2. Autophagy Neuronal Signaling
  3. Autophagy Amyloid-β Tau Protein
  4. F-SLOH

F-SLOH is a brain-penerant and orally active TFEB activator and amyloid-β inhibitor with an IC50 of 3.4 μM against amyloid-β. F-SLOH promotes nuclear translocation of TFEB, driving autophagy and lysosomal biogenesis. F-SLOH reduces amyloid-β oligomers and Tau aggregates via autophagy lysosomal degradation pathway. F-SLOH can be used for the research of Alzheimer’s disease.

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F-SLOH

F-SLOH Chemical Structure

CAS No. : 1620896-55-0

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F-SLOH Related Antibodies

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Description

F-SLOH is a brain-penerant and orally active TFEB activator and amyloid-β inhibitor with an IC50 of 3.4 μM against amyloid-β. F-SLOH promotes nuclear translocation of TFEB, driving autophagy and lysosomal biogenesis. F-SLOH reduces amyloid-β oligomers and Tau aggregates via autophagy lysosomal degradation pathway. F-SLOH can be used for the research of Alzheimer’s disease[1].

In Vitro

F-SLOH potently inhibits Aβ fibril formation in a cell-free biochemical assay with an IC50 of 3.4 μM[1].
F-SLOH (12.5-200 μM) exhibits low cytotoxicity in N2a-APP cells, with significant toxicity only observed at 200 μM[1].
F-SLOH (6.25-50 μM) dose-dependently reduces Aβ1-40 and Aβ1-42 levels in the media of N2a-APP cells[1].
F-SLOH (6.25-25 μM; 24 h) dose-dependently reduces full-length APP and CTFs protein levels in N2a-APP cells after 24 h of treatment[1].
F-SLOH reduces full-length APP levels in N2a-APP cells via a lysosomal degradation pathway[1].
F-SLOH (6.25-25 μM; 24 h) dose-dependently induces TFEB nuclear translocation in cultured microglial cells after 24 h of treatment[1].
F-SLOH (6.25-25 μM; 24 h) dose-dependently induces autophagy in HT-22 cells[1].
F-SLOH (6.25-25 μM; 24 h) dose-dependently promotes lysosomal biogenesis in HT-22 cells after 24 h of treatment[1].
F-SLOH (25 μM; 24 h) promotes autophagy flux and autophagosome-lysosome fusion in HT-22 cells stably expressing tf-LC3[1].
F-SLOH (24 h) increases lysosome number in HT-22 cells[1].
F-SLOH (6.25-25 μM；1-24 小时) inhibits the MAPK1/ERK2 pathway in HT-22 cells in both a dose-dependent and time-dependent manner[1].

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

F-SLOH Related Antibodies

Western Blot Analysis[1]

Cell Line: N2a-APP cells (N2a cells overexpressing APP695)
Concentration: 6.25 μM; 12.5 μM; 25 μM
Incubation Time: 24 h
Result: Dose-dependently reduced protein levels of full-length APP and its metabolite CTFs.
Caused significant reductions at all tested concentrations relative to control.

Western Blot Analysis[1]

Cell Line: HT-22 cells
Concentration: 6.25 μM; 12.5 μM; 25 μM
Incubation Time: 24 h
Result: Dose-dependently increased LC3-II protein levels, indicating induction of autophagy.
Effect was comparable to the positive control Torin1.\nDose-dependently increased protein levels of LAMP1 and mature Cathepsin D, indicating promotion of lysosomal biogenesis.
Effect was comparable to the positive control Torin1.

