E137
IRL-1620
powder
Synonym(s):
N-Succinyl-[Glu9, Ala11,15]-Endothelin 1 fragment 8-21
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About This Item
Recommended Products
form
powder
color
white
storage temp.
−20°C
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Amino Acid Sequence
Suc-Asp-Glu-Glu-Ala-Val-Tyr-Phe-Ala-His-Leu-Asp-Ile-Ile-Trp
Biochem/physiol Actions
Selective ETB endothelin receptor agonist.
Signal Word
Danger
Hazard Statements
Precautionary Statements
Hazard Classifications
Acute Tox. 1 Inhalation - Acute Tox. 1 Oral
Storage Class Code
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Pharmacological research, 60(5), 402-410 (2009-08-12)
IRL-1620, a highly selective ET(B) receptor agonist, is presently in a phase I clinical trial (NCT00613691) in the United States for patients with recurrent or progressive carcinoma. The effect of acute repeated administration of IRL-1620 on the development of tachyphylaxis
Biochemical and biophysical research communications, 185(3), 867-873 (1992-06-30)
Suc-[Glu9,Ala11,15]-endothelin(ET)-1(8-21), IRL 1620, is a linear ET-analog specific for the ET-isopeptide-nonselective ETB receptor. The radio-iodinated analog, [125I]IRL 1620, showed a single class of saturable binding to the ETB receptors in porcine lung membranes with a Kd of 18 pM and
American journal of physiology. Gastrointestinal and liver physiology, 294(5), G1219-G1226 (2008-03-08)
Endotoxemia produces hepatic vascular dysregulation resulting from inhibition of endothelin (ET)-stimulated NO production. Mechanisms include overexpression of caveolin-1 (Cav-1) and altered phosphorylation of endothelial nitric oxide (NO) synthase (NOS; eNOS) in sinusoidal endothelial cells. Since ischemia-reperfusion (I/R) also causes vascular
Brain research, 1464, 14-23 (2012-05-15)
We have earlier shown that stimulation of endothelin B receptors by IRL-1620 provides significant neuroprotection at 24h following cerebral ischemia. However, the effect of IRL-1620 is not known in the subacute phase of cerebral ischemia, where development of cerebral edema
Canadian journal of physiology and pharmacology, 86(8), 516-525 (2008-09-02)
We hypothesized that constitutive endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) have opposite effects on the regulation of endothelin and its receptors. We therefore sought to determine whether deletions of iNOS or eNOS genes in mice modulate pressor
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