TFLLR-NH2
TFLLR-NH2 Basic information
- Product Name:
- TFLLR-NH2
- Synonyms:
-
- H-THR-PHE-LEU-LEU-ARG-NH2
- THR-PHE-LEU-LEU-ARG-NH2
- THROMBIN RECEPTOR (PAR-1), HYBRIDE HUMAN-XENOPE
- TFLLR-AMIDE
- TFLLR-NH2
- (Thr1)-TRAP-5 amide
- TFLLR-NH2 Protease-Activated Receptor 1 (PAR1) Agonist
- (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
- CAS:
- 197794-83-5
- MF:
- C31H53N9O6
- MW:
- 647.81
- Product Categories:
-
- Proteinase-activated receptor (PAR)
- Peptide Receptors
- Mol File:
- 197794-83-5.mol
TFLLR-NH2 Chemical Properties
- Density
- 1.31±0.1 g/cm3(Predicted)
- storage temp.
- Desiccate at -20°C
- pka
- 12.10±0.45(Predicted)
- form
- Powder
- Water Solubility
- Soluble to 1 mg/ml in water
- Sequence
- Thr-Phe-Leu-Leu-Arg-NH2
TFLLR-NH2 Usage And Synthesis
Uses
TFLLR-NH2 is a PAR-1 activator.
in vivo
Injection of TF-NH2 into the rat paw stimulates a marked and sustained oedema. An NK1R antagonist and ablation of sensory nerves with capsaicin inhibit oedema by 44% at 1?h and completely by 5?h. In wild-type but not PAR1?/? mice, TF-NH2 stimulates Evans blue extravasation in the bladder, oesophagus, stomach, intestine and pancreas by 2–8 fold. Extravasation in the bladder, oesophagus and stomach is abolished by an NK1R antagonist[1]. TFp-NH2 produces notable contraction at 3-50 μM and relaxation at 0.3-50 μM, in the absence of apamin. The concentration-response curve for TFp-NH2-induced contraction is remarkably shifted left, when the TFp-NH2-induced relaxation is blocked by apamin at 0.1 μM[3].
IC 50
PAR1: 1.9 μM (EC50)
storage
-20°C
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