Western Blot Analysis[1]

Cell Line: HT-22 cells
Concentration: 6.25 μM; 12.5 μM; 25 μM
Incubation Time: 1 h; 2 h; 4 h; 6 h; 8 h; 24 h
Result: Dose-dependently reduced phospho-TFEB (S142) levels over 24 h.
Time-dependently reduced phospho-TFEB (S142) levels over 1-8 h.
Increased total TFEB levels, indicating TFEB dephosphorylation.
Dose-dependently reduced phospho-ERK1/2 and phospho-MEK levels over 24 h.
Time-dependently reduced phospho-ERK1/2 and phospho-MEK levels over 0-8 h.
Indicated inhibition of the MAPK1/ERK2 pathway.
Parmacokinetics
Species Dose Route Cmax Tmax
Mice[1] 20 mg/kg i.p. 81.134 ng/g 1 h
In Vivo

F-SLOH (10-20 mg/kg; i.p.; alternate days; 4 months) dose-dependently reduces Alzheimer's disease pathology, improves cognitive function, and activates TFEB-mediated autophagy-lysosomal pathway in 5XFAD mice[1].
F-SLOH (10-20 mg/kg; p.o.; ad libitum; 6 months) dose-dependently reduces Alzheimer's disease pathology, improves cognitive function, and activates TFEB-mediated autophagy-lysosomal pathway in 3XTg-AD mice[1].
F-SLOH (10-20 mg/kg; 1 week) activates TFEB-mediated autophagy-lysosomal pathway in wild-type mice without causing body weight changes[1].

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

Animal Model: C57BL/6 (heterozygous 5XFAD transgenic, 2 months old, male/female)[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: i.p.; alternate days; 4 months
Result: Reduced levels of Aβ monomers (Aβ1-40, Aβ1-42), Aβ oligomers, and Aβ plaques in soluble and insoluble brain fractions.
Reduced full-length APP and its CTF metabolites.
Reduced astrocytic activation (GFAP staining) and microgliosis (Iba1 staining).
Increased hippocampal-dependent memory, as shown by prolonged freezing time in contextual fear conditioning tests relative to vehicle-treated mice.
Increased synaptic formation and postsynaptic density protein 95 (PSD-95)/synaptophysin expression.
Activated TFEB, increasing nuclear TFEB translocation, LC3B-II levels, LAMP1 levels, and mature cathepsin D levels to promote autophagy and lysosomal biogenesis.
Increased lysosome and autolysosome formation in hippocampal tissue.
Animal Model: B6;129 (female heterozygous 3XTg-AD transgenic, 6-12 months old, N=8 per group)[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: p.o.; 6 months
Result: Reduced levels of Aβ monomers (Aβ1-40, Aβ1-42), Aβ oligomers, and Aβ plaques in soluble and insoluble brain fractions.
Reduced full-length APP and its CTF metabolites.
Reduced insoluble phosphorylated Tau (AT8, PHF1, CP13, MC1, HT7) levels and AT8/HT7-positive neuron load.
Reduced astrocytic activation (GFAP staining) and microgliosis (Iba1 staining).
Rescued learning impairment (shorter escape latency in Morris water maze), improved spatial memory (increased time spent in target quadrant during probe trial), and increased hippocampal-dependent memory (prolonged freezing time in contextual fear conditioning tests) relative to vehicle-treated mice.
Improved exploratory and locomotor function in open-field tests.
Increased dendritic spine density and postsynaptic density protein 95 (PSD-95)/synaptophysin expression.
Activated TFEB, increasing nuclear TFEB translocation, LC3B-II levels, LAMP1 levels, and mature cathepsin D levels to promote autophagy and lysosomal biogenesis.
Animal Model: C57BL/6 (wild-type, N=8 per group)[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: 1 week
Result: Increased nuclear TFEB translocation, reduced cytoplasmic TFEB levels, and increased LC3B-II, LAMP1, and mature cathepsin D levels in brain tissue to promote autophagy and lysosomal biogenesis.
Showed no significant change in mouse body weight.
Molecular Weight

521.02

Formula

C30H30ClFN2O3
CAS No.
SMILES

COCCOCCN1C2=CC=C(/C=C/C3=CC=[N+](CCO)C4=C3C=CC=C4)C=C2C5=CC(F)=CC=C51.[Cl-]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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F-SLOH 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:

F-SLOH1620896-55-0AutophagyAmyloid-βTau Proteinβ-amyloid peptideAβAbeta5XFAD micelysosomal biogenesisAlzheimer’s diseaseMAPK1/ERK2 pathwayTFEBautophagyN2a-APP cellsHT-22 cells3XTg-AD miceamyloid-βInhibitorinhibitorinhibit

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