| Identification | Back Directory | [Name]
S 17092 | [CAS]
176797-26-5 | [Synonyms]
S 17092
S 17092-1
S 17092 >=98% (HPLC)
(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
Methanone, [(2S,3aS,7aS)-octahydro-1-[[(1R,2R)-2-phenylcyclopropyl]carbonyl]-1H-indol-2-yl]-3-thiazolidinyl-
[(2S,3aS,7aS)-2-(1,3-thiazolidine-3-carbonyl)-2,3,3a,4,5,6,7,7a-octahydroindol-1-yl]-[(1R,2R)-2-phenylcyclopropyl]methanone | [Molecular Formula]
C22H28N2O2S | [MDL Number]
MFCD00948255 | [MOL File]
176797-26-5.mol | [Molecular Weight]
384.53 |
| Chemical Properties | Back Directory | [Boiling point ]
622.6±55.0 °C(Predicted) | [density ]
1.268±0.06 g/cm3(Predicted) | [storage temp. ]
2-8°C | [solubility ]
DMSO: ≥10mg/mL | [form ]
powder | [pka]
-1.12±0.20(Predicted) | [color ]
white to tan | [Optical Rotation]
[α]/D -140 to -170° in dichloromethane | [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 | [InChIKey]
NXSXRIHXEQSYEZ-KNJMJIDISA-N | [SMILES]
O=C([C@@H]1C[C@@H]2CCCC[C@@H]2N1C(=O)[C@@H]3C[C@H]3c4ccccc4)N5CCSC5 |
| Safety Data | Back Directory | [Hazard Codes ]
Xn | [Risk Statements ]
22 | [WGK Germany ]
3 | [Storage Class]
11 - Combustible Solids | [Hazard Classifications]
Acute Tox. 4 Oral |
| Hazard Information | Back Directory | [Uses]
S 17092 may be used in prolyl endopeptidase-mediated cell signaling studies. | [Biological Activity]
S-17092 is a potentselective 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 neuropeptideswhich 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 differentiationis pro-angiogenic and antifibrogenic. | [in vivo]
S 17092 (1-10 mg/kg; p.o.; 7 days) improves the performance of cognitive tasks (VDR, DMS, DA) in a dose-dependent manner in MPTP (HY-15608)-treated monkeys[1].
S 17092 (10 mg/kg; p.o.; 7 days and again 1 h before each daily memory test) alleviates the Scopolamine (HY-N0296)-induced memory deficit, improves learning and working memory performances in young, elderly and old C57BL/6 mice[1].
S 17092 (0.01-30 mg/kg; i.p.; 60 or 120 min before session 1 then 24 h later 60 or 120 min before session 2, respectively) dose-dependently increases the retention time, alleviating scopolamine-induced amnesia in rats[1].
S 17092 is a long acting PEP inhibitor (t1/2 > 9 h). The 50% inhibitory dose (ID50) for cortical PEP activity are 7.4 and 13.4 mg/kg at one hour after p.o. in Wistar rat and NMRI mouse, respectively[1].
| Animal Model: | 3-5 months old male C57BL/6 mice[1] | | Dosage: | 10 mg/kg | | Administration: | Oral gavage (p.o.); twice daily for 7 days and 60 min prior to the training sessions | | Result: | Correct responses in the experimental group were 55, 58, and 74% in sessions 1, 2, and 3, respectively. Performance in experimental group was similar to that in non-amnesic controls.
Improved learning and memory performances in young amnesic C57BL/6 mice.
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| Animal Model: | Adult male Macaca fascicularis monkeys treated with MPTP[1] | | Dosage: | 1, 3, 10 mg/kg | | Administration: | Oral gavage (p.o.); 7 days | | Result: | Significantly improved variable delayed response (VDR) performance (76.9% correct responses vs. post-MPTP only) at 3 mg/kg, but not at 1 or 10 mg/kg doses.
VDR performance tended to revert back to a normal delay-dependent pattern of response, performance significantly improved on shorter (2, 5, and 10 sec delay) but not on longer delay trials at the 3mg/kg dose. Improved performance on shorter delay trials was not seen with either the 1 or 10 mg/kg doses.
Significant improvements in DMS (delayed matching-to-sample) performance were observed after administration at either 3 or 10 mg/kg doses.
Significantly improved DA (delayed alternation) performance at the 3 mg/kg dose, from 79% at baseline to 90.6% after 7-days or longer treatments.
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| Animal Model: | 21-22 and 25 months old C57BL/6 mice[1] | | Dosage: | 10 mg/kg | | Administration: | Oral gavage (p.o.); 7 days and again 1 h before each daily memory test | | Result: | With correct responses of 45 and 70% in control and experimental animals, respectively, in session 5 and 46 and 65%, respectively, in session 6 in 21-22 months old C57BL/6 mice.
Had a beneficial effect on the selective deficit observed 25 months old C57BL/6 mice.
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| Animal Model: | Rats treated with scopolamine[1] | | Dosage: | 0.01-30 mg/kg | | Administration: | Intraperitoneal injection (i.p.); 60 or 120 min before session 1 then 24 h later 60 or 120 min before session 2, respectively | | Result: | Dose-dependently increased the retention time, alleviating scopolamine-induced amnesia.
The maximum effect using 10 mg/kg with the 60 min pretest dosing interval was achieved using 3 mg/kg in the 120 min tests, suggesting that brain neuropeptide turnover may have been increased by increasing the time interval between the administration and the test.
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| Company Name: |
Energy Chemical
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| Telephone: |
400-0056266 |
| Website: |
www.energy-chemical.com |
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