SLIGRL-NH2|CAS 171436-38-7

Cas No.:	171436-38-7
Chemical Name:	SLIGRL-NH2
Synonyms:	L-Leucinamide,L-seryl-L-leucyl-L-isoleucylglycyl-L-arginyl-;SLIGRL-NH2;PAR-2 (1-6) amide (mouse, rat);SER-LEU-ILE-GLY-ARG-LEU-NH2;SLIGRL-NH2;H2N-SLIGRL-AMIDE;H-SER-LEU-ILE-GLY-ARG-LEU-NH2;PAR2-AP;REF DUPL: H-Ser-Leu-Ile-Gly-Arg-Leu-NH2;SER-LEU-ILE-GLY-ARG-LEU-AMIDE;SLIGRLAMIDE;PAR2-AP, SLIGRL-NH2;CHEMBL238078;Ser-Leu-Ile-Gly-Arg-Leu-NH(2);CS-0029354;AKOS040763878;CAS_171436-38-7;PAR-2 (1-6) amide (mouse, rat) trifluoroacetate salt, >=97% (HPLC);PAR-2 Activating Peptide;Ser-Leu-Ile-Gly-Arg-Leu-NH2;SL-NH2;BDBM85517;BDBM50477070;seryl-leucyl-isoleucyl-glycyl--arginyl-leucinamide;HB2920;AS-82543;AKOS024456619;171436-38-7;C29H56N10O7;HY-P1308;Ser-Leu-Ile-Gly-Arg-Leu-amide;(2S,3S)-2-[[(2S)-2-[[(2S)-2-amino-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-N-[2-[[(2S)-1-[[(2S)-1-amino-4-methyl-1-oxopentan-2-yl]amino]-5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-2-oxoethyl]-3-methylpentanamide;SLIGRL (modifications: C-terminal amide);PAR-2 activation peptide;PAR-2 (1-6) AMIDE (MOUSE, RAT)
SMILES:	CC[C@@H]([C@H](NC([C@@H](NC([C@@H](N)CO)=O)CC(C)C)=O)C(NCC(N[C@H](C(N[C@H](C(N)=O)CC(C)C)=O)CCCNC(N)=N)=O)=O)C
Formula:	C₂₉H₅₆N₁₀O₇
M.Wt:	656.81774
Purity:	>98%
Sotrage:	2 years -20°C Powder, 2 weeks4°C in DMSO,6 months-80°C in DMSO

Description:	Protease-Activated Receptor-2 Activating Peptide is an agonist of Protease-Activated Receptor-2 (PAR-2).
Target:	PAR-2[1]
In Vitro:	Protease-Activated Receptor-2 Activating Peptide (SLIGRL-NH2) is an agonist of PAR-2 and MrgprC11[1]. Protease-Activated Receptor-2 Activating Peptide (SLIGRL-NH2) causes an L-NAME-inhibited relaxation. Based on SLIGRL-NH2 causing a concentration-dependent relaxation with an EC50 of 10 µM in endothelium-free preparations in the presence of perivascular adipose tissue (PVAT) , 20 µM is used as a suitable ‘test’ concentration of peptide in subsequent experiments designed to evaluate the effects of potential inhibitors of ADRF release/action. In the endothelium-free aorta preparations, SLIGRL-NH2 causes a concentration-dependent relaxation in preparations only in the presence of PVAT [+PVAT, -ENDO (endothelium)][2].
Kinase Assay:	Tissues are routinely contracted with 100 mM potassium chloride (KCl) to test their viability. Then, after re-equilibration for 20 min in fresh buffer, tissues are contracted with 1 µM of phenylephrine and a test concentration of 1 µM ACh is added and the presence or absence of a relaxant response is monitored to verify the presence or absence of an intact functional endothelium. The contractile response to phenylephrine is expressed as a percentage of the contractile response caused by 100 mM KCl (% KCl). Upon standardizing the preparation with the use of KCl and ACh, the effects of added SLIGRL-NH2, 2-furoyl-LIGRLO-NH2, LRGILS-NH2, LSIGRL-NH2 and 2-furoyl-OLRGIL-NH2 on the tension of the phenylephrine-contracted preparations (1 µM phenylephrine) is monitored for tissues with/without an intact endothelium and with/without adherent PVAT. Relaxation (%) is expressed as a percentage reduction of the plateau tension developed in the presence of phenylephrine. The effects of the inhibitors (L-NAME, ODQ, indomethacin, 4-aminopyridine, combined apamin + charybdotoxin, glibenclamide, genistein, H89 and catalase) are measured by treating the tissues with the inhibitors for 15 min before their contraction with 1 µM phenylephrine, then followed by the addition of test concentrations of SLIGRL-NH2, 2-furoyl-LIGRLO-NH2, LRGILS-NH2, LSIGRL-NH2 and 2-furoyl-OLRGIL-NH2. In most experiments evaluating a role for PAR2, SLIGRL-NH2 is used at a concentration of 20 µM to ensure selectivity for PAR2[2].
References:	[1]. Akiyama T, et al. Behavioral model of itch, alloknesis, pain and allodynia in the lower hindlimb and correlativeresponses of lumbar dorsal horn neurons in the mouse. Neuroscience. 2014 Apr 25;266:38-46. [2]. Li Y, et al. Perivascular adipose tissue-derived relaxing factors: release by peptide agonists via proteinase-activated receptor-2 (PAR2) and non-PAR2 mechanisms. Br J Pharmacol. 2011 Dec;164(8):1990-2002.

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