TFLLR-NH2(TFA)

1313730-19-6

C33H54F3N9O8

DMSO : 100 mg/mL (131.26 mM; Need ultrasonic)

GPCR/G Protein

TFLLR-NH2 (TFA) is a selective PAR1 agonist with an EC₅₀ of 1.9 uM. IC50 & Target: EC50: 1.9 uM (PAR1)^[1] In Vitro: 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?um 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 the in vitro platelet culture system, a TFLLR-NH2 dose-dependent increase of secreted TGF-beta1 is detected in the supernatant^[2]. 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 uM and relaxation at 0.3-50 uM, 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 uM^[3].