This library is being continuously updated to include all new and current peptides including Peptide 34 (GPR54) ,Fertilization promoting peptide (TCP11), Head Activator Neuropeptide (GPR37), Obestatin( GPR39), Neuromedin S, Neuropeptide S, QRFP-43,PBAN, P518, NPB & NPW, INSL 3 & 7, Endokinin A/B, AF9, BK), receptors (FM-4/TGR-1, NPSR, GPR100, GPR135, GPR142, GPR103, GPR7 & 8, LGR7 & 8, CG6986, NPR-1, PBAN-R) and references.
Please contact us to get an updated peptide list!

Library Format : Packaged in 96 well plates 1.5 nanomoles of peptide in 15 micrograms BSA

Want To Discover New Orphan Receptors? Try Phoenix's G Protein-Coupled Receptor Peptide Ligand Library

More than 50 families of identified or suspected G Protein Coupled Receptor Peptide Ligands plus its related agonists and antagonists enable a "reverse pharmacology approach" for large scale screening. Now over Eight Hunderd Peptides Orphan G Protein Coupled Receptors are included which are HPLC-purified and fluorescein free. This library covers various newly identified G Protein Coupled Receptor Ligands including new Obestatin (GPR39), RF-amide related peptide QRFP-43, QRFP-26/P518 (GPR103/SP9155/AQ27), Gln-Alltostatin C(CG7285 & CG13702), Proctolin (CG6986), Endokinin A/B (NK1), Adipokinetic hormone (ADHR), CCAP (CG6111), PBAN (PBAN-R), H3 Relaxin (LGR7 & 8), NPB and NPW (GPR7 & GPR8), Icilin (CMR-1), Neuropeptide F (DmNPFR1), RFamide Related Peptides (OT7T022), Neuromedin U (NmU R-1/FM-3 and NmU R-2/FM-4), human Urotensin II (GPR14), Neuropeptide AF/FF(NPFF-1 and NPFF-2), Ghrelin(GHS-Rs), Motilin(GPR-38-A), MCH(SLC-1, MCH-R2), Orexins and Hypocretins (HFGAN-72), Prolactin Releasing Peptide (HGR-3/GPR-10/UHR-1), Orphanin FQ (ORL-1) and Apelin(APJ), NEP 1-40(Nogo-66 receptor)
Contact us to get an updated peptide list!

Potential GPCR dimer interfaces. Contact dimers, in which the interface between GPCR monomers involves surface contact between helices of two independent monomers (indicated by color), and domain-swapped dimers, in which helices 6 and 7 are exchanged or "swapped" between GPCR monomers (indicated by color), are illustrated, viewed at the cytoplasmic face of the membrane. Note the origins and locations of the intracellular loops (i1 loop, blue; i2 loop, black; i3 loop, red) contributing to the putative G protein binding surface in the two models.
Breitwieser G.E. Circulation Research. 2004;94:17

Receptor-mediated G protein activation. The interaction of an endogenous ligand with its cell surface receptor (R) facilitates the coupling of the activate receptor (R*) with intracellular heterotrimeric G proteins. The R*-G protein coupling promotes the exchange of GDP for GTP on the G-subunit. G-GTP then dissociates from Gß and R*. Both subunits are free to modulate the activity of a wide variety of intracellular effectors. Termination of the signal occurs when the -phosphate of GTP is removed by the intrinsic GTPase activity of the G-subunit, leaving GDP in the nucleotide binding pocket on G. G-GDP then reassociates with Gß and the cycle is complete. RGS proteins accelerate the intrinsic GTPase activity of G-subunits, thereby reducing the duration of signaling events.
Cabrera-Vera T. M., et al. Endocrine Reviews 2003, 24 (6): 765-781

NAB1 negatively regulates pathologic cardiac hypertrophy. Hypertrophic stimuli (such as isoproterenol-phenylephrine or myocardial pressure overload) induce Egr-1 expression, which in turn can activate pathologic cardiac hypertrophy. These hypertrophic stimuli also increase NAB1, which interacts with Egr-1 through its R1 domain, thereby reducing left ventricular hypertrophy and potentially cardiac failure. RV, right ventricle; LV, left ventricle.
Levon M Khachigian. Nature Medicine 11, 828 - 829 (2005)

Sarah M. Assmann. G Proteins Go Green: A Plant G Protein Signaling FAQ Sheet. Science, Vol 310, Issue 5745, 71-73 , 7 October 2005

Limited G Protein-Coupled Receptor Peptide list: Click to send E-mail request.