The Administrators of the Tulane Educational Fund

The United States Government As Represented by the Department of Veterans Affairs

University of Miami

Other

Dresden University of Technology

Augusta University Research Institute, Inc.

Debiopharm S.a.

Andrew V Schally

Marta Zarandi

Ren Zhi Cai

Jozsef L Varga

David H Coy

Sandor Bajusz

Norman L Block

Joshua Hare

Stefan Bornstein

Tamas Janaky

Attila A Nagy

Samirah Gomes

Ren-Zhi Cai

Barbara Ludwig

Renzhi Cai

Rosemeire M Kanashiro-Takeuchi

Thomas R Tice

Piero Orsolini

Rudolf Lucas

Attila Juhasz

Robert M Jackson

Jozsef Gulyas

Neal Weintraub

Atilla Juhasz

Jan Izdebski

Katalin Toth

Chester A Meyers

Mehdi Mirsaeidi

Maritza Romero-Lucas

Rosemeire Miyuki Kanashiro Takeuchi

Chongxu Zhang

Zarandi Marta

Cai Renzhi

Samirah A Gomes

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

GHRH antagonists for use in a method of treating sarcoidosis

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.

Treating inflammatory lung disease

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.

GHRH agonists for the treatment of ischemic disorders

Described herein are materials and methods for treating dyslipidemia in a mammalian subject in need thereof comprising administering a growth hormone-releasing hormone (GHRH) antagonist or variant thereof to the subject.

Materials and methods of treating dyslipidemia

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. In some embodiments, the at least one agonist of GHRH is administered pre-transplantation, concurrently with transplantation, post-transplantation or any combinations thereof.

GHRH agonists for islet cell transplantation and function and the treatment of diabetes

There is provided a novel series of synthetic analogs of hGH-RH(1-29)NH(SEQ ID NO: 1) and hGH-RH(1-30)NH. 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 CH&#x2014;(CH)&#x2014;CO-Ada, at the N-Terminus and &#x3b2;-Ala, Amc, Apa, Ada, AEA, AEP, &#x3b5;-Lys(&#x3b1;-NH), 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.

N- and C-terminal substituted antagonistic analogs of GH-RH

There are provided a novel series of peptide analogs of hGH-RH(1-29)NHand hGH-RH(1-30)NHwhich 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.

GH-RH analogs with potent agonistic effects

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

Agonists of growth hormone releasing hormone as effectors for survival and proliferation of pancreatic islets

N- and C- terminal substituted antagonistic analogs of GH-RH

Whether the growth hormone (GH)/Insulin-like growth factor 1(IGF-I) axis exerts cardioprotective effects remains controversial; and the underlying mechanism(s) for such actions are unclear. Here we tested the hypothesis 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 &#x3bc;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. The receptor for GHRH was detectable on myocytes supporting direct activation of cardiac signal transduction. Collectively, these findings demonstrate that within the heart GHRH-agonists can activate cardiac repair following MI, suggesting the existence of a potential signaling pathway based on GHRH in the heart. The phenotypic profile of the response to a potent GHRH agonist has therapeutic implications.

Cardioprotective effects of GHRH agonists

Novel fluorinated synthetic analogs of hGH-RH(1-30)NHthat inhibit the release of growth hormone from the pituitary in mammals as well as inhibit the proliferation of human cancers through a direct effect on the cancer cells, and to therapeutic compositions containing these novel peptides and their use.

Fluorinated GHRH antagonists

There is provided a novel series of synthetic antagonistic analogs of hGH-RH(1-29)NH. These analogs inhibit the activity of endogenous hGH-RH on the pituitary GH-RH receptors, and therefore prevent the release of growth hormone. The analogs also inhibit the proliferation of human cancers through a direct effect on the cancer cells. The higher inhibitory potencies of the new analogs, as compared to previously described ones, results from replacement of various amino acids.

Antagonistic analogs of GH RH (2003)

There is provided a novel series of synthetic analogs of hGH-RH(1&#x2013;29)NH. These analogs inhibit the activity of endogenous hGH-RH, and therefore prevent the release of growth hormone. The stronger inhibitory potencies of the new analogs, as compared to previously described ones, results from replacement of various amino acids.

Antagonistic analogs of GH-RH inhibiting IGF-I and -II

Growing community of inventors

Metairie, LA, United States of America

Andrew V Schally