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Sermorelin

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

Quick Stats
Studies 223
Trials 41
2024 pubmed 2 citations

Exploring the role of GHRH antagonist MIA-602 in overcoming Doxorubicin-resistance in acute myeloid leukemia.

Gaumond. Simonetta I SI; Abdin. Rama R; Costoya. Joel J; Schally. Andrew V AV; Jimenez. Joaquin J JJ

Key Findings

  • MIA-602 significantly reduced viability of wild‑type AML cell lines in vitro.
  • Doxorubicin‑resistant AML clones were equally sensitive to MIA-602.
  • In mice implanted with doxorubicin‑resistant K‑562 cells, MIA-602 treatment lowered tumor volume compared to control.

Practical Outcomes

  • The findings are specific to a cancer‑type drug and do not provide actionable guidance for everyday health optimization, dosing, or safety in healthy individuals. There is no protocol or recommendation for using GHRH antagonists like MIA-602 outside of a clinical oncology setting.

Summary

The study tested a drug called MIA-602, which blocks growth‑hormone‑releasing hormone receptors, and found it can kill certain leukemia cells in the lab and shrink tumors in mice, even when those cells are resistant to the chemotherapy drug doxorubicin. This research is focused on cancer treatment, not on improving longevity, metabolism, or performance for healthy people.

Abstract

Acute myeloid leukemia (AML) is characterized by the rapid proliferation of mutagenic hematopoietic progenitors in the bone marrow. Conventional therapies include chemotherapy and bone marrow stem cell transplantation; however, they are often associated with poor prognosis. Notably, growth hormone-releasing hormone (GHRH) receptor antagonist MIA-602 has been shown to impede the growth of various human cancer cell lines, including AML. This investigation examined the impact of MIA-602 as monotherapy and in combination with Doxorubicin on three Doxorubicin-resistant AML cell lines, KG-1A, U-937, and K-562. The <i>in vitro</i> results revealed a significant reduction in cell viability for all treated wild-type cells. Doxorubicin-resistant clones were similarly susceptible to MIA-602 as the wild-type counterpart. Our <i>in vivo</i> experiment of xenografted nude mice with Doxorubicin-resistant K-562 revealed a reduction in tumor volume with MIA-602 treatment compared to control. Our study demonstrates that these three AML cell lines, and their Doxorubicin-resistant clones, are susceptible to GHRH antagonist MIA-602.

Study Information

Provider

pubmed

Year

2024

Date

2024-04-08T00:00:00.000Z

DOI

10.18632/oncotarget.28579

Citations

2

References

19