerama Shetty, Steven Idell
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Patent number: 10175255Abstract: An assay that informs precision-based intrapleural fibrinolytic therapy (IPFT) is disclosed. Provided is a simple assay based on measurement of the Fibrinolytic Potential (FP)—total fibrinolytic activity in pleural fluid when plasminogen activator inhibitors (PAIs) are neutralized and endogenous plasminogen (PLG) is activated. The assay is used to determine FP in baseline pleural fluids of patients undergoing IPFT with agents such as tPA or scuPA to determine the dose and dose intervals for the particular patient. Pleural fluids are also collected after IPFT to confirm that intrapleural fibrinolysis is inhibited and endogenous PLG accumulates in the pleural fluid. Inhibition of intrapleural fibrinolysis in combination with its increase after supplementation of pleural fluid with a plasminogen activator indicates whether or not the subject should be treated with more or higher doses of an IPFT drug.Type: GrantFiled: March 31, 2016Date of Patent: January 8, 2019Assignee: Board of Regents, The University of Texas SystemInventors: Andrey A. Komissarov, Galina Florova, Steven Idell
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Publication number: 20180140547Abstract: Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).Type: ApplicationFiled: May 6, 2016Publication date: May 24, 2018Inventors: Robert O. WILLIAMS, III, Steven IDELL
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Publication number: 20180086791Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO: 1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: ApplicationFiled: October 9, 2017Publication date: March 29, 2018Inventors: Sreerama SHETTY, Steven IDELL
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Publication number: 20180050084Abstract: Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).Type: ApplicationFiled: February 26, 2016Publication date: February 22, 2018Inventors: Robert O. WILLIAMS, III, Steven IDELL, Sreerama SHETTY
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Patent number: 9808505Abstract: The influence of TF, endothelial cell protein C receptor (EPCR) and protease activated receptor-1 (PAR1) on tumor growth of malignant pleural mesothelioma (MPM) is disclosed. MPM cells that lack or express TF, EPCR or PAR1 and a murine orthotopic model of MPM led to the discovery that intrapleural administration into nude mice of REN MPM cells expressing TF and PAR1 but lacking EPCR and PAR2 generated large pleural cavity tumors. Suppression of TF or PAR1 expression markedly reduced tumor growth. Overexpression of TF in non-aggressive MPM cells expressing EPCR and PAR1 but exhibiting minimal levels of TF failed to alter their tumorigenicity. Introduction of EPCR expression in aggressive MPM cells attenuated tumor growth whereas EPCR silencing in non-aggressive MPM cells overexpressing TF increased tumorigenicity of non-aggressive cells. Expression of EPCR by MPM cells suppresses tumor growth and treats MPM.Type: GrantFiled: March 10, 2014Date of Patent: November 7, 2017Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Usha R. Pendurthi, Vijaya M. R. Lella, Shivakeshava Gaddam, Steven Idell
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Publication number: 20170253632Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: ApplicationFiled: March 10, 2017Publication date: September 7, 2017Inventors: Sreerama SHETTY, Steven IDELL
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Patent number: 9630990Abstract: In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.Type: GrantFiled: March 17, 2014Date of Patent: April 25, 2017Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEMInventors: Sreerama Shetty, Steven Idell
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Publication number: 20160291043Abstract: The present invention is directed to an assay that informs precision-based intrapleural fibrinolytic therapy (IPFT). Provided is a simple assay based on measurement of the Fibrinolytic Potential (FP)—total fibrinolytic activity in pleural fluid when plasminogen activator inhibitors (PAIs) are neutralized and endogenous plasminogen (PLG) is activated. The assay is used to determine FP in baseline pleural fluids of patients undergoing IPFT with agents such as tPA or scuPA to determine the dose and dose intervals for the particular patient. Pleural fluids are also collected after IPFT to confirm that intrapleural fibrinolysis is inhibited and endogenous PLG accumulates in the pleural fluid. Inhibition of intrapleural fibrinolysis in combination with its increase after supplementation of pleural fluid with a plasminogen activator indicates whether or not the subject should be treated with more or higher doses of an IPFT drug.Type: ApplicationFiled: March 31, 2016Publication date: October 6, 2016Inventors: Andrey A. Komissarov, Galina Florova, Steven Idell