64190-70-1

Usage

Uses

Used in Pharmaceutical Industry:
FMRFamide is used as a pharmaceutical agent for its cardioacceleratory effects. It has been shown to increase heart rate and contractility in various species, making it a potential treatment for conditions such as heart failure.
Used in Research:
FMRFamide is also used as a research tool in the study of various biological processes. It has been used to investigate the role of neuropeptides in the nervous system, as well as to explore the mechanisms of pain and inflammation.
Used in Neuropeptide Research:
FMRFamide is used as a neuropeptide in research to understand its role in the nervous system. It has been found to have a variety of functions, including the modulation of neurotransmitter release and the regulation of feeding behavior.
Used in Drug Development:
FMRFamide is used in drug development as a potential therapeutic agent for a variety of conditions. Its diverse biological activities make it a promising candidate for the development of new drugs to treat a range of diseases, including cardiovascular disorders and neurological conditions.

Biological functions

Target cells and function The predominant effect of FaRPs is the reduction of spontaneous muscle contractions, such as in the intestinal muscle and the heart rate. Among FaRP subtypes, some FaRPs function in gut contraction and other subtypes do not.?Physiological discrimination according to different?subtype of FaRPs results in extensive functions.For example, FaRPs exert acceleratory effects on the heart rate, inhibitory effects on gut motility, and modulate synaptic activity. Furthermore, sequential ecdysis behavior is also regulated by FaRPs, consequently activating the downstream of the eclosion hormone (EH) and ecdysistriggering hormone (ETH).During ecdysis, FaRP-expressing Tv neurons are activated by ETH.

Synthesis

Gene, mRNA, and precursor D. melanogaster FMRFa mRNA produces a deduced prepropeptide composed of 347 aa. The prepropeptide is composed of a signal sequence, and 10 copies of FMRFa and extended FaRPs. The mature peptides are processed proteolytically and amidated at each C-terminal of the peptides.

InChI:InChI=1/C29H42N8O4S/c1-42-16-14-23(35-26(39)21(30)17-19-9-4-2-5-10-19)28(41)36-22(13-8-15-34-29(32)33)27(40)37-24(25(31)38)18-20-11-6-3-7-12-20/h2-7,9-12,21-24H,8,13-18,30H2,1H3,(H2,31,38)(H,35,39)(H,36,41)(H,37,40)(H4,32,33,34)/t21-,22-,23-,24-/m0/s1

Upstream product

• 5241-58-7 L-Phenylalanine amide 
• 123197-18-2 H-Phe-Met-Arg-OH 
• 123197-28-4 Boc-Phe-Met-Arg(Mts)-Phe-NH₂ 
• 85642-22-4 N-benzoxycarbonyl-L-phenylalanyl-L-methionyl-N-^γ-nitro-L-arginyl-L-phenylalaninamide 
• 2488-15-5 N-tert-butoxycarbonyl-L-methionine 
• 13734-34-4 N-tert-butoxycarbonyl-L-phenylalanine 
• 13726-76-6 t-butyloxycarbonyl-L-arginine 
• 2188-18-3 Boc-Arg(NO₂)-OH 
• 85642-21-3 N^α-tert-butoxycarbonyl-N^γ-nitro-L-arginyl-L-phenylalaninamide 
• 85651-85-0 N-tert-butoxycarbonyl-L-methionyl-N^γ-nitro-L-arginyl-L-phenylalaninamide 
• 58810-06-3 H-Arg(Mts)-OH 
• 123197-27-3 Boc-Phe-Met-Arg(Mts)-OH 
• 123197-26-2 Boc-Met-Arg(Mts)-OH 
• 16948-13-3 Boc-Met-OTcp 

Relevant academic research and scientific papers

Novel Modified Carboxy Terminal Fragments of Neutropeptide Y with High Affinity for Y2-Type Receptors and Potent Functional Antagonism at a Y1-Type Receptor

Peptide analogs of neuropeptide Y (NPY) with a Tyr-32 and Leu-34 replacement resulted in the decapeptide TyrIleAsnLeuIleTyrArgLeuArgTyr-NH2 (9; Table 1) and a 3700-fold improvement in affinity at Y2 (rat brain; IC50 = 8.2 +/- 3 nM) receptors when compared to the native NPY(27-36) C-terminal fragment.In addition, compound 9 was an agonist at Y1 (human erythroleukemia (HEL) cell; ED50 = 8.8 +/- 0.5 nM) receptors with potency comparable to that of NPY(1-36) (ED50 = 5 nM).Molecular dynamics and 1H-NMR were used to propose a solution structure of decapeptide 9 and for subsequent analog design.The replacement of Leu with Pro at position 4 of decapeptide 9 afforded an antagonist of NPY in HEL cells (18, TyrIleAsnProIleTyrArgLeuArgTyr-NH2; IC50 = 100 +/- 5 nM).Deletion of the N-terminal tyrosine of 18 resulted in a 10-fold improvement in antagonistic activity with a parallel 4-fold decrease in Y2 affinity.This potent antagonist may provide further insight into the physiological role(s) for NPY in the mammalian and peripheral nervous system.