2. Immunology/Inflammation Stem Cell/Wnt MAPK/ERK Pathway PI3K/Akt/mTOR Autophagy
  3. PD-1/PD-L1 ERK mTOR Autophagy
  4. Acesulfame

Acesulfame is a synthetic sweetener. Long-term use of Acesulfame can affect cognitive function. Acesulfame potassium can suppress autophagic degradation of PD-L1 in RIL-175 and SK-Hep1 cells through the ERK1/2-mTORC1-ULK1 pathway, which may be related to immune evasion in cancer cells. Acesulfame can be used in research on neurological diseases, metabolic disorders, cancer, and immune evasion.

For research use only. We do not sell to patients.

Acesulfame

Acesulfame Chemical Structure

CAS No. : 33665-90-6

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Acesulfame Related Antibodies

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Description

Acesulfame is a synthetic sweetener. Long-term use of Acesulfame can affect cognitive function. Acesulfame potassium can suppress autophagic degradation of PD-L1 in RIL-175 and SK-Hep1 cells through the ERK1/2-mTORC1-ULK1 pathway, which may be related to immune evasion in cancer cells. Acesulfame can be used in research on neurological diseases, metabolic disorders, cancer, and immune evasion[1][2][3][4].

In Vitro

Acesulfame (1 mM, 24 hours) upregulates PD-L1 protein levels in RIL-175 and SK-Hep1 cells[2].
Acesulfame (1 mM, 24 hours) increases granzyme B production in RIL-175 and SK-Hep1 cells co-cultured with T cells[2].
Acesulfame (1 mM, 24 hours) activates ERK1/2-mTORC1-ULK1 pathway to suppress autophagic degradation of PD-L1 in RIL-175 and SK-Hep1 cells[2].
. Acesulfame (5-25 mM, 24 hours) inhibites mitochondrial metabolism in SH-SY5Y cells[4].
Acesulfame (5-25 mM, 24 hours) inhibites ATP production in cells and reduced phosphorylation of neuroprotective proteins, impaires energy metabolism and neuroprotective functions in SH-SY5Y cells[4].

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

Acesulfame Related Antibodies

Western Blot Analysis[2]

Cell Line: RIL-175 (mouse hepatocellular carcinoma), SK-Hep1 (human hepatocellular carcinoma)
Concentration: 1 mM
Incubation Time: 24 hours
Result: Significantly increased PD-L1 protein levels.

Cell Viability Assay[4]

Cell Line: SH-SY5Y (neuroblastoma cells)
Concentration: 5-25 mM
Incubation Time: 24 hours
Result: Reduced the extracellular acidification rate (ECAR) in SH-SY5Y cells.
In Vivo

Acesulfame (37.5 mg/kg, p.o., once daily for 4 weeks) increases body weight in male CD-1 mice and altered their gut microbiome composition[3].
Acesulfame (12.5 mM, administered via drinking water for 40 weeks) affects the neurometabolic functions in C57BL/6J mice[4].

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

Animal Model: CD-1 mice (male and female)[3]
Dosage: 37.5 mg/kg
Administration: Oral gavage (p.o.), once daily for 4 weeks
Result: Increased body weight in male CD-1 mice.
Significantly altered the gut microbiome composition in both male and female mice.
Animal Model: C57BL/6J mice[3]
Dosage: 12.5 mM
Administration: Administered via drinking water, once daily for 40 weeks
Result: Significant increase in fasting blood glucose and insulin levels in treated mice, without altering insulin sensitivity.
Molecular Weight

163.15

Formula

C4H5NO4S
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C1C=C(C)OS(=O)(N1)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
In solvent -80°C 6 months
-20°C 1 month
Purity & Documentation
References
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Acesulfame 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:

Acesulfame33665-90-6PD-1/PD-L1ERKmTORAutophagyPD-1/Programmed death-ligand 1Extracellular signal regulated kinasesMammalian target of RapamycinSweetenercognitive functionsneuro-metabolicInhibitorinhibitorinhibit

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