Patents by Inventor Ruth T. Yu
Ruth T. Yu 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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Patent number: 10450277Abstract: Novel compounds having a formula embodiments of a method of making the same, and of a composition comprising them are disclosed herein. Also disclosed are embodiments of a method of treating or preventing a metabolic disorder in a subject, comprising administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and treating or preventing a metabolic disorder in the subject. Additionally disclosed are embodiments of a method of treating or preventing inflammation in an intestinal region of a subject, comprising administering to the subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and thereby treating or preventing inflammation in the intestinal region of the subject.Type: GrantFiled: November 27, 2018Date of Patent: October 22, 2019Assignees: The Salk Institute for Biological Studies, University of SydneyInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Sungsoon Fang, Jae Myoung Suh, Thomas J. Baiga, Ruth T. Yu, John F. W. Keana, Christopher Liddle
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Publication number: 20190276510Abstract: The present disclosure provides FGF1 mutant proteins, which include an N-terminal deletion, point mutation(s), or combinations thereof, as well as FGF1-vagus targeting chimeric proteins which include an FGF1 portion (e.g., native FGF1 or mutant FGF1) and a portion that targets the chimera to the vagus nerve (e.g., GLP or exendin-4). Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants and FGF1-vagus targeting chimeric proteins can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.Type: ApplicationFiled: May 22, 2019Publication date: September 12, 2019Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu, Sihao Liu
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Publication number: 20190192630Abstract: The present disclosure provides FGF1 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Such mutant FGF1 proteins can be part of a chimeric protein that includes a ?-Klotho-binding protein, an FGFR1c-binding protein, a ?-Klotho-binding protein and a FGFR1c-binding protein, a C-terminal region from FGF19 or FGF21. In some examples, mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed molecules to reduce blood glucose levels are also provided.Type: ApplicationFiled: March 7, 2019Publication date: June 27, 2019Applicant: Salk Institute for Biological StudiesInventors: Jae Myoung Suh, Michael Downes, Ronald M. Evans, Annette Atkins, Ruth T. Yu
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Patent number: 10301268Abstract: Novel compounds having a formula embodiments of a method of making the same, and of a composition comprising them are disclosed herein. Also disclosed are embodiments of a method of treating or preventing a metabolic disorder in a subject, comprising administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and treating or preventing a metabolic disorder in the subject. Additionally disclosed are embodiments of a method of treating or preventing inflammation in an intestinal region of a subject, comprising administering to the subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and thereby treating or preventing inflammation in the intestinal region of the subject.Type: GrantFiled: September 12, 2016Date of Patent: May 28, 2019Assignees: The Salk Institute for Biological Studies, University of SydneyInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Sungsoon Fang, Jae Myoung Suh, Thomas J. Baiga, Ruth T. Yu, John F. W. Keana, Christopher Liddle
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Publication number: 20190151416Abstract: The present disclosure provides FGF1 mutant proteins, which include an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.Type: ApplicationFiled: January 18, 2019Publication date: May 23, 2019Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu, Sihao Liu
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Publication number: 20190084939Abstract: Novel compounds having a formula embodiments of a method of making the same, and of a composition comprising them are disclosed herein. Also disclosed are embodiments of a method of treating or preventing a metabolic disorder in a subject, comprising administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and treating or preventing a metabolic disorder in the subject. Additionally disclosed are embodiments of a method of treating or preventing inflammation in an intestinal region of a subject, comprising administering to the subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and thereby treating or preventing inflammation in the intestinal region of the subject.Type: ApplicationFiled: November 27, 2018Publication date: March 21, 2019Applicants: Salk Institute for Biological Studies, The University of SydneyInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Sungsoon Fang, Jae Myoung Suh, Thomas J. Baiga, Ruth T. Yu, John F.W. Keana, Christopher Liddle
