Phe-Met-Arg-Phe, amide

Phe-Met-Arg-Phe, amide dose dependently (ED₅₀=23 nM) activates a K⁺ current in the peptidergic caudodorsal neurons. Sequence: Phe-Met-Arg-Phe-NH2. IC50 & Target: ED50: 23 nM (K⁺ current)^[1] In Vitro: 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]. In Vivo: Phe-Met-Arg-Phe, amide (FMRFamide) stimulates growth hormone secretion in conscious OVX rats. The presence of Phe-Met-Arg-Phe, amide-like immunoreactivity in neuronal elements in the hypothalamus suggested a role for this in the hypothalamic control of the anterior pituitary function. The injection of 200 ng (313.8 picomoles) of FMRFamide (in 2 uL) produces a significantly increased plasma GH 15 min after injection. The GH-increasing effect of 400-800 ng (627-1255 picomoles) of FMRFamide is already developed after 5 min and lasted up to 30 min^[3].