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ChemicalBook--->CAS DataBase List--->1313730-19-6

1313730-19-6

1313730-19-6 Structure

1313730-19-6 Structure
IdentificationBack Directory
[Name]

TFLLR-NH2(TFA)
[CAS]

1313730-19-6
[Synonyms]

TFLLR-NH2(TFA)
197794-83-5 (Thr1)-TRAP-5 amide
[Molecular Formula]

C33H54F3N9O8
[MDL Number]

MFCD05663482
[MOL File]

1313730-19-6.mol
[Molecular Weight]

761.85
Chemical PropertiesBack Directory
[storage temp. ]

Store at -20°C
[solubility ]

Water: 100 mg/mL (131.26 mM); DMSO: 100 mg/mL (131.26 mM)
[form ]

Solid
[color ]

White to off-white
[Sequence]

H-Thr-Phe-Leu-Leu-Arg-NH2
Hazard InformationBack Directory
[Biological Activity]

TFLLR-NH2 (TFA) is a selective PAR1 agonist with an EC50 of 1.9 μM.
[in vitro]

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.

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[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. 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.

[target]

EC50: 1.9 μM (PAR1)

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