Anti-Neuropeptide FF Receptor 1 (extracellular) Antibody

Neuropeptide FF receptor 1, NPFFR1, also known as GPR147 and RFamide-related peptide receptor 0T7T022, is a Gi/o protein-coupled receptor that mainly couples to Gα_i3 and Gα_s proteins and binds NPFF and RF-amide related peptides that are characterized by a conserved C-terminal RF-amide motif.^1,2

NPFF has been identified in various species, including humans, rodents, bovines, and guinea pigs, indicating its physiological significance. NPFF has been detected in discrete areas of the rat central nervous system (CNS), with the highest levels observed in the dorsal spinal cord and the posterior lobe of the pituitary gland.  The distribution of NPFF mRNA at the tissue level generally corresponds with NPFF immunoreactivity, except in the hypothalamic region where differences have been observed. The NPFF gene was found to be upregulated in the dorsal horn by inflammatory pain.¹ 

NPFFR1 is expressed at a higher level than NPFFR2 in the human CNS, while NPFFR2 is more abundant than NPFFR1 in the rat brain. NPFFR1 mRNA is more abundant than NPFFR2 in the human spinal cord, whereas only NPFFR2 is found in the spinal cord of rats.¹

NPFFR1 displayed a sex-biased role in food intake and metabolic homeostasis. NPFFR1 knockout male mice demonstrated reduced spontaneous food intake and suppressed leptin- and ghrelin-induced feeding. In contrast, food intake was unaltered in NPFFR1 knockout female mice. Ablation of NPFFR1 did not cause any overt alterations in body weight of male mice but increased body weight in female mice associated with increased fat mass. NPFFR1 ablation worsened glucose tolerance and insulin sensitivity caused by a high fat diet in male but not in female mice.¹

NPFF has been widely recognized as an endogenous peptide that modulates the effects of opioids, with its ability to either block or potentiate morphine-induced analgesia depending on the site of administration. The increased presence of NPFF in the central nervous system (CNS) has been implicated in the development of opioid tolerance and dependence. Pharmacological blockade of NPFFR1/2 prevented the development of opioid-induced hyperalgesia and analgesic tolerance. Furthermore, the NPFF system has been shown to play a crucial role in modulating the effects of other drugs of abuse, as well as various physiological processes such as neuroendocrine and cardiovascular functions and energy homeostasis, including insulin release, food intake, memory, blood pressure, electrolyte balance, and neural regeneration. Consequently, the NPFF system has gained significant attention as a promising target for therapeutic interventions.^1,3