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Merck
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Documenti fondamentali

SML2908

Sigma-Aldrich

A71915 trifluoroacetate

≥95% (HPLC)

Sinonimo/i:

(Arg6, β-cyclohexyl-Ala8, D-Tic16, Arg17, Cys18)-Atrial Natriuretic Factor (6-18) amide (Cys7→Cys18 disulfide), TFA salt, A 71915, A-71915, Arg-Cys-β-cyclohexyl-Ala-Gly-Gly-Arg-Ile-Asp-Arg-Ile-D-Tic-Arg-Cys-NH2 (Cys2→Cys13 disulfide), TFA salt, RC-(Cha)-GGRIDRI-(D-Tic)-RC-NH2 (Cys2→Cys13 disulfide, TFA salt, [Arg6, Cha8]ANP-(6-15)-D-Tic-Arg-Cys-NH2 (Cys7→Cys18 disulfide), TFA salt

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About This Item

Formula empirica (notazione di Hill):
C69H116N26O15S2 · xC2HF3O2
Numero CAS:
132956-87-7
Peso molecolare:
1613.95 (free base basis)
Codice UNSPSC:
12352200
NACRES:
NA.77

Livello qualitativo

100

Saggio

≥95% (HPLC)

Forma fisica

powder

Colore

white to off-white

Temperatura di conservazione

−20°C

Azioni biochim/fisiol

A71915 is a potent atrial natriuretic peptide A (ANP, NPPA) receptor (NPR1, ANP-A, ANPR-A, NPR-A) antagonist (pKi = 9.18 (Ki = 650 nM) by competitive binding against 300 nM rat ANP1-28 to human neuroblastoma NB-OK-1 cells; pA2 = 9.45 against rat ANP-induced cGMP production in NB-OK-1 cells). A71915 is reactive toward dog, human, mouse, rabbit, and rat species, and commonly employed both in cultures (1-10 μM) and in vivo for studying NPR-A-mediated responses.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Certificati d'analisi (COA)

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Shuyuan Chu et al.
Peptides, 90, 1-9 (2017-02-24)
Atrial natriuretic peptide (ANP) is increasingly expressed on airway and inhibits pulmonary arterial remodeling. However, the role of ANP in remodeling of respiratory system is still unclear. The role of ANP on airway remodeling and the possible mechanism was explored
L L Norling et al.
Biology of the neonate, 66(5), 294-301 (1994-01-01)
Atrial natriuretic peptide (ANP) regulates glomerular hemodynamics by interaction with biologic receptors (GC-A/ANP) that possess particulate guanylyl cyclase activity. In a previous study we have shown a developmental difference in glomerular response to ANP where preweaned glomeruli produced significantly less
Norikazu Kiguchi et al.
The Journal of pharmacology and experimental therapeutics, 356(3), 596-603 (2015-12-17)
B-type natriuretic peptide (BNP)-natriuretic peptide receptor A (NPRA) and gastrin-releasing peptide (GRP)-GRP receptor (GRPR) systems contribute to spinal processing of itch. However, pharmacological and anatomic evidence of these two spinal ligand-receptor systems are still not clear. The aim of this
C Delporte et al.
European journal of pharmacology, 224(2-3), 183-188 (1992-12-02)
The effects of seven competitive atrial natriuretic peptide (ANP) receptor antagonists were compared on cultured human neuroblastoma NB-OK-1 cells expressing exclusively ANPA receptors, by evaluating their capacity to inhibit [125I]ANP binding and to suppress ANP-stimulated cyclic GMP elevation. In ANP
G J Trachte
The Journal of pharmacology and experimental therapeutics, 264(3), 1227-1233 (1993-03-01)
Atrial natriuretic factor (ANF) suppresses adrenergic and purinergic neurotransmission in the rabbit vas deferens. The neuromodulatory mechanism of action for ANF is not established, but is thought to be independent of cyclic GMP (cGMP) generation. This study directly tested for
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