| Identification | Back Directory | [Name]
Ethyl 8'-methyl-2',4-dioxo-2-(piperidin-1-yl)-2'H-spiro[cyclopent[2]ene-1,3'-imidazo[1,2-a]pyridine]-3-carboxylate | [CAS]
1256269-87-0 | [Synonyms]
SAK3 >=98% (HPLC)
Ethyl 8'-methyl-2',4-dioxo-2-(piperidin-1-yl)-2'H-spiro[cyclopent[2]ene-1,3'-imidazo[1,2-a]pyridine]-3-carboxylate | [Molecular Formula]
C20H23N3O4 | [MOL File]
1256269-87-0.mol | [Molecular Weight]
369.41 |
| Chemical Properties | Back Directory | [Boiling point ]
539.3±60.0 °C(Predicted) | [density ]
1.37±0.1 g/cm3(Predicted) | [storage temp. ]
Store at 4°C | [solubility ]
Soluble in DMSO | [form ]
Solid | [pka]
3.36±0.20(Predicted) | [color ]
White to off-white | [InChIKey]
WZHBYTVHUFURPY-UHFFFAOYSA-N | [SMILES]
O=C(OCC)C1=C(C2(CC1=O)N3C=CC=C(C3=NC2=O)C)N4CCCCC4 |
| Hazard Information | Back Directory | [Uses]
SAK3 is a potent CaV3.1 and CaV3.3 activator. Enhances CaV3.1 and CaV3.3, but not CaV3.2 activity at concentrations of 0.01 - 10 M in neuro2A cells in vitro. Elevates ACh levels in hippocampus. Rescues impaired memory-related behaviors in OBX mice. Orally bioavailable. | [Biological Activity]
SAK3 is a potent and orally active spiroimidazopyridine derivative th at enhances Cav3.1 and Cav3.3but not Cav3.2T-type voltage-gated Ca2+ channel (T-VGCC) activity (∼20% peak current increase with 0.1 nM SAK3 by whole-cell patch-clamp using human Cav3.1 or Cav3.3 transfected neuro2A; no effect up to 10 nM using Cav3.2 transfectant). Acute SAK3 oral administration (0.5 mg/kg) significantly enhances hippocampal CA1 region acetylcholine (ACh) release in na?ve miceas well as increases hippocampal ACh levels and improves memory deficits among olfactory-bulbectomized (OBX) mice. Daily SAK3 oral administration 24 hrs following hypothyroidism induction by methimazole (MMI) is efficacious against MMI-induced medial septum (MS) cholinergic neurons loss (0.5-1 mg/kg/day) and cognitive deficits (1 mg/kg/day). | [in vivo]
Acute SAK3 (0.5 mg/kg) oral administration promotes acetylcholine (ACh) release in hippocampal CA1 via T-VGCC stimulation via enhancing T-type Ca2+ channel[1]. | Animal Model: | Animal Model:Cav3.1 knockout (KO) mice[1] | | Dosage: | 0.5 mg/kg | | Administration: | Administered p.o. | | Result: | Significantly increased ACh release in CA1, peaking at 20 min after oral administration.
|
| [IC 50]
T-type calcium channel | [storage]
Store at 4°C |
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| Company Name: |
BOC Sciences
|
| Tel: |
|
| Website: |
https://www.bocsci.com |
| Company Name: |
Energy Chemical
|
| Tel: |
021-58432009 400-005-6266 |
| Website: |
http://www.energy-chemical.com |
| Company Name: |
Merck KGaA
|
| Tel: |
21-20338288 |
| Website: |
www.sigmaaldrich.cn |
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