Molecular Formula | C31H53N9O6 |
Molar Mass | 647.81 |
Density | 1.31±0.1 g/cm3(Predicted) |
pKa | 12.10±0.45(Predicted) |
Storage Condition | -20℃ |
In vitro study | PAR1 agonists stimulate concentration-dependent increases in [Ca 2+ ]i and in the proportions of neurones. The maximal increase in [Ca 2+ ]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. 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-β1 is detected in the supernatant. |
In vivo study | 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. 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. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 1.544 ml | 7.718 ml | 15.437 ml |
5 mM | 0.309 ml | 1.544 ml | 3.087 ml |
10 mM | 0.154 ml | 0.772 ml | 1.544 ml |
5 mM | 0.031 ml | 0.154 ml | 0.309 ml |