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Sermorelin

GHRH (1-29), GRF 1-29 NH2, Sermorelin acetate

Quick Stats
Studies 223
Trials 41
Score 1
2005 pubmed

Effective treatment of experimental human non-Hodgkin's lymphomas with antagonists of growth hormone-releasing hormone.

Keller. Gunhild G; Schally. Andrew V AV; Groot. Kate K; Toller. Gabor L GL; Havt. Alexandre A; Köster. Frank F; Armatis. Patricia P; Halmos. Gabor G; Zarandi. Marta M; Varga. Jozsef L JL; Engel. Jörg B JB

Key Findings

  • GHRH antagonists MZ-5-156 and MZ-J-7-138 cut tumor growth by roughly 60‑74% in mouse models of human NHL
  • Treated mice showed lower serum IGF‑1 levels and reduced tumor bFGF, while VEGF was unchanged
  • Both lymphoma cell lines expressed GHRH and its receptor, indicating a direct drug target

Practical Outcomes

  • This research points to a possible new way to treat certain lymphomas, but it’s far from ready for self‑experimentation or clinical use. Biohackers should not try these antagonists now; more human trials are needed to confirm safety and effectiveness.

Summary

In a mouse study, drugs that block the hormone that normally tells the body to release growth hormone (called GHRH antagonists) slowed the growth of two types of human lymphoma tumors by about 60‑74%. The treatment also lowered a growth‑promoting protein (IGF‑1) in the blood and reduced another factor (bFGF) inside the tumors, but didn’t affect VEGF. These findings are early‑stage and done in animals, so they don’t translate into a usable protocol for people right now.

Abstract

Antagonists of growth hormone-releasing hormone (GHRH) were shown to inhibit the growth of various cancers. We investigated the antitumor activity and the mechanism of action of GHRH antagonists in human non-Hodgkin's lymphomas (NHL). Nude mice bearing xenografts of RL and HT human NHL were treated with GHRH antagonists MZ-5-156 and MZ-J-7-138 at a dose of 40 microg twice daily. The concentrations of serum IGF-1 and GHRH, bFGF, and VEGF in tumor tissue were measured by radioimmunoassays. Expression of GHRH and splice variant 1 of the GHRH receptor in both cell lines was examined by RT-PCR. The effects of MZ-5-156, MZ-J-7-138 and GHRH on cell proliferation were evaluated in vitro. Treatment with MZ-5-156 and MZ-J-7-138 significantly (P < 0.05) inhibited the growth of RL and HT tumors by 59.9-73.9%. High-affinity binding sites for GHRH and mRNA for GHRH and splice variant-1 of the GHRH receptors were found on RL and HT tumors. RL and HT cells contained GHRH peptide, and their growth in vitro was significantly inhibited by both antagonists. IGF-I levels in serum of mice were significantly decreased by antagonist MZ-5-156. Therapy with GHRH antagonists also significantly reduced tumoral bFGF, whereas VEGF levels were not suppressed. Our findings suggest that GHRH antagonists inhibit the growth of RL and HT lymphomas by direct effects mediated by tumoral receptors for GHRH. GHRH antagonists could offer a new therapeutic modality for the management of advanced NHL.

Study Information

Provider

pubmed

Year

2005

Date

2005-07-18T00:00:00.000Z

DOI

10.1073/pnas.0504102102