Abstract: The present disclosure is directed to a method of treating an inflammatory disorder, such as sarcoidosis, using a growth hormone-releasing hormone (GHRH) antagonist.

Abstract: The disclosure provides a method of treating sarcoidosis, the method comprising administering a GHRH antagonist to mammalian subject in need thereof.

Abstract: Described herein are compositions and methods for treating pulmonary fibrosis and cancer. The compositions include growth hormone releasing hormone peptides. The methods include reducing lung inflammation, lung scarring, reducing expression of T cell receptor complex genes as well as inhibiting tumor growth.

Abstract: Described herein are compositions and methods for treating pulmonary fibrosis and cancer. The compositions include growth hormone releasing hormone peptides. The methods include reducing lung inflammation, lung scarring, reducing expression of T cell receptor complex genes as well as inhibiting tumor growth.

Abstract: Disclosed herein are compositions of GHRH agonists and peptides, and methods to treat disorders, such as ischemia and reperfusion injury. In one embodiment, a method of treating a reperfusion injury in a subject in need may involve administering a therapeutically effective amount of at least one GHRH agonist peptide to the subject. In additional embodiment, a method of promoting vasculogenesis in a mammal may involve administering a therapeutically effective amount of at least one GHRH agonist peptide to the subject. In a further embodiment, a method of promoting differentiation of mesenchymal stem cells into endothelial cells may involve contacting mesenchymal stem cells with at least one GHRH agonist peptide.

Abstract: Disclosed herein are compositions of GHRH agonists and peptides, and methods to treat diabetes. In one embodiment, a method of promoting survival of grafted cells and/or tissues may involve exposing the cells and/or tissues to an effective amount of at least one agonist of GHRH. In some embodiments, the grafted cells and/or tissues may be pancreatic cells. In some embodiments, the grafted cells may be islet cells co-cultured with non-pancreatic cells. In a further embodiment, a method of treating a patient diagnosed with diabetes involves transplanting and/or grafting the islet cells and/or tissues comprising islet cells into a patient, and administering a therapeutically effective amount of at least one agonist of GHRH to the patient. In some embodiments, the islet cells and/or tissues comprising islet cells may be optionally exposed to GHRH and/or at least one agonist of GHRH prior to transplantation into a patient.

Abstract: There is provided a novel series of synthetic analogs of hGH-RH(1-29)NH2 (SEQ ID NO: 1) and hGH-RH(1-30)NH2. Of particular interest are those carrying PhAc, N-Me-Aib, Dca, Ac-Ada, Fer, Ac-Amc, Me-NH-Sub, PhAc-Ada, Ac-Ada-D-Phe, Ac-Ada-Phe, Dca-Ada, Dca-Amc, Nac-Ada, Ada-Ada, or CH3—(CH2)10—CO-Ada, at the N-Terminus and ?-Ala, Amc, Apa, Ada, AE2A, AE4P, ?-Lys(?-NH2), Agm, Lys(Oct) or Ahx, at the C-terminus. These analogs inhibit the release of growth hormone from the pituitary in mammals as well as inhibit the proliferation of human cancers, and inhibit the hyperplastic and benign proliferative disorders of various organs, through a direct effect on the cancerous and non-malignant cells. The stronger inhibitory potencies of the new analogs, as compared to previously described ones, result from replacement of various amino acids.

Abstract: There is provided a novel series of synthetic analogs of hGH-RH(1-29)NH2 (SEQ ID NO: 1) and hGH-RH(1-30)NH2. Of particular interest are those carrying PhAc, N-Me-Aib, Dca, Ac-Ada, Fer, Ac-Amc, Me-NH-Sub, PhAc-Ada, Ac-Ada-D-Phe, Ac-Ada-Phe, Dca-Ada, Dca-Amc, Nac-Ada, Ada-Ada, or CH3—(CH2)10—CO-Ada, at the N-Terminus and ?-Ala, Amc, Apa, Ada, AE2A, AE4P, ?-Lys(?-NH2), Agm, Lys(Oct) or Ahx, at the C-terminus. These analogs inhibit the release of growth hormone from the pituitary in mammals as well as inhibit the proliferation of human cancers, and inhibit the hyperplastic and benign proliferative disorders of various organs, through a direct effect on the cancerous and non-malignant cells. The stronger inhibitory potencies of the new analogs, as compared to previously described ones, result from replacement of various amino acids.

