Phe-Met-Arg-Phe, amide

Research use only, not for human use.

Phe-Met-Arg-Phe, amide 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.

Phe-Met-Arg-Phe, amide 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 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. 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).(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.

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. 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).

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 FMR Famide (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.

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Cell Cycle/DNA Damage

Potassium Channel

ED50: 23 nM (K+ current)

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64190-70-1

598.76

C29H42N8O4S

>98% (HPLC)

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Sequence:Phe-Met-Arg-Phe-NH2

(-20℃)

With Ice Pack

≥ 2 years