Patents by Inventor Sreerama Shetty

Sreerama Shetty 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).

  • Publication number: 20240082342
    Abstract: Chronic tobacco smoke exposure (TSE)-induced lung injury includes increased alveolar and airway inflammation, type II alveolar epithelial cells (A2Cs) senescence and apoptosis, and mucus hypersecretion by airway epithelial cells (AECs) that can be treated by the caveolin-1 peptide CSP7 (SEQ ID NO:1). Caveolin-1 and p53 mediated induction of plasminogen activator inhibitor-1 (PAI-1) expression by interleukin 17A, TSE, pollution and other causes leads to lung injury, which can be abrogated by CSP7 treatment, which abolishes A2Cs senescence and apoptosis and AEC mucus hypersecretion. CSP7 treatment of lung tissue of patients with TSE-induced lung injury decreases A2C apoptosis and AEC mucus hypersecretion. Lung injury with A2Cs senescence and apoptosis and AEC mucus hypersecretion caused by TSE-induced PAI-1 expression in lung tissue of patients is abolished by CSP7.
    Type: Application
    Filed: October 25, 2023
    Publication date: March 14, 2024
    Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventor: Sreerama SHETTY
  • Publication number: 20240067713
    Abstract: Methods for treating, reducing, ameliorating or inhibiting symptoms idiopathic pulmonary fibrosis (IPF) or interstitial pneumonia, comprising administering to a subject in need of an effective amount of a) multiple EGF-like-domains-9 (MEGF9) or a biologically active fragment thereof; b) uncoordinated receptor 5A (UNC5A) or a biologically active fragment thereof; c) dolichyl-phosphate beta-glucosyltransferase (ALG5) or a biologically active fragment thereof; d) a combination of two or three of a)-c); e) an antibody specifically binding to a); f) an antibody specifically binding to b); g) an antibody specifically binding to c); h) a combination of two or three of e)-g); or i) a combination of at least one of a)-c) and at least one of e)-g). Pharmaceutical compositions and processes for making and using the compositions are also disclosed.
    Type: Application
    Filed: October 5, 2023
    Publication date: February 29, 2024
    Applicant: Board of Regents, The University of Texas System
    Inventor: Sreerama SHETTY
  • Publication number: 20240059736
    Abstract: 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: Application
    Filed: August 15, 2023
    Publication date: February 22, 2024
    Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventors: Sreerama SHETTY, Steven IDELL
  • Patent number: 11780879
    Abstract: 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: Grant
    Filed: October 12, 2021
    Date of Patent: October 10, 2023
    Assignee: Board of Regents, the University of Texas System
    Inventors: Sreerama Shetty, Steven Idell
  • Publication number: 20230190861
    Abstract: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease encompassing chronic bronchitis, emphysema and remodeling of small airways that can be treated by the caveolin-1 peptide CSP7 (SEQ ID NO:1). Chronic tobacco smoke exposure (TSE)-induced lung injury includes increased alveolar and airway inflammation, type II alveolar epithelial cells (A2Cs) senescence and apoptosis, and mucus hypersecretion by AECs. Interleukin 17A-mediated induction of plasminogen activator inhibitor-1 (PAI-1) expression through caveolin-1 led to TSE-induced lung injury, which was abrogated by CSP7 treatment which abolished A2Cs senescence and apoptosis, and AECs mucus hypersecretion in TSE wild type (WT) mice. Ex vivo CSP7 treatment of lung tissue of COPD patients decreased A2C apoptosis and AEC mucus hypersecretion. Lung injury induced by PAI-1 expression in COPD lung tissue and WT mice (20 weeks TSE), with A2Cs senescence and apoptosis, and AEC mucus hypersecretion was abolished by CSP7.
    Type: Application
    Filed: February 22, 2023
    Publication date: June 22, 2023
    Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventor: Sreerama SHETTY
  • Publication number: 20230100467
    Abstract: 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: Application
    Filed: December 2, 2022
    Publication date: March 30, 2023
    Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventors: Sreerama SHETTY, Steven IDELL
  • Publication number: 20220370544
    Abstract: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease encompassing chronic bronchitis, emphysema and remodeling of small airways that can be treated by the caveolin-1 peptide CSP7 (SEQ ID NO:1). Chronic tobacco smoke exposure (TSE)-induced lung injury includes increased alveolar and airway inflammation, type II alveolar epithelial cells (A2Cs) senescence and apoptosis, and mucus hypersecretion by AECs. Interleukin 17A-mediated induction of plasminogen activator inhibitor-1 (PAI-1) expression through caveolin-1 led to TSE-induced lung injury, which was abrogated by CSP7 treatment which abolished A2Cs senescence and apoptosis, and AECs mucus hypersecretion in TSE wild type (WT) mice. Ex vivo CSP7 treatment of lung tissue of COPD patients decreased A2C apoptosis and AEC mucus hypersecretion. Lung injury induced by PAI-1 expression in COPD lung tissue and WT mice (20 weeks TSE), with A2Cs senescence and apoptosis, and AEC mucus hypersecretion was abolished by CSP7.
