Abstract: The disclosure is directed in non-limiting embodiments to compounds, compositions, and methods of treating conditions and diseases associated with activation of the gonadotropin GnRH receptor (GnRHR), particularly those involving GnRHR activating autoantibodies (GnRHR AAbs). In one non-limiting embodiment, the disease is Polycystic Ovary Syndrome (PCOS). The therapeutic compounds in at least certain embodiments include peptides which at least partially comprise D-amino acids, such as retro-inverso D-amino acid (RID) peptides, which are able to bind with high affinity to GnRHR AAbs.

Abstract: Compounds, compositions, and delivery devices, for treating and diagnosing conditions and diseases associated with activation of the gonadotropin releasing hormone receptor (GnRHR), particularly those involving GnRHR activating autoantibodies (GnRHR AAbs). In one non-limiting embodiment, the disease is Polycystic Ovary Syndrome (PCOS). The therapeutic compounds in at least certain non-limiting embodiments include peptides which comprise D-amino acids (D-amino acid peptides) which are able to bind with high affinity to GnRHR AAbs.

Abstract: The disclosure is directed in non-limiting embodiments to compounds, compositions, and methods of treating conditions and diseases associated with activation of the gonadotropin GnRH receptor (GnRHR), particularly those involving GnRHR activating autoantibodies (GnRHR AAbs). In one non-limiting embodiment, the disease is Polycystic Ovary Syndrome (PCOS). The therapeutic compounds in at least certain embodiments include peptides which at least partially comprise D-amino acids, such as retro-inverso D-amino acid (RID) peptides, which are able to bind with high affinity to GnRHR AAbs.

Abstract: Compositions are disclosed that include D-amino acid peptides and that are capable of specifically binding to at least one autoantibody against a G-protein coupled receptor. The autoantibody is produced in a patient having or being predisposed to a disease, condition, or disorder, and the autoantibody is capable of binding to a specific epitope of the G-protein coupled receptor. Methods of production and use of said compositions are also disclosed.

Abstract: Compositions are disclosed that include D-amino acid peptides and that are capable of specifically binding to at least one autoantibody against a G-protein coupled receptor. The autoantibody is produced in a patient having or being predisposed to a disease, condition, or disorder, and the autoantibody is capable of binding to a specific epitope of the G-protein coupled receptor. Methods of production and use of said compositions are also disclosed.

Abstract: Compositions are disclosed that include D-amino acid peptides and that are capable of specifically binding to at least one autoantibody against a G-protein coupled receptor. The autoantibody is produced in a patient having or being predisposed to a disease condition or disorder, and the autoantibody is capable of binding to a specific epitope of the G-protein coupled receptor. Methods of production and use of said compositions are also disclosed.

Abstract: Compositions are disclosed that include D-amino acid peptides and that are capable of specifically binding to at least one autoantibody against a G-protein coupled receptor. The autoantibody is produced in a patient having or being predisposed to a disease condition or disorder, and the autoantibody is capable of binding to a specific epitope of the G-protein coupled receptor. Methods of production and use of said compositions are also disclosed.

Abstract: Methods of preventing sustained monomorphic ventricular tachycardia following myocardial ischemia, decreasing infarct size and/or decreasing the incidence and/or maximum intrinsic rate of very rapid ventricular triplets following myocardial ischemia is disclosed. The methods involve administering an effective amount of a composition that inhibits substantial loss of beta-adrenergic receptor kinase (?-ARK) activity and/or ?-ARK expression.

Abstract: Methods of preventing sustained monomorphic ventricular tachycardia following myocardial ischemia, decreasing infarct size and/or decreasing the incidence and/or maximum intrinsic rate of very rapid ventricular triplets following myocardial ischemia is disclosed. The methods involve administering an effective amount of a composition that inhibits substantial loss of beta-adrenergic receptor kinase (?-ARK) activity and/or ?-ARK expression.