University of Michigan

Phrixus Pharmaceuticals, Inc.

Merck Sharp + Dohme Corp.

University of Minnesota

Indiana University

Msd Italia S.r.l.

Istituto Di Ricerche Di Biologia Molecolare P. Angeletti S.r.l.

Joseph M Metzger

Lorraine E Reeve

Bruce Edward Markham

Dewayne Townsend

Daniel E Michele

Soichiro Yasuda

Rainer Ng

Richard Dennis DiMarchi

Elisabetta Bianchi

Antonello Pessi

Alessia Santoprete

Paul E Carrington

Brian P Ward

Donald J Marsh

Paolo Ingallinella

George J Eiermann

Ranabir Sinha Roy

Gianluigi Veglia

Margaret Westfall

Sharlene Day

Elena Capito

Alessandro Pocai

Brian Raymond Thompson

Raffaello Verardi

Meng Jing

Michael T Bowser

Richard Dimarchi

Dan Michele

This disclosure describes, in one aspect, a composition that generally includes an xNA molecule comprising at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method of treating cardiac disease. Generally, the method includes administering to a subject a composition that includes an xNA molecule having at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function, and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method for evaluating the efficacy of treatment of cardiac disease. Generally, the method includes administering to a subject a composition that includes a first xNA molecule comprising a predetermined length in an amount effective to increase myocyte relaxation, then selecting a predetermined length of a second xNA molecule for at least one subsequent treatment. If treatment with the first xNA results in more myocyte relaxation than is desired, then the predetermined length of the second xNA molecule is shorter than the predetermined length of the first xNA. If, on the other hand, treatment with the first xNA results in less myocyte relaxation than is desired then the predetermined length of the second xNA molecule is longer than the predetermined length of the first xNA.

Therapeutic polynucleotides, compositions, and methods

Peptide analogs of oxyntomodulin (OXM, glucagon-37), which have been modified to be resistant to cleavage and inactivation by dipeptidyl peptidase IV (DPP-IV) and to increase in vivo half-life of the peptide analog while enabling the peptide analog to act as a dual GLP-1/glucagon receptor (GCGR) agonist are described. The peptide analogs are useful for treatment of metabolic disorders such as diabetes and obesity.

Oxyntomodulin analogs

The present invention relates to compositions and methods for treating and preventing skeletal muscle deficiencies. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing skeletal muscle deficiencies and injuries (e.g., dystrophin-deficient skeletal muscle; skeletal muscle having a contraction force deficit; skeletal muscle having a Caimbalance; skeletal muscle having microtears).

Compositions and methods for treating and preventing skeletal muscle deficiencies

The present invention relates to compositions and methods for treating and preventing heart disease. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing heart disease (e.g., in subjects with muscular dystrophy) and for treating cells and tissue damage caused by ischemia and cell death (e.g., for treating dystrophin-deficient cells (e.g., myocytes)).

Compositions and methods for treating and preventing cardiomyopathy and heart disease

The present invention relates to cardiac performance, in particular to regulating cardiac performance via recombinant troponin I (TnI) protein and nucleic acids encoding recombinant TnI. The present invention provides nucleic acids encoding gain of function TnI proteins (e.g., cTnlA164H), vectors containing such nucleic acids, host cells containing such vectors, transgenic animals carrying a gain of function TnI protein (e.g., a cTnlA164H transgene), and therapeutic agents (e.g., comprising recombinant TnI, TnI analogues, synthetic TnI, or the like) or agents for gene therapy of heart failure or disease for research and therapeutic uses.

Compositions and methods for regulating cardiac performance

The present invention relates to compositions and methods for treating and preventing heart disease. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188&#x2014;P188) and methods of using the same for treating and preventing heart disease (e.g., in subjects with muscular dystrophy) and for treating cells and tissue damage caused by ischemia and cell death (e.g., for treating dystrophin-deficient cells (e.g., myocytes)).

The present invention relates to the overexpression of a calcium binding protein in cardiac myocytes in vivo and in vitro, and in particular, to the correction of diastolic dysfunction. Expression of the calcium binding protein parvalbumin in cardiac myocytes results in an increase in the rate of relaxation of the cardiac myocyte, in vivo and in vitro. The parvalbumin is expressed from an adenovirus vector, adeno-associated virus vector, or gutted adenovirus vector. The transfected in vivo and in vitro cardiac myocytes are also useful in drug screens.

Correcting diastolic dysfunction in heart failure

Growing community of inventors

Ann Arbor, MI, United States of America

Joseph M Metzger