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Publication number: 20180319857Abstract: The present disclosure provides FGF2 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Thus, the disclosed mutant FGF2 proteins can be used to treat one or more metabolic diseases. In some examples, mutant FGF2 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed molecules to reduce blood glucose levels, for example to treat a metabolic disorder are also provided.Type: ApplicationFiled: July 13, 2018Publication date: November 8, 2018Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu
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Publication number: 20180267059Abstract: The invention features compositions and methods treating or preventing for age-related insulin resistance, type 2 diabetes and related disorders. The method involves depleting fTreg cells with an anti-ST2 antibody to decrease age-related fTreg accumulation and restore insulin sensitivity, thereby treating age-related insulin resistance, type 2 diabetes and related disorders.Type: ApplicationFiled: January 12, 2016Publication date: September 20, 2018Applicant: SALK INSTITUTE FOR BIOLOGICAL STUDIESInventors: SAGAR P. BAPAT, YE ZHENG, RONALD EVANS, MICHAEL DOWNES, ANNETTE R. ATKINS, RUTH T. YU
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Publication number: 20180228869Abstract: Methods of using FGF1 analogs, such as FGF1 mutant proteins having an N-terminal deletion, point mutation(s), or combinations thereof, to reduce blood glucose levels in subjects with steroid-induced diabetes, hypercortisolemia, or diabetes due to treatment with an antipsychotic agent, are provided. Such mutant FGF1 proteins can be part of a chimeric protein that includes a ?-Klotho-binding protein, an FGFR1-binding protein, a ?-Klotho-binding protein and a FGFR1-binding protein, a C-terminal region from FGF19 or FGF21.Type: ApplicationFiled: April 13, 2018Publication date: August 16, 2018Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu
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Publication number: 20180207114Abstract: Brown adipose tissue (BAT) plays a role in keeping an organism warm in response to a cold environment. In response to cold, transcription factors, including peroxisome proliferator receptor alpha (PGC1?), mediate the adaptive changes in the expression of oxidative and thermogenic genes in BAT. However, even without cold, BAT exhibits high expression of these genes relative to white adipose tissue (WAT). It is shown herein that estrogen related receptor gamma (ERR?) is a critical factor that controls the expression of key metabolic genes in BAT under basal conditions. ERR? is highly expressed in BAT versus WAT, yet is not transcriptionally induced by cold, suggesting it plays an important role in innate basal BAT function rather than in the adaptive response to cold. Based on these observations, methods of increasing thermogenesis in a subject by administering a therapeutically effective amount of one or more agents that increase ERR? activity are provided.Type: ApplicationFiled: March 21, 2018Publication date: July 26, 2018Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu, Maryam Ahmadian
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Publication number: 20180193418Abstract: The present disclosure provides FGF1 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Such mutant FGF1 proteins can be part of a chimeric protein that includes a ?-Klotho-binding protein, an FGFR1c-binding protein, a ?-Klotho-binding protein and a FGFR1c-binding protein, a C-terminal region from FGF19 or FGF21. In some examples, mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed molecules to reduce blood glucose levels are also provided.Type: ApplicationFiled: March 2, 2018Publication date: July 12, 2018Applicant: Salk Institute for Biological StudiesInventors: Jae Myoung Suh, Michael Downes, Ronald M. Evans, Annette Atkins, Ruth T. Yu
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Patent number: 9925241Abstract: The present disclosure provides FGF1 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Such mutant FGF1 proteins can be part of a chimeric protein that includes a ?-Klotho-binding protein, an FGFR1c-binding protein, a ?-Klotho-binding protein and a FGFR1c-binding protein, a C-terminal region from FGF19 or FGF21. In some examples, mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed molecules to reduce blood glucose levels are also provided.Type: GrantFiled: October 21, 2014Date of Patent: March 27, 2018Assignee: Salk Institute for Biological StudiesInventors: Jae Myoung Suh, Michael Downes, Ronald M. Evans, Annette Atkins, Ruth T. Yu
