2. Others NF-κB Metabolic Enzyme/Protease Immunology/Inflammation
  3. Drug Derivative Reactive Oxygen Species (ROS)
  4. Glutathione monoethyl ester

Glutathione monoethyl ester is a glutathione derivative that can be transported into cells and hydrolyzed into glutathione. Glutathione monoethyl ester downregulates the gene expression of TEN1 and CTC1 while upregulating TERT expression. Glutathione monoethyl ester enhances telomerase activity, promotes proliferation and differentiation in aged bone marrow stromal cells, while elevating glutathione levels and reducing oxidative stress, protein aggregation and cell death in motor neuronal cells. Glutathione monoethyl ester confers broad multi-organ protection against cerebral ischemia, renal injury, liver damage, and pancreatitis. Glutathione monoethyl ester can be used for the research of amyotrophic lateral sclerosis, stroke, acute renal failure, liver injury, and acute pancreatitis.

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Glutathione monoethyl ester

Glutathione monoethyl ester Chemical Structure

CAS No. : 118421-50-4

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Glutathione monoethyl ester Related Antibodies

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Description

Glutathione monoethyl ester is a glutathione derivative that can be transported into cells and hydrolyzed into glutathione. Glutathione monoethyl ester downregulates the gene expression of TEN1 and CTC1 while upregulating TERT expression. Glutathione monoethyl ester enhances telomerase activity, promotes proliferation and differentiation in aged bone marrow stromal cells, while elevating glutathione levels and reducing oxidative stress, protein aggregation and cell death in motor neuronal cells. Glutathione monoethyl ester confers broad multi-organ protection against cerebral ischemia, renal injury, liver damage, and pancreatitis. Glutathione monoethyl ester can be used for the research of amyotrophic lateral sclerosis, stroke, acute renal failure, liver injury, and acute pancreatitis[1][2][3][4][5][6].

In Vitro

Glutathione monoethyl ester (1-3 mM; 24 h) treatment of aged rat BMSCs significantly increases cell proliferation at 2 mM[1].
Glutathione monoethyl ester (2 mM; 24 h) treatment of aged rat BMSCs significantly increases absolute telomere length to 628.68 kb per diploid genome[1].
Glutathione monoethyl ester (2 mM; 24 h) treatment of aged rat BMSCs significantly increases relative TERT expression and decreases relative CTC1 and TEN1 expression, while leaving TERC and STN1 expression unchanged[1].
Glutathione monoethyl ester (2 mM; 24 h) treatment of aged rat BMSCs significantly increases relative telomerase activity[1].
Glutathione monoethyl ester (2 mM; 24 h) treatment of aged rat BMSCs significantly increases differentiation potential, as shown by higher percentages of nestin-positive neural stem cells, ChAT-positive cholinergic neuron-like cells, and NF160-positive cholinergic neuron-like cells[1].
Glutathione monoethyl ester (5 mM) prevents Ethacrynic acid (HY-B1640)‑induced GSH depletion, ROS accumulation, and TDP‑43