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Merck

SML0181

Sigma-Aldrich

S 17092

≥98% (HPLC)

别名:

(2S,3aS,7aS)-1-(((R,R)-2-Phenylcyclopropyl)carbonyl)-2-((thiazolidin-3-yl)carbonyl)octahydro-1H-indole, [(2S,3aS,7aS)-Octahydro-1-[[(1R,2R)-2-phenylcyclopropyl]carbonyl]-1H-indol-2-yl]-3-thiazolidinyl--methanone

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About This Item

经验公式(希尔记法):
C22H28N2O2S
分子量:
384.53
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77

化驗

≥98% (HPLC)

形狀

powder

光學活性

[α]/D -140 to -170° in dichloromethane

顏色

white to tan

溶解度

DMSO: ≥10 mg/mL

儲存溫度

2-8°C

SMILES 字串

O=C([C@@H]1C[C@@H]2CCCC[C@@H]2N1C(=O)[C@@H]3C[C@H]3c4ccccc4)N5CCSC5

InChI

1S/C22H28N2O2S/c25-21(18-13-17(18)15-6-2-1-3-7-15)24-19-9-5-4-8-16(19)12-20(24)22(26)23-10-11-27-14-23/h1-3,6-7,16-20H,4-5,8-14H2/t16-,17-,18+,19-,20-/m0/s1

InChI 密鑰

NXSXRIHXEQSYEZ-KNJMJIDISA-N

應用

S 17092 may be used in prolyl endopeptidase-mediated cell signaling studies.

生化/生理作用

S-17092 is a potent, selective inhibitor of Prolyl oligopeptidase (POP), also known as prolyl endopeptidase (PEP or PE). Ki=1.5 nM. Nootropic.

S-17092 inhibition of POP prevents breakdown and thus increases the activity of a number of neuropeptides, which is likely the basis for its nootropic activity. S 17092 has been shown to improve cognition. It improved cognitive task performance in chronic low dose MPTP-treated monkeys. S-17092 was recently used to inhibit the formation of AcSDKP from its precursor 43-mer thymosin ?4 (T?4). Ac-SDKP is involved in hemopoietic stem cell differentiation, is pro-angiogenic and antifibrogenic.

特點和優勢

This compound is featured on the Neuropeptidases page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

象形圖

Exclamation mark

訊號詞

Warning

危險聲明

危險分類

Acute Tox. 4 Oral

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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访问文档库

Sokrates Stein et al.
Cardiovascular research, 117(4), 1060-1069 (2020-05-14)
Fibroblast activation protein (FAP) is upregulated at sites of tissue remodelling including chronic arthritis, solid tumours, and fibrotic hearts. It has also been associated with human coronary atherosclerotic plaques. Yet, the causal role of FAP in atherosclerosis remains unknown. To
Tommi P Kilpeläinen et al.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 128, 110253-110253 (2020-05-25)
Previous studies have shown that prolyl oligopeptidase (PREP) negatively regulates autophagy and increases the aggregation of alpha-synuclein (αSyn), linking it to the pathophysiology of Parkinson's disease. Our earlier results have revealed that the potent small molecular PREP inhibitor KYP-2047 is
Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice.
Kim JD, Toda C, D'Agostino G, et al.
Proceedings of the National Academy of Sciences of the USA, 111(32), 11876-11881 (2014)

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