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B150

Sigma-Aldrich

BQ-123

≥99%, sodium salt, lyophilized powder

Synonym(s):

BQ123, Cyclo(D-Trp-D-Asp-Pro-D-Val-Leu)

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About This Item

Empirical Formula (Hill Notation):
C31H41N6O7 Na
CAS Number:
Molecular Weight:
632.68
MDL number:
UNSPSC Code:
12352204
PubChem Substance ID:
NACRES:
NA.32

Quality Level

Assay

≥99%

form

lyophilized powder

storage temp.

−20°C

SMILES string

[H][C@@]12CCCN1C(=O)[C@@H](CC(O)=O)NC(=O)[C@@H](Cc3c[nH]c4ccccc34)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](NC2=O)C(C)C

InChI

1S/C31H42N6O7/c1-16(2)12-21-27(40)33-22(13-18-15-32-20-9-6-5-8-19(18)20)28(41)35-23(14-25(38)39)31(44)37-11-7-10-24(37)29(42)36-26(17(3)4)30(43)34-21/h5-6,8-9,15-17,21-24,26,32H,7,10-14H2,1-4H3,(H,33,40)(H,34,43)(H,35,41)(H,36,42)(H,38,39)/t21-,22+,23+,24-,26+/m0/s1

InChI key

VYCMAAOURFJIHD-PJNXIOHISA-N

Gene Information

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Amino Acid Sequence

cyclo-Asp-Pro-Val-Leu-Trp

Application

BQ-123 has been used as a selective endothelin-A receptor antagonist to study its effects on tumor necrosis factor α (TNFα)-induced human airway smooth muscle cells (HASMCs) proliferation. It is also used as endothelin-A receptor antagonist to study its effects on TNFα-induced granulocyte–macrophage colony-stimulating factor (GM-CSF) expression.

Biochem/physiol Actions

BQ-123 is an endothelin(Et) receptor antagonist and is exquisite for endothelin A (ETA) receptor. It is a cyclic pentapeptide.
Selective ETA endothelin receptor antagonist.

Storage Class Code

11 - Combustible Solids

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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F Cosentino et al.
Journal of cardiovascular pharmacology, 22 Suppl 8, S332-S335 (1993-01-01)
The present study was designed to determine whether an endothelinA (ETA)-receptor antagonist BQ-123 (cyclo[Dtrp, Dasp, pro-D-Val-Leu]) or an ET-converting enzyme inhibitor phosphoramidon may prevent development of cerebral vasospasm after subarachnoid hemorrhage (SAH). A "double hemorrhage" canine model of the disease
J Knobloch et al.
Thorax, 64(12), 1044-1052 (2009-10-24)
There is an urgent need to inhibit endothelin-1 (ET-1) induced chronic inflammatory processes in early stages of lung diseases in order to prevent untreatable irreversible stages often accompanied by lung fibrosis and pulmonary hypertension. Nothing is known about the airway
M Clozel et al.
Life sciences, 52(9), 825-834 (1993-01-01)
The aim of this study was to evaluate the role of endothelin and endothelin ETA receptor in the early cerebral vasoconstriction following subarachnoid hemorrhage (SAH) in the rat. SAH induced by injection of autologous blood in the cisterna magna reduced
Jürgen Knobloch et al.
Biochemical pharmacology, 116, 188-199 (2016-07-17)
Pathological proliferation of human airway smooth muscle cells (HASMCs) causes hyperplasia in chronic lung diseases. Signaling pathways that link airway inflammation to HASMC proliferation might provide therapeutic targets for the prevention of airway remodeling and chronic lung diseases. Endothelin-1 (ET-1)
Sarah Pisarcik et al.
American journal of physiology. Lung cellular and molecular physiology, 304(8), L549-L561 (2013-02-19)
Numerous cellular responses to hypoxia are mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1). HIF-1 plays a central role in the pathogenesis of hypoxic pulmonary hypertension. Under certain conditions, HIF-1 may utilize feedforward mechanisms to amplify its activity. Since hypoxia

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