Phe-Met-Arg-Phe, amide acetate dose dependently (ED50=23 nM) activates a K+ current in the peptidergic caudodorsal neurons. This peptide appears to localize with neuropeptide Y in some regions of the brain.

In the molluscan central nervous system, Phe-Met-Arg-Phe, amide (FMRFa) acts on K+ channels in sensory, motor-, and neuroendocrine neurones. Phe-Met-Arg-Phe, amide activates a novel K+ current that is characterized by a combined voltage- and receptor-dependent gating mechanism, with both factors being necessary for opening of the channels[1]. Phe-Met-Arg-Phe, amide (1 μM) significantly inhibits glucose stimulated (300 mg/dL) insulin release (p<0.005) and somatostatin release (p<0.01) from the isolated perfused pancreas. Phe-Met-Arg-Phe, amide (FMRF-NH2) (1 and 10 μM) is without effect on glucagon secretion, either in low glucose (50 mg/dL), high glucose (300 mg/dL), or during arginine stimulation (5 mM)[2].

Phe-Met-Arg-Phe amide (FMRFamide) has been identified to stimulate growth hormone secretion in conscious ovariectomized (OVX) rats. Its immunoreactivity within hypothalamic neuronal elements hints at its involvement in regulating anterior pituitary functions. Administration of 200 ng (313.8 picomoles) of FMRFamide in a 2 uL volume significantly elevates plasma growth hormone (GH) levels within 15 minutes post-injection. Moreover, a dose range of 400-800 ng (627-1255 picomoles) of FMRFamide induces a rapid increase in GH levels, observable as early as 5 minutes and persisting for up to 30 minutes.