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Publication number: 20180057554Abstract: The present disclosure provides FGF1 mutant proteins, which include an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.Type: ApplicationFiled: October 16, 2017Publication date: March 1, 2018Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu
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Publication number: 20180044642Abstract: The invention generally features compositions comprising induced pluripotent stem cell progenitors (also termed reprogramming progenitor cells) and methods of isolating such cells. The invention also provides compositions comprising induced pluripotent stem cells (iPSCs) derived from such progenitor cells. Induced pluripotent stem cell progenitors generate iPSCs at high efficiency. In particular embodiments the invention is predicated upon increased expression of an estrogen related receptor and changes in the oxidative and glycolytic pathways.Type: ApplicationFiled: February 26, 2016Publication date: February 15, 2018Applicant: Salk Institute for Biological StudiesInventors: Ronald EVANS, Michael DOWNES, Yasuyuki KIDA, Teruhisa KAWAMURA, Zong WEI, Ruth T. YU, Annette R. ATKINS
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Publication number: 20180015057Abstract: Provided herein are methods and kits for increasing cardiac contraction, increasing mitochondrial activity, and/or increasing oxphos activity. Such methods include use of therapeutically effective amounts of one or more agents that increases estrogen-related receptor (ERR) ? activity and one or more agents that increases ERR? activity. In some examples, the method further includes administering a therapeutically effective amount of one or more agents that increases mitofusin 1 (Mfn1) activity.Type: ApplicationFiled: September 19, 2017Publication date: January 18, 2018Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Liming Pei, Michael Downes, Ruth T. Yu, Annette Atkins
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Publication number: 20180000768Abstract: Disclosed are embodiments of a method of treating or preventing latent autoimmune diabetes of adults (LADA) in a subject. Such embodiments include administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or farnesoid X receptor (FXR) agonist compounds, thereby activating FXR receptors in the intestines, and treating or preventing latent autoimmune diabetes of adults (LADA) in the subject.Type: ApplicationFiled: September 6, 2017Publication date: January 4, 2018Applicant: Salk Institute for Biological StudiesInventors: Sungsoon Fang, Eiji Yoshihara, Ruth T. Yu, Annette Atkins, Michael Downes, Ronald M. Evans
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Publication number: 20170355739Abstract: The present disclosure provides FGF1 mutant proteins having one or more mutations in the heparin binding domain. Such mutants may also have an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.Type: ApplicationFiled: August 21, 2017Publication date: December 14, 2017Applicants: Salk Institute for Biological Studies, The Florida State University Research Foundation, IncorporatedInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu, Michael Blaber, Xue Xia
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Publication number: 20170355740Abstract: The present disclosure provides FGF1 mutant proteins having one or more mutations in the heparin binding domain. Such mutants may also have an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.Type: ApplicationFiled: August 21, 2017Publication date: December 14, 2017Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Ruth T. Yu
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Publication number: 20170291931Abstract: The present disclosure provides FGF2 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Thus, the disclosed mutant FGF2 proteins can be used to treat one or more metabolic diseases. In some examples, mutant FGF2 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed molecules to reduce blood glucose levels, for example to treat a metabolic disorder are also provided.Type: ApplicationFiled: June 8, 2017Publication date: October 12, 2017Applicant: Salk Institute for Biological StudiesInventors: Ronald M. Evans, Michael Downes, Annette Atkins, Jae Myoung Suh, Ruth T. Yu
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Publication number: 20170189485Abstract: This application provides methods of increasing vascularization, muscle performance, muscle rehabilitation, and/or mitochondrial activity in subjects in need thereof, by administering a therapeutically effective amount of one or more agents that increases ERR? activity to the subject. Such agents can include one or more ERR? agonists. In some examples the method does not require that the subject exercise, and as such, the subject may be sedentary (such as bedridden or in a wheelchair).Type: ApplicationFiled: January 17, 2017Publication date: July 6, 2017Applicant: Salk Institute for Biological StudiesInventors: Vihang A. Narkar, Michael Downes, Ruth T. Yu, Ronald M. Evans