MR 409, a selective growth hormone-releasing hormone (GHRH) agonist, exhibits notable neuroprotective properties by augmenting endogenous neurogenesis in cerebral ischemic mice and demonstrates the ability to inhibit in vivo lung cancer growth [1] [2] [3] [4].

One week after myocardial infarction (MI), MR 409 (MR-409) significantly diminishes plasma concentrations of IL-2, IL-6, IL-10, and TNF-α compared to placebo [1]. At a concentration of 1 μM, MR-409 attenuates p53 expression in bovine pulmonary arterial endothelial cells (BPAECs) and activates JAK2, STAT3, and ERK1/2 signaling pathways [2]. Furthermore, MR-409 (1 and 5 μM) reduces lipopolysaccharide (LPS)-induced PGE2 and 8-iso-PGF2α production in a dose-responsive manner, whereas it decreases LPS-induced lactate dehydrogenase (LDH) activity and nitrite levels independently of dose variation [3]. Similarly, gene expression of COX-2, NF-κB, and iNOS in colon specimens induced by LPS is mitigated by MR-409 at concentrations of 1 and 5 μM, again without showing dose-dependency [3]. Additionally, MR-409 stimulates endogenous neurogenesis and counteracts tMCAO-induced neuroplasticity deficits, along with promoting proliferation and reducing apoptosis in neural stem cells subjected to oxygen and glucose deprivation-reperfusion [4].

MR 409 (MR-409) suppresses lung cancer growth in vivo when xenografted into nude mice [3]. Additionally, when administered subcutaneously at a dose of 5 μg daily for four weeks, MR 409 diminishes the nociceptive response in mice [3].