TFLLR-NH2 (BAT-006103)
* For research use only

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

Peptide Inhibitors
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BAT-006103 5 mg $198 In stock
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(Thr1)-TRAP-5 amide; (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; PAR-1-activating peptide; PAR-1-AP; threonyl-phenylalanyl-leucyl-leucyl-argininamide
1.31±0.1 g/cm3
Store in a cool and dry place (or refer to the Certificate of Analysis).
InChI Key
Canonical SMILES
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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Tip: Chemical formula is case sensitive. C22H30N4O c22h30n40
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