Abstract: There are provided a novel series of peptide analogs of hGH-RH(1-29)NH2 and hGH-RH(1-30)NH2 which show high activities in stimulating the release of pituitary GH in animals. They retain their physiological activity in solution for extended periods of time and resist enzymic degradation in the body. These novel and useful properties appear to be due to novel substitution patterns ant at the 1, 15, 27 and 29 positions on the peptide.

Abstract: There are provided a novel series of peptide analogs of hGH-RH(1-29)NH2 and hGH-RH(1-30)NH2 which show high activities in stimulating the release of pituitary GH in animals. They retain their physiological activity in solution for extended periods of time and resist enzymic degradation in the body. These novel and useful properties appear to be due to novel substitution patterns ant at the 1, 15, 27 and 29 positions on the peptide.

Abstract: Embodiments of the present disclosure are directed to methods to treat a subject having cancer. In one embodiment, a method of treating a subject with cancer may comprise administering a therapeutically effective amount of at least one GHRH agonist peptide in combination with at least one anticancer agent. In another embodiment, a method of killing cancer cells may comprise contacting the cancer cells with a composition comprising at least one GHRH agonist peptide and at least one anticancer agent. In some embodiments, the method may be in vitro or in vivo. In an additional embodiment, a method of killing cancer stem cells may comprise contacting the cancer stem cells with a composition comprising at least one GHRH agonist peptide and at least one anticancer agent.

Abstract: Disclosed herein are compositions of GHRH peptide antagonists, and methods to treat Alzheimer's disease and other neurodegenerative disorders. Such compounds are useful for therapeutics, for protecting neuronal cells from cell-death and for promoting neuronal cell viability.

Abstract: Agonists of growth hormone releasing hormone promote islet graft growth and proliferation in patients. Methods of treating patients comprise the use of these agonists.

Abstract: There is provided a novel series of synthetic analogs of hGH-RH(1-29)NH2 (SEQ ID NO: 1) and hGH-RH(1-30)NH2. Of particular interest are those carrying PhAc, N-Me-Aib, Dca, Ac-Ada, Fer, Ac-Amc, Me-NH-Sub, PhAc-Ada, Ac-Ada-D-Phe, Ac-Ada-Phe, Dca-Ada, Dca-Amc, Nac-Ada, Ada-Ada, or CH3—(CH2)10—CO-Ada, at the N-Terminus and ?-Ala, Amc, Apa, Ada, AE2A, AE4P, ?-Lys(?-NH2), Agm, Lys(Oct) or Ahx, at the C-terminus. These analogs inhibit the release of growth hormone from the pituitary in mammals as well as inhibit the proliferation of human cancers, and inhibit the hyperplastic and benign proliferative disorders of various organs, through a direct effect on the cancerous and non-malignant cells. The stronger inhibitory potencies of the new analogs, as compared to previously described ones, result from replacement of various amino acids.

Abstract: Disclosed herein are compositions of GHRH agonists and peptides, and methods to treat diabetes. In one embodiment, a method of promoting survival of grafted cells and/or tissues may involve exposing the cells and/or tissues to an effective amount of at least one agonist of GHRH. In some embodiments, the grafted cells and/or tissues may be pancreatic cells. In some embodiments, the grafted cells may be islet cells co-cultured with non-pancreatic cells. In a further embodiment, a method of treating a patient diagnosed with diabetes involves transplanting and/or grafting the islet cells and/or tissues comprising islet cells into a patient, and administering a therapeutically effective amount of at least one agonist of GHRH to the patient. In some embodiments, the islet cells and/or tissues comprising islet cells may be optionally exposed to GHRH and/or at least one agonist of GHRH prior to transplantation into a patient.

