TFLLR-NH2 trifluoroacetate salt

>98% (HPLC)

L-Threonyl-L-phenylalanyl-L-leucyl-L-leucyl- L-argininamide trifluoroacetate salt, Thr-Phe-Leu-Leu-Arg-NH2 trifluoroacetate salt
Empirical Formula (Hill Notation):
C31H53N9O6 · xC2HF3O2
Peso molecular:
647.81 (free base basis)
MDL number:
PubChem Substance ID:
En este momento no podemos mostrarle ni los precios ni la disponibilidad


>98% (HPLC)


lyophilized powder


white to tan


H2O: >2 mg/mL

storage temp.


SMILES string




InChI key


Amino Acid Sequence



TFLLR-NH2 trifluoroacetate salt has been used as a protease-activated receptor-1 (PAR-1) agonist to study its effects on hippocampal CA1 pyramidal neurons and Swell1 knock out mice (cKO).


5, 25 mg in glass bottle

Biochem/physiol Actions

TFLLR-NH2 is a protease-activated receptor (PARs) agonist which is more selective to PAR-1 than SFLLRN-NH2. Protease-activated receptors (PARs) are present on various organs including, plateles, mast cell, gallblader, oesophagus etc, and regulate various physiological processes including human platelet aggregation, vascular contraction/relaxation, and an increase in endothelial permeability. Recent papers indicated that PAR′s are also involved in sensory processing. Specificly PAR ligands enhance glutamatergic excitatory transmission in substantia gelatinosa (SG) neurons of adult rat spinal cord slices.

Preparation Note

TFLLR-NH2 trifluoroacetate is soluble in water at a concentration that is greater than 2 mg/ml.


NONH for all modes of transport

WGK Germany


Flash Point F

Not applicable

Flash Point C

Not applicable

Hui Sun et al.
American journal of physiology. Lung cellular and molecular physiology, 318(1), L192-L199 (2019-10-31)
We evaluated the mechanisms underlying protease-activated receptor 1 (PAR1)-mediated activation of nodose C-fibers in mouse lungs. The PAR1-induced action potential discharge at the terminals was strongly inhibited in phospholipase C-β3 (PLCβ3)-deficient animals. At the level of the cell soma, PAR1...
Glutamate-releasing SWELL1 channel in astrocytes modulates synaptic transmission and promotes brain damage in stroke
Yang J, et al.
Neuron, 102(4), 813-827 (2019)
Junhua Yang et al.
Neuron, 102(4), 813-827 (2019-04-16)
By releasing glutamate, astrocytes actively regulate synaptic transmission and contribute to excitotoxicity in neurological diseases. However, the mechanisms of astrocytic glutamate release have been debated. Here, we report non-vesicular release of glutamate through the glutamate-permeable volume-regulated anion channel (VRAC). Both...

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