    Type: Application
    Filed: November 21, 2019
    Publication date: November 24, 2022
    Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventor: Sreerama SHETTY
  • Publication number: 20220098239
    Abstract: 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: Application
    Filed: October 12, 2021
    Publication date: March 31, 2022
    Inventors: Sreerama SHETTY, Steven IDELL
  • Patent number: 11161875
    Abstract: 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: Grant
    Filed: December 3, 2019
    Date of Patent: November 2, 2021
    Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventors: Sreerama Shetty, Steven Idell
  • Publication number: 20210330741
    Abstract: 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: Application
    Filed: July 5, 2021
    Publication date: October 28, 2021
    Applicant: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventors: Robert O. WILLIAMS, III, Steven IDELL, Sreerama SHETTY
  • Publication number: 20200164028
    Abstract: 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: Application
    Filed: November 27, 2019
    Publication date: May 28, 2020
    Inventors: Robert O. WILLIAMS, III, Steven IDELL, Sreerama SHETTY
  • Publication number: 20200165298
    Abstract: 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: Application
    Filed: December 3, 2019
    Publication date: May 28, 2020
    Inventors: Sreerama SHETTY, Steven IDELL
  • Patent number: 10377796
    Abstract: 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: Grant
    Filed: March 10, 2017
    Date of Patent: August 13, 2019
    Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventors: Sreerama Shetty, Steven Idell
  • Publication number: 20180086791
    Abstract: 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: Application
    Filed: October 9, 2017
    Publication date: March 29, 2018
    Inventors: Sreerama SHETTY, Steven IDELL
  • Publication number: 20180050084
    Abstract: 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: Application
    Filed: February 26, 2016
    Publication date: February 22, 2018
    Inventors: Robert O. WILLIAMS, III, Steven IDELL, Sreerama SHETTY
  • Publication number: 20170253632
    Abstract: 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: Application
    Filed: March 10, 2017
    Publication date: September 7, 2017
    Inventors: Sreerama SHETTY, Steven IDELL
  • Patent number: 9630990
    Abstract: 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: Grant
    Filed: March 17, 2014
    Date of Patent: April 25, 2017
    Assignee: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM
    Inventors: Sreerama Shetty, Steven Idell
  • Publication number: 20160272678
    Abstract: 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: Application
    Filed: March 17, 2014
    Publication date: September 22, 2016
    Inventors: Sreerama SHETTY, Steven IDELL
  • Patent number: 8697840
    Abstract: During lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). In the bleomycin lung injury model, p53 and PAI-1 are induced while uPA and uPAR are inhibited. A 20 residue peptide DGIWKASFTTFTVTKYWFYR termed PP-1 (the Cav-1 scaffolding domain) or peptide NYHYLESSMTALYTLGH, termed PP-2, protected LECs from bleomycin-induced apoptosis in vitro and in vivo and prevented subsequent pulmonary fibrosis by attenuating lung epitheilial damage. Pharmaceutical compositions, peptide multimers and deliverable polypeptides comprising the above peptides are dislcosed.
    Type: Grant
    Filed: March 5, 2009
    Date of Patent: April 15, 2014
    Assignee: Board of Regents, The University of Texas System
    Inventors: Sreerama Shetty, Steven Idell
  • Publication number: 20090227515
    Abstract: During lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). In the bleomycin lung injury model, p53 and PAI-1 are induced while uPA and uPAR are inhibited. A 20 residue peptide DGIWKASFTTFTVTKYWFYR termed PP-1 (the Cav-1 scaffolding domain) or peptide NYHYLESSMTALYTLGH, termed PP-2, protected LECs from bleomycin-induced apoptosis in vitro and in vivo and prevented subsequent pulmonary fibrosis by attenuating lung epitheilial damage. Pharmaceutical compositions, peptide multimers and deliverable polypeptides comprising the above peptides are dislcosed.
    Type: Application
    Filed: March 5, 2009
    Publication date: September 10, 2009
    Applicant: Board of Regents, The University of Texas System
    Inventors: Sreerama Shetty, Steven Idell