Abstract: Disclosed herein are compositions of GHRH agonists and peptides, and methods to treat disorders, such as ischemia and reperfusion injury. In one embodiment, a method of treating a reperfusion injury in a subject in need may involve administering a therapeutically effective amount of at least one GHRH agonist peptide to the subject. In additional embodiment, a method of promoting vasculogenesis in a mammal may involve administering a therapeutically effective amount of at least one GHRH agonist peptide to the subject. In a further embodiment, a method of promoting differentiation of mesenchymal stem cells into endothelial cells may involve contacting mesenchymal stem cells with at least one GHRH agonist peptide.

Abstract: There is provided a novel series of synthetic analogs of hGH-RH(1-29)NH2 (SEQ ID NO: 1) and hGH-RH(1-30)NH2. Of particular interest are those carrying PhAc, N-Me-Aib, Dca, Ac-Ada, Fer, Ac-Amc, Me-NH-Sub, PhAc-Ada, Ac-Ada-D-Phe, Ac-Ada-Phe, Dca-Ada, Dca-Amc, Nac-Ada, Ada-Ada, or CH3—(CH2)10—CO-Ada, at the N-Terminus and ?-Ala, Amc, Apa, Ada, AE2A, AE4P, ?-Lys(?-NH2), Agm, Lys(Oct) or Ahx, at the C-terminus. These analogs inhibit the release of growth hormone from the pituitary in mammals as well as inhibit the proliferation of human cancers, and inhibit the hyperplastic and benign proliferative disorders of various organs, through a direct effect on the cancerous and non-malignant cells. The stronger inhibitory potencies of the new analogs, as compared to previously described ones, result from replacement of various amino acids.

Abstract: Disclosed herein are methods demonstrating that growth-hormone releasing hormone (GHRH) directly activates cellular reparative mechanisms within the injured heart, in a GH/IGF-I independent fashion. Following experimental myocardial infarction (MI), rats were randomly assigned to receive, during a 4 week period, either placebo (n=14), rat recombinant GH (rrGH, n=8) or JI-38 (n=8; 50 ?g/Kg/day), a potent GHRH-agonist. JI-38 did not elevate serum levels of GH or IGF-I, but markedly attenuated the degree of cardiac functional decline and remodeling after injury. In contrast, GH administration markedly elevated body weight, heart weight, circulating GH and IGF-I, but did not offset the decline in cardiac structure and function. Whereas, both JI-38 and GH augmented levels of cardiac precursor cell proliferation, only JI-38 increased anti-apoptotic gene expression. Collectively, these findings demonstrate that within the heart, GHRH-agonists can activate cardiac repair following MI.

Abstract: There are provided a novel series of peptide analogs of hGH-RH(1-29)NH2 and hGH-RH(1-30)NH2 which show high activities in stimulating the release of pituitary GH in animals. They retain their physiological activity in solution for extended periods of time and resist enzymic degradation in the body. These novel and useful properties appear to be due to novel substitution patterns ant at the 1, 15, 27 and 29 positions on the peptide.

Abstract: There is provided a novel series of synthetic analogs of hGH-RH(1-29)NH2 (SEQ ID NO: 96) and hGH-RH(1-30)NH2. Of particular interest are those carrying PhAc, N-Me-Aib, Dca, Ac-Ada, Fer, Ac-Amc, Me-NH-Sub, PhAc-Ada, Ac-Ada-D-Phe, Ac-Ada-Phe, Dca-Ada, Dca-Amc, Nac-Ada, Ada-Ada, or CH3—(CH2)10—CO-Ada, at the N-Terminus and ?-Ala, Amc, Apa, Ada, AE2A, AE4P, ?-Lys(?-NH2), Agm, Lys(Oct) or Ahx, at the C-terminus. These analogs inhibit the release of growth hormone from the pituitary in mammals as well as inhibit the proliferation of human cancers, and inhibit the hyperplastic and benign proliferative disorders of various organs, through a direct effect on the cancerous and non-malignant cells. The stronger inhibitory potencies of the new analogs, as compared to previously described ones, result from replacement of various amino acids.