One week post-myocardial infarction (MI), MR 409 (MR-409) significantly reduces plasma levels of IL-2, IL-6, IL-10 and TNF-α compared to placebo[1].
MR 409 (MR-409; 1 μM) suppresses p53 expression in bovine pulmonary arterial endothelial cells (BPAECs)[2].
MR 409 (1 μM) induces the activation of JAK2, STAT3 and ERK1/2[2].
MR 409 (MR-409; 1 and 5 μM) decreases LPS-induced PGE2 and 8-iso-PGF2α levels, in a dose-dependent manner[3].
MR 409 (1 and 5μM) decreases LPS-induced lactate dehydrogenase (LDH) activity and nitrite production, without showing a dose-dependent effect[3].
MR 409 (1 and 5 μM) decreases LPS-induced gene expression of COX-2, NF-κB and iNOS in colon specimens, without a dose-dependent effect[3].
MR 409 (MR-409) can stimulate endogenous neurogenesis and improve the tMCAO-induced loss of neuroplasticity. MR 409 also enhances the proliferation and inhibits apoptosis of neural stem cells treated with oxygen and glucose deprivation-reperfusion[4].
MR 409 (MR-409) inhibits the in vivo growth of lung cancer xenografted into nude mice[3].
MR 409 (5 μg; s.c. treated daily for 4 weeks) reduces nociceptive response in mice[3].
References:
[1]. Rosemeire M Kanashiro-Takeuchi, et al. New therapeutic approach to heart failure due to myocardial infarction based on targeting growth hormone-releasing hormone receptor. Oncotarget. 2015;6(12):9728-39.
[2]. Mohammad A Uddin, et al. GHRH antagonists support lung endothelial barrier function. Tissue Barriers. 2019;7(4):1669989.
[3]. Lucia Recinella, et al. Protective effects of growth hormone-releasing hormone analogs in DSS-induced colitis in mice. Sci Rep. 2021 Jan 28;11(1):2530.
[4]. Yueyang Liu, et al. Agonistic analog of growth hormone-releasing hormone promotes neurofunctional recovery and neural regeneration in ischemic stroke. Proc Natl Acad Sci U S A. 2021 Nov 23;118(47):e2109600118.