endothelin-1 (et-1)

Aminaftone, a derivative of 4-aminobenzoic acid, inhibits endothelin-1 (ET-1) production and is used to study hypertension and systemic sclerosis.

Clazosentan (Ro 61-1790) is a selective antagonist of the endothelin A receptor (ETAreceptor) that inhibits ET-1-mediated vasoconstriction, preventing cerebral vasospasm and vasospasm-associated cerebral infarction.

A-192621 is a potent, nonpeptide, orally active, and selective endothelin B (ETB) receptor antagonist with an IC50 of 4.5 nM and a Ki of 8.8 nM. A-192621 promotes apoptosis in PASMCs and elevates both arterial blood pressure and plasma ET-1 levels[1][2][3]. Its selectivity is 636-fold higher for ETB than ETA (IC50 of 4280 nM and Ki of 5600 nM).

ENDOTHELIN-1 (ET-1), the principal peptide of the endothelin family, has been shown to have a variety of biological activities in both vascular and nonvascular tissues. The C-terminal fragment, which is a highly conserved sequence in the peptides of t

Ac-Endothelin-1 (16-21), human acetate, the principal peptide of the endothelin family, has been shown to have a variety of biological activities in both vascular and nonvascular tissues. The C-terminal fragment, which is a highly conserved sequence in th

J-104132 is a potetn and selective endothelin A B receptor antagonist (Ki: cloned human ETA = 0.034 nM; cloned human ETB = 0.104 nM) . In vitro, J-104132 is a potent antagonist of ET-1-induced accumulation of [3H]inositol phosphates in Chinese hamster ova

Ro 46-2005 is a synthetic non-peptide endothelin receptor antagonist, inhibits the specific binding of 125I-ET-1 to human vascular smooth muscle cells (ETA receptor, IC50: 220 nM).

ACT-373898 is a metabolite of the endothelin (ET) receptor type A (ETA) and ETBdual antagonist macitentan .1 1.Dingemanse, J., Sidharta, P.N., Maddrey, W.C., et al.Efficacy, safety and clinical pharmacology of macitentan in comparison to other endothelin receptor antagonists in the treatment of pulmonary arterial hypertensionExpert Opin. Drug Saf.13(3)391-405(2013)

Nebentan (YM598) is a potent, selective and orally active non-peptide endothelin ETA receptor antagonist through the modification of Bosentan . Nebentan inhibits [125I] endothelin-1 binding to cloned human endothelin ETA and ETB receptor, with Ki of 0.697 nM and 569 nM, respectively[1]. YM598 can ameliorate the progression of cor pulmonale and myocardial infarction in vivo[2]. Nebentan inhibits the specific binding of [125I] endothelin-1 to endothelin ETA and ETB receptors in a concentration dependent manner,Ki values are 0.697 nM and 1.53 nM for human and rat endothelin ETA receptors, respectively. In contrast, YM598 exhibits low affinities for human and rat endothelin ETB receptors, with Ki values of 569 nM and 155 nM,respectively[1].In measurement of intracellular Ca2+ concentration, Nebentan concentration-dependently inhibits the increase in [Ca2+]i induced by 10 nM endothelin-1 in both CHO cells and A10 cells, the IC50 values are 26.2 nM for CHO cells and 26.7 nM for A10 cells, respectively[1]. Nebentan (oral administration; 0.1-1 mg kg; 4 weeks) significantly inhibits the progression of pulmonary hypertension and the development of right ventricular hypertrophy[2].Nebentan (oral administration; 1 mg kg; 30 weeks) significantly ameliorates the poor survival rate of CHF rats, it markedly reduces the hypertrophy of both ventricles as well as pulmonary congestion[2]. [1]. Hironori Yuyama, et al. Pharmacological Characterization of YM598, an Orally Active and Highly Potent Selective Endothelin ET(A) Receptor Antagonist. Eur J Pharmacol. 2003 Sep 30;478(1):61-71. [2]. Akira Fujimori, et al. YM598, an Orally Active ET(A) Receptor Antagonist, Ameliorates the Progression of Cardiopulmonary Changes and Both-Side Heart Failure in Rats With Cor Pulmonale and Myocardial Infarction. J Cardiovasc Pharmacol. 2004 Nov;44 Suppl 1:S354-7.

Human Big ET-1 comprises residues 53-90 of the endothelin precursor (preproendothelin). Compared to the mature endothelin-1 (hET-1), the peptide show less vasoconstrictor activity in vitro, but similar pressor effects in vivo. Former CAS-number 121014-53-7.

The big endothelins comprise residues 53-90 (human big ET-1) and 53-91 (porcine big ET-1) of the endothelin precursor (preproendothelin). Compared to the mature endothelin-1 (ET-1), both peptides show less vasoconstrictor activity in vitro, but similar pressor effects in vivo. Former CAS-number 121014-54-8.

