2. Neuronal Signaling Membrane Transporter/Ion Channel Stem Cell/Wnt PI3K/Akt/mTOR Metabolic Enzyme/Protease TGF-beta/Smad
  3. Amyloid-β Cholinesterase (ChE) Calcium Channel GSK-3 Tau Protein Phosphatase Akt PKA
  4. SCR1693

SCR1693 is a selective, reversible, orally active and noncompetitive inhibitor of AChE (IC50 = 0.68 μM) as well as a calcium channel blocker. SCR1693 reduces tau phosphorylation levels, and inhibits the generation and release of Aβ. SCR1693 restores insulin signaling and improves cognitive deficits. SCR1693 can be used for the study of Alzheimer's disease, especially which complicated with type 2 diabetes mellitus.

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SCR1693

SCR1693 Chemical Structure

CAS No. : 1442559-20-7

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SCR1693 Related Antibodies

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AChE BChE

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N-type calcium channel L-type calcium channel P/Q-type calcium channel T-type calcium channel Calcium Channel

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GSK-3 GSK-3α GSK-3β

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Akt Akt1 Akt2 Akt3

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PKA PKAR PKACα

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Description

SCR1693 is a selective, reversible, orally active and noncompetitive inhibitor of AChE (IC50 = 0.68 μM) as well as a calcium channel blocker. SCR1693 reduces tau phosphorylation levels, and inhibits the generation and release of Aβ. SCR1693 restores insulin signaling and improves cognitive deficits. SCR1693 can be used for the study of Alzheimer's disease, especially which complicated with type 2 diabetes mellitus[1][2][3].

IC50 & Target[1]

AChE

 

In Vitro

SCR1693 (0.4-5 μM, 24 h) reduces total and phosphorylated tau levels in HEK293/tau cells[1].
SCR1693 (0.8-20 μM, 6 h) induces tau dephosphorylation and increases total tau levels in HEK293/tau cells with short-term treatment[1].
SCR1693 (0.4-4 μM, 24 h) inhibits Aβ generation and release in N2a/APP cells[1].
SCR-1693 (3.3-30 μM, 6 h) downregulates tau phosphorylation mainly by regulating its phosphatases in Neuro-2a-tau cells[2].
SCR-1693 (10 μM , 6 h) activates PKA/Akt, inhibits GSK-3β, and enhances PP2A/PP1 activity in Neuro-2a-tau cells[2].
SCR-1693 (10 μM, 6 h) reduces insulin resistance by regulating PP1/PP2A in Neuro-2a-tau cells[2].
SCR-1693 (0.004-2.5 μM, 48 h) inhibits Aβ25-35 (HY-P0128)-induced SH-SY5Y cell death[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

SCR1693 Related Antibodies

Western Blot Analysis[1]

Cell Line: HEK293/tau cells
Concentration: 0.4, 2, 5 μM
Incubation Time: 24 h
Result: Increased tau dephosphorylation level at Ser198/199/202 sites (Tau 1 epitope) concentration dependently.
Reduced total tau level significantly at 5 μM.

Western Blot Analysis[1]

Cell Line: HEK293/tau cells
Concentration: 0.8, 4, 20 μM
Incubation Time: 6 h
Result: Induced tau dephosphorylation at Ser198/199/202 (Tau-1) sites and increased total tau level (4 μM and 20 μM).

Western Blot Analysis[2]

Cell Line: Neuro-2a-tau cells
Concentration: 3.3, 10, 30 μM
Incubation Time: 6 h
Result: Decreased tau phosphorylation levels at the sites of Ser199/202, Ser202/T205, T212/Ser214, Thr231, Ser262 and Ser356, rather than Ser422,and increased tau dephosphorylation level.
Activated PKA and Akt, and inhibited GSK-3β activation.
Decreased the negatively regulated phosphorylation of PP2AC and PP1 at the site of Tyr307 and Thr320, respectively.
Enhanced PP2A and PP1 activity.
Enlarged insulin signaling, especially p-IRS-1 Tyr632 and p-Akt Ser473.
In Vivo

SCR1693 (1-4 mg/kg, i.g., once daily, 20 days) attenuates intracerebroventricular Streptozotocin (STZ) (HY-13753) induced cognitive deficits in rats[2].
SCR1693 (3-30 mg/kg, p.o. single dose) dose-dependently causes the inhibition of brain homogenate AChE activity in wistar rats[3].
SCR1693 (0.1-1 mg/kg, p.o., once daily, 12 days) improves spatial memory in Aβ25-35-treated mice [3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: STZ (3 mg/kg) was administered intracerebroventricularly twice in male wistar rats (220-250 g)[2]
Dosage: 1, 2, 4 mg/kg
Administration: i.g., once daily for 20 days
Result: Shortened STZ-injection induced lengthening of escape latency during the training period.
Showed a significant improvement of behavioral performance in the probe trails test.
Restored the levels of GPAF and PSD-95.
Decreased STZ-induced tau hyperphosphorylation in hippocampus of rats.
Decreased deactivated phosphorylation of PP1 and PP2A in a dose-dependent manner.
Animal Model: A single intracerebroventricular (icv) injection of aggregated Aβ25-35 in mice[3]
Dosage: 0.1, 0.3, 1 mg/kg
Administration: p.o. once daily for 12 days
Result: Improved Aβ25-35-impaired learning and both long-term and short-term memory and its effects were stronger than Donepezil (HY-14566) and Memantine (HY-B0591).
Decreased AChE activity.
Prevented Aβ25-35-induced loss of hippocampal pyramidal cells.
Protected hippocampal synaptic transmission and LTP.
Regulated hippocampal protein phosphorylation in Aβ25–35-treated mice.
Molecular Weight

425.95

Formula

C24H28ClN3O2
CAS No.
SMILES

O=C(C1=C(C)N=C2NC3=C(CC(C)(CC3)C)C(N)=C2C1C4=C(Cl)C=CC=C4)OCC
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Room temperature in continental US; may vary elsewhere.
Storage

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Purity & Documentation
References
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SCR1693 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

SCR16931442559-20-7SCR 1693SCR-1693Amyloid-βCholinesterase (ChE)Calcium ChannelGSK-3Tau ProteinPhosphataseAktPKAβ-amyloid peptideAβAbetaCa2+ channelsCa channelsGlycogen synthase kinase-3Glycogen synthase kinase 3PKBProtein kinase BProtein kinase AAlzheimer's diseasetauAChEtype 2 diabetesNeura-2a-tau cellsHEK293/tau cellsInhibitorinhibitorinhibit

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