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IRL-1620 TFA Sale

目录号 : GC38641

IRL-1620 (TFA) 是高效,选择性的内啡肽受体 (endothelin receptor) B 型激动剂,Ki 值为 16 pM。

IRL-1620 TFA Chemical Structure

规格 价格 库存 购买数量
500μg
¥900.00
现货
1mg
¥1,530.00
现货
5mg
¥5,310.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

IRL-1620 (TFA) is a potent and selective endothelin receptor type B (ETB) agonist with a Ki of 16 pM[1].

IRL-1620 (TFA) is the most potent and specific ligand for the ETB receptor (KiETA/ KiETB=120,000) as judged by the Ki values for ETA (19 μM) and ETB (16 PM) receptors[1]. IRL-1620 (TFA) is 60 times more selective for the ETB receptor than ET-3 (KiETA/ KiETB=1,900)[1].

IRL-1620 (TFA) (1-100 nM) induces contractions of the guinea pig trachea. The effective concentration that produces 30 % of 60 mM KCI-induced contraction is estimated to be 28 nM for IRL-1620[1]. IRL-1620 (TFA) (1-100 nM) increases cytosolic Ca2+ in the vascular endothelium ([Ca]E) with little effect on resting muscle tone, and relaxes the norepinephrine-stimulated tone with an increase in [Ca]E, in rat aorta,[1]. IRL-1620 (TFA) improves both acquisition (learning) and retention (memory) on the water maze task and enhances angiogenic and neurogenic remodeling. Rats treated with IRL-1620 significantly reduces the cognitive impairment induced by Aβ. IRL-1620 treatment enhances the number of blood vessels labeled with VEGF compared to vehicle treatment[2].IRL-1620 (TFA), restores analgesic tolerance to morphine and oxycodone, but it does not affect morphine and oxycodone induced decrease in NGF/PI3K expression. IRL-1620 attenuates opioid tolerance without the involvement of NGF/PI3K pathway[3].

[1]. Takai M, et al. A potent and specific agonist, Suc-[Glu9,Ala11,15]-endothelin-1(8-21), IRL 1620, for the ETB receptor. Biochem Biophys Res Commun. 1992 Apr 30;184(2):953-9. [2]. Briyal S, et al. Stimulation of endothelin B receptors by IRL-1620 decreases the progression of Alzheimer's disease. Neuroscience. 2015 Aug 20;301:1-11. [3]. Gulati S, et al. Attenuation of opioid tolerance by ETB receptor agonist, IRL-1620, is independent of an accompanied decrease in nerve growth factor in mice. Heliyon. 2017 Jun 7;3(6):e00317.

Chemical Properties

Cas No. SDF
分子式 C88H118F3N17O29 分子量 1934.97
溶解度 Soluble in DMSO 储存条件 -20°C, protect from light
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 0.5168 mL 2.584 mL 5.168 mL
5 mM 0.1034 mL 0.5168 mL 1.0336 mL
10 mM 0.0517 mL 0.2584 mL 0.5168 mL
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Research Update

Endothelin receptor B enhances liver injury and pro-inflammatory responses by increasing G-protein-coupled receptor kinase-2 expression in primary biliary cholangitis

Sci Rep 2022 Nov 17;12(1):19772.PMID:36396948DOI:PMC9672122

Severe diseases like cirrhosis and liver failure can be developed from primary biliary cholangitis (PBC). Endothelin-2 (EDN2) and endothelin receptor B (EDNRB) are related to the pathogenesis of PBC. However, the roles of EDN2 and EDNRB in PBC-related liver injury and inflammation along with molecular mechanisms are poorly defined. In this study, histopathologic alterations of liver tissues were assessed through hematoxylin-eosin staining. Alanine transaminase (ALT), alkaline phosphatase (ALP), aspartate transaminase (AST), and γ-Glutamyltranspetidase (GGT) (4 liver function indexes) serum levels were detected with corresponding activity assay kits. Also, we determined the levels of M2 subtype anti-mitochondrial antibody (AMA-M2), interferon-gamma (IFN-γ), and tumor-necrosis factor alpha (TNFα) in serum with ELISA assay. Later, RT-qPCR assay was used to measure the expression of genes at mRNA levels, while western blotting and immunohistochemical techniques were used to detect protein levels of genes. Our results showed that the liver tissues of PBC patients and mice presented with severe hepatocyte injury and inflammatory cell infiltration as well as destruction of intrahepatic small bile ducts. ALP, AST, ALT, GGT, AMA-M2, IFN-γ, and TNF-α serum levels were higher in PBC patients and mice. Besides, EDN2 and EDNRB were highly expressed in serums and livers of PBC patients and mice. EDNRB potentiated PBC-related liver injury and pro-inflammatory responses, as evidenced by observation of serious liver pathologic injury and increased serum levels of ALP, AST, ALT, AMA-M2, IFN-γ, and TNF-α in PBC mice following EDNRB overexpression. EDNRB overexpression or activation via its agonist IRL-1620 TFA triggered liver injury and pro-inflammatory responses, increased GRK2 expression and induced NF-κB expression and activation in wild-type mice. EDNRB knockdown or inhibition by Bosentan alleviated liver damage and inflammation, reduced GRK2 expression, and inhibited NF-κB in PBC mice. These findings suggested EDNRB loss or inhibition weakened liver injury and pro-inflammatory responses by down-regulating GRK2 and inhibiting the NF-κB pathway in PBC mice.