Thrombin receptor agonist peptide (TRAP-14) is a 14-amino acid peptide agonist of the α-thrombin receptor. It induces aggregation of washed platelets as well as platelets in citrated and hirudin plasma. TRAP-14 (100 μM) increases the cytosolic calcium concentration in isolated guinea pig pulmonary smooth muscle cells 5-fold over baseline. It increases pulmonary arterial pressure in isolated guinea pig lung when used at a concentration of 1 μM, which is comparable to the effect induced by 10 nM α-thrombin. TRAP-14 also induces contraction of isolated rat aortic rings and increases endothelin-1 (ET-1) levels in a dose-dependent manner, an effect that is reversed by the ETA antagonist BQ-123 and the nitric oxide synthase (NOS) inhibitor L-NNA .

Desmethyl bosentan, an active metabolite of the endothelin receptor antagonist bosentan, activates the pregnane X receptor (PXR) in CV-1 monkey kidney cells expressing the human receptor in a reporter assay at a concentration of 25 μM.

BE-24566B is a polyketide fungal metabolite originally isolated fromS. violaceusniger.1It is active againstB. subtilis,B. cereus,S. aureus,M. luteus,E. faecalis, andS. thermophilus(MICs = 1.56, 1.56, 1.56, 1.56, 3.13, and 3.13 μg/ml, respectively). BE-24566B is an endothelin (ET) receptor antagonist (IC50s = 11 and 3.9 μM for ETAand ETBreceptors, respectively).2 1.Kojiri, K., Nakajima, S., Fuse, A., et al.BE-24566B, a new antibiotic produced by Streptomyces violaceusnigerJ. Antibiot. (Tokyo)48(12)1506-1508(1995) 2.Lam, Y.K.T., Hensens, O., Helms, G., et al.L-755,805, a new polyketide endothelin binding inhibitor from an actinomyceteTetrahedron Lett.36(12)2013-2016(1995)

Bosentan (Benzenesulfonamide) is a sulfonamide-derived, competitive and specific endothelin receptor antagonist with a slightly higher affinity for the endothelin A receptor than endothelin B receptor. Bosentan blocks the action of endothelin 1, an extremely potent endogenous vasoconstrictor and bronchoconstrictor, by binding to endothelin A and endothelin B receptors in the endothelium and vascular smooth muscle. Bosentan decreases both pulmonary and systemic vascular resistance and is particularly used in the treatment of pulmonary arterial hypertension.

Bosentan hydrate (Ro 47-0203) is a competitive and dual antagonist of endothelin-1 at the endothelin-A (ET-A) and endothelin-B (ET-B) receptors.

Bosentan-d4, the deuterium-labeled variant of Bosentan, serves as a competitive dual antagonist against endothelin-1 (ET) by targeting both ET A and ET B receptors. It exhibits binding affinities with K i values of 4.7 nM for ET A and 95 nM for ET B in human SMC.

Endothelin 1 (swine, human) (TFA) is a synthetic peptide mirroring the sequence of the potent endogenous vasoconstrictor found in both human and swine Endothelin 1, operating via two receptor types, ET A and ET B [1].

Endothelin 1 (swine, human), Alexa Fluor 488-labeled, is a synthetic peptide mirroring human and swine Endothelin 1, an endogenous vasoconstrictor, and is tagged with Alexa Fluor 488 for fluorescence, operating via two receptor types, ET A and ET B [1].

[Ala2] Endothelin-3, human is a linear analog of endothelin-3 (ET-3) with Ala substituting for Cys residues. ET-3, a vasoactive peptide produced by human rhabdomyosarcoma cell lines and not expressed in non-muscle-origin human sarcoma cell lines, serves as a paracrine factor by promoting endothelial cell migration [1] [2].

Endothelin-1 (1-31) (Human) is a potent vasoconstrictor and hypertensive agent, derived from the specific hydrolysis of big ET-1 by chymase [1].

Endothelin-1 (1-31) (Human) acetate, a potent vasoconstrictor and hypertensive agent, is produced through the selective hydrolysis of big ET-1 by chymase [1].

Endothelin-1 (1-31) (Human) TFA, a potent vasoconstrictor and hypertensive agent, originates from chymase-mediated selective hydrolysis of big ET-1 [1].

BQ-3020 ammonium, a selective endothelin receptor (ET B receptor) agonist, demonstrates inhibition of [125 I] ET-1 binding to ET B receptors with an IC50 of 0.2 nM and induces vasoconstriction in rabbit pulmonary arteries. Additionally, it promotes relaxation of the pig urinary bladder neck, rendering it useful for research into cardiovascular diseases [1] [2].