Shanghai Nianxing Industrial Co., Ltd
China
Product Name: TFLLR-NH2TFA
Price:
Purity: 98.0%
Stocking Period: 10 Day
Contact: Yang

Taiwan Oyi peptide Co. Ltd
China
Product Name: TFLLR-NH2 TFA
Price: $Inquiry/1mg $Inquiry/100kg
Purity: 98.0%
Stocking Period: 1 Day
Contact: Vinnie

1313730-19-6

1313730-19-6 structure

1313730-19-6 structure

Name: TFLLR-NH2 TFA
Chemical Name: TFLLR-NH2(TFA)
CAS Number: 1313730-19-6
Molecular Formula: C₃₃H₅₄F₃N₉O₈
Molecular Weight: 761.83
Catalog: Peptides
Create Date: 2018-11-18 07:56:02
Modify Date: 2024-01-10 15:39:44
TFLLR-NH2 (TFA) is a selective PAR1 agonist with an EC50 of 1.9 μM.

Name	TFLLR-NH2(TFA)
Synonyms	MFCD05663482

Description	TFLLR-NH2 (TFA) is a selective PAR1 agonist with an EC50 of 1.9 μM.
Related Catalog	Signaling Pathways >> GPCR/G Protein >> Protease-Activated Receptor (PAR) Research Areas >> Others Peptides
Target	EC50: 1.9 μM (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 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 the in vitro platelet culture system, a TFLLR-NH2 dose-dependent increase of secreted TGF-β1 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 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].
Animal Admin	Mice[1] Mice are anaesthetized with isofluorane, and saline or TF-NH2 (3 μmol/kg in 25 μL physiological saline) is injected into the lateral tail vein. Evans blue (33.3 mg/kg in 50 μL saline) is co-injected with the peptide. Mice are perfused transcardially at 10 min after administration of TF-NH2 with physiological saline containing 20 u/mL heparin at a pressure of 80-100 mmHg for 2-3 min. Excised tissues are incubated in 1 mL of formamide for 48 h, and Evans blue content is measured spectrophotometrically at 650 nm[1].
References	[1]. de Garavilla L, et al. Agonists of proteinase-activated receptor 1 induce plasma extravasation by a neurogenic mechanism. Br J Pharmacol. 2001 Aug;133(7):975-87. [2]. Kawabata A, et al. Characterization of the protease-activated receptor-1-mediated contraction and relaxation in the rat duodenal smooth muscle. [3]. Jia Y, et al. Activation of platelet protease-activated receptor-1 induces epithelial-mesenchymal transition and chemotaxis of colon cancer cell line SW620. Oncol Rep. 2015 Jun;33(6):2681-8.

Molecular Formula	C₃₃H₅₄F₃N₉O₈
Molecular Weight	761.83

Hazard Codes	Xi