TFLLR-NH2 is a selectivePAR1agonist with anEC₅₀of 1.9 μM.

EC50: 1.9 μM (PAR1)^[1]

PAR1 agonists stimulate concentration-dependent increases in [Ca²⁺]i and in the proportions of neurones. The maximal increase in [Ca²⁺]i above basal is detected in response to 10 μm TF-NH2(peak 196.5±20.4 nM, n=25) when 50–80% of identified neurones responded^[1]. SW620 cells cultured in the supernatant of TFLLR-NH2-activated platelets upregulate E-cadherin expression and downregulate the vimentin expression. In thein vitroplatelet culture system, a TFLLR-NH2 dose-dependent increase of secreted TGF-β1 is detected in the supernatant^[2].

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].

647.81

C₃₁H₅₃N₉O₆

197794-83-5

Thr-Phe-Leu-Leu-Arg-NH2

TFLLR-NH2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.