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Merck

SML2908

A71915 trifluoroacetate

≥95% (HPLC)

동의어(들):

(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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크기 선택

제품정보 (DICE 배송 시 비용 별도)

실험식(Hill 표기법):
C69H116N26O15S2 · xC2HF3O2
CAS 번호:
132956-87-7
Molecular Weight:
1613.95 (free base basis)
NACRES:
NA.77
UNSPSC Code:
12352200

주요 문서

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기술 서비스
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도움 문의

assay

≥95% (HPLC)

form

powder

color

white to off-white

storage temp.

−20°C

Quality Level

100

Biochem/physiol Actions

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.
Atrial natriuretic peptide A (ANP, NPPA) receptor (NPR1, ANPRA, NPRA) antagonist with in vitro and in vivo efficacy.

저장 등급

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

가장 최신 버전 중 하나를 선택하세요:

시험 성적서(COA)

Lot/Batch Number
0000139665
0000139665
0000133526

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COA 검색

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문서 라이브러리에서 최근에 구매한 제품에 대한 문서를 찾아보세요.

문서 라이브러리 방문

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
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
Jun Zhao et al.
Journal of the renin-angiotensin-aldosterone system : JRAAS, 17(1), 1470320315627409-1470320315627409 (2016-03-25)
The objective of this article is to investigate the possible role of atrial natriuretic peptide (ANP) in Angiotensin-(1-7) (Ang-(1-7)) signaling pathway on atrial electrical and structural remodeling in a chronic rapid atrial pacing canine model. Twenty-four dogs were randomly assigned
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
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
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