Endothelins and Related Peptides

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CAT# Product Name M.W Molecular Formula Inquiry
B1501 Big Endothelin-1 (1-38), human 4282.9 C₁₈₉H₂₈₂N₄₈O₅₆S₅ Inquiry
B1503 Big Endothelin-1 (1-39), bovine 4370.7 Inquiry
B1505 Big Endothelin-1 (1-39), porcine 4384 C₁₉₃H₂₈₉N₄₉O₅₈S₅ Inquiry
B1507 Big Endothelin-1 (1-39), rat 4389.1 Inquiry
B1509 Big Endothelin-1 (19-38), human 2221.7 Inquiry
B1513 Big Endothelin-1 (22-39), bovine 1896.2 Inquiry
B1515 Big Endothelin-1 (22-39), porcine 1910.1 Inquiry
B1517 Big Endothelin-1 (22-39), rat 1915.2 Inquiry
B1519 Big Endothelin-2 (1-37), human 4183.7 Inquiry
B1521 Big Endothelin-2 (22-37), human 1654.8 Inquiry
B1523 Big Endothelin-2 (22-38), human 1811 Inquiry
B1525 Big Endothelin-3 (1-41), amide, human 4923.7 Inquiry
B1526 Big Endothelin-3 (22-41), amide, human 2298.6 Inquiry
B1529 [Tyr123] Prepro Endothelin (110-130), amide, human 2402.8 Inquiry
E09004 RES-701-1 0.0 C103H115N23O23 Inquiry
E09005 IRL-1038 1410.0 C68H92N14O15S2 Inquiry
E09006 Endothelin-1 (1-15), amide, human 1713.4 C70H105N17O23S5 Inquiry
E09007 Endothelin-1 (1-15), human 1714.0 C70H104N16O24S5 Inquiry
E09008 IRL-1720 1762.0 C85H120N18O23 Inquiry
E09009 Big Endothelin-1 fragment (22-38) (human) 1809.01 C80H125N23O25 Inquiry

Introduction

Endothelin is a vasoactive peptide secreted by endothelial cells. There are three types of endothelin in the human body: ET-1, ET-2, and ET-3, and their biological activities are different. It is mainly caused by autocrine or paracrine release of endothelial cells, which is of great significance for the stability of cardiovascular hemodynamics. Endothelin binds to its receptor and exerts its corresponding biological activity. Three endothelin receptors have been identified: ETA, ETB, and ETC. Endothelin is closely related to hypertension. The level of endothelin in plasma is higher than that in healthy people, and its level is positively correlated with the severity of hypertension. Endothelin is the strongest endogenous vasoconstrictor peptide ever discovered.

Mechanism of action

In humans, the receptors for endothelin are mainly ETA and ETB, all of which are G protein-coupled receptors. Endothelin, by binding to the corresponding receptor, stimulates its chemical activity and thus manifests its function in the human body. ETA is mainly expressed in muscle cells and binds to ET-1 and ET-2. ETB is mainly expressed in endothelial cells, endocrine cells, and nerve cells and can be combined with ET-1, 2, and 3. ETA activation promotes vascular smooth muscle contraction and proliferation, and ETB-1 promotes the release of vasodilating substances such as nitric oxide (NO). The relationship between blood pressure and elevated endothelin is a causal relationship: plasma ET-1 may be directly or indirectly involved in the development and progression of hypertension; elevated blood pressure and blood pressure variability are important risk factors for elevated plasma ET-1 levels.

Application of Endothelins and Related Peptides

ETA receptor antagonists can alleviate vascular inflammation, reduce vascular smooth muscle cell differentiation, calcification and sclerosing, suggesting that endothelin receptor antagonists will be a promising new drug that is expected to play a special role in the treatment of hypertension. In addition, endothelin receptor antagonists can play a good role in reducing mortality in patients with heart failure. The expression of vasoactive substances released by endothelial cells has been shown to be closely related to pulmonary hypertension (PAH), and endothelin-1 (ET-1) is particularly effective for pulmonary hypertension. Most endothelin receptor antagonists on the market are currently designed and developed around ETA, for example, Bosentan, macitentan, ambrisentan, and sitaxsentan.

References

  1. Davenport, A. P., Kuc, R. E., Southan, C., & Maguire, J. J. (2018). New drugs and emerging therapeutic targets in the endothelin signaling pathway and prospects for personalized precision medicine. Physiological Research, 67(Supplementum 1), S37.
  2. Mcmahon, T. J. , & Bryan, N. S. . (2017). Biomarkers in pulmonary vascular disease: gauging response to therapy. The American Journal of Cardiology, 120(8), S89-S95.
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