TFLLR-NH2
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TFLLR-NH2

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TFLLR-NH2, derived from the protease-activated receptor-1 (PAR1), is a selective PAR1 agonist with an EC50 of 1.9 μM.

Category
Peptide Inhibitors
Catalog number
BAT-010746
CAS number
197794-83-5
Molecular Formula
C31H53N9O6
Molecular Weight
647.81
TFLLR-NH2
Size Price Stock Quantity
5 mg $199 In stock
IUPAC Name
(2S)-N-[(2S)-1-[[(2S)-1-amino-5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]-2-[[(2S)-2-[[(2S,3R)-2-amino-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-4-methylpentanamide
Synonyms
TFLLR amide; (Thr1)-TRAP-5 amide; (Thr1)-PAR-1 (1-5) amide (human); PAR-1-activating peptide; PAR-1-AP; L-threonyl-L-phenylalanyl-L-leucyl-L-leucyl-L-argininamide
Related CAS
1313730-19-6 (TFA salt)
Appearance
White Lyophilized Powder
Purity
98%
Density
1.31±0.1 g/cm3(Predicted)
Sequence
H-Thr-Phe-Leu-Leu-Arg-NH2
Storage
Store at -20°C
Solubility
Soluble in 20% Acetonitrile (1 mg/mL), sterile Water (1 mg/mL)
InChI
InChI=1S/C31H53N9O6/c1-17(2)14-22(27(43)37-21(26(33)42)12-9-13-36-31(34)35)38-28(44)23(15-18(3)4)39-29(45)24(16-20-10-7-6-8-11-20)40-30(46)25(32)19(5)41/h6-8,10-11,17-19,21-25,41H,9,12-16,32H2,1-5H3,(H2,33,42)(H,37,43)(H,38,44)(H,39,45)(H,40,46)(H4,34,35,36)/t19-,21+,22+,23+,24+,25+/m1/s1
InChI Key
ANAMCEKSRDPIPX-GFGQVAFXSA-N
Canonical SMILES
CC(C)CC(C(=O)NC(CC(C)C)C(=O)NC(CCCN=C(N)N)C(=O)N)NC(=O)C(CC1=CC=CC=C1)NC(=O)C(C(C)O)N
1.Endothelium-dependent contractile actions of proteinase-activated receptor-2-activating peptides in human umbilical vein: release of a contracting factor via a novel receptor.
Saifeddine M;Roy SS;Al-Ani B;Triggle CR;Hollenberg MD Br J Pharmacol. 1998 Dec;125(7):1445-54.
The contractile actions of the proteinase-activated receptor-2-activating peptides (PAR2APs), SLIGRL-NH2 (SL-NH2), SLIGKV-NH2 (KV-NH2), trans-cinnamoyl-LIGRLO-NH2 (tc-NH2), and the PAR1-AP. TFLLR-NH2 (TF-NH2) as well as trypsin and thrombin were studied in endothelium-denuded and intact human umbilical vein (HUV) ring preparations. In HUV rings with, but not without an intact endothelium, PAR2APs caused a concentration-dependent contractile response, whereas LSIGRL-NH2 trypsin and PAR1APs were inactive. The contractile response was not affected by the endothelin ETA receptor antagonist, BQ123, the cyclooxygenase inhibitor, indomethacin, the leukotriene synthesis inhibitor, MK886, or the epoxygenase/P450 inhibitor, SKF-525A. Other pharmacological antagonists (prazosin, Losartan") were similarly inactive. The order of potencies of the PAR2APs to cause a contraction in the endothelium-intact preparation was: SL-NH2 > > KV-NH2 > or = tc-NH2. Using an endothelium-free rat aorta ring as a reporter tissue, surrounded with endothelium-intact HUV as a donor tissue in a 'sandwich assay,' we also monitored the ability of SL-NH2, TF-NH2, trypsin and thrombin to release either contractile (EDCF) or relaxant (EDRF) factors.
2.Dual endothelium-dependent vascular activities of proteinase-activated receptor-2-activating peptides: evidence for receptor heterogeneity.
Roy SS;Saifeddine M;Loutzenhiser R;Triggle CR;Hollenberg MD Br J Pharmacol. 1998 Apr;123(7):1434-40.
1. The vascular actions of the proteinase-activated receptor-2-activating peptides (PAR2APs), SLIGRL-NH2 (SL-NH2) and SLIGKV-NH2 (KV-NH2) as well as the reverse-sequence peptide, LSIGRL-NH2 (LS-NH2) and an N-acylated PAR2AP derivative, trans-cinnamoyl-LIGRLO-NH2 (tcLI-NH2), were studied in rat intact and endothelium-denuded artery ring preparations, primarily from the pulmonary artery (RPA). 2. In RPA rings with but not without a functional endothelium, SL-NH2 (but not LS-NH2) caused either an endothelium-dependent relaxation (at concentrations: < 10 microM) or (at higher concentrations: > 10 microM), an endothelium-dependent contraction. No contractile response was observed in endothelium-denuded preparations, that otherwise contracted in response to the PAR1AP, TFLLR-NH2. 3. The endothelium-dependent contractile response to SL-NH2 was not blocked by the alpha-adrenoceptor antagonist prazosin, the endothelin antagonist BQ123, the angiotensin II antagonist DuP753, by tetrodotoxin; nor by the enzyme inhibitors, N(omega)-nitro-L-arginine-methylester (NO-synthase), indomethacin (cyclo-oxygenase), SKF-525A (epoxygenase) and MK886 (leukotriene synthesis inhibitor). 4. In the relaxation assay, KV-NH2 was 5 fold less potent than SL-NH2, whereas in the contractile assay KV-NH2 was about equipotent with SL-NH2.
3.The PAR-1-activating peptide facilitates pepsinogen secretion in rats.
Kawao N;Hiramatsu K;Inoi N;Kuroda R;Nishikawa H;Sekiguchi F;Kawabata A Peptides. 2003 Sep;24(9):1449-51.
Protease-activated receptor-2 (PAR-2) is abundantly expressed in gastric mucosal chief cells, facilitating pepsinogen secretion. In the present study, we investigated whether PAR-1, a thrombin receptor, could modulate pepsinogen secretion in rats. The PAR-1-activating peptide TFLLR-NH(2) as well as the PAR-2-activating peptide SLIGRL-NH(2), administered i.v. repeatedly at 1-h intervals, significantly increased gastric pepsinogen secretion over 2-4 h (after two to four doses). In contrast, the control peptide FTLLR-NH(2), given in the same manner, had no such effect. Thus, PAR-1, like PAR-2, might function to facilitate pepsinogen secretion, suggesting a novel role of the thrombin-PAR-1-pathway in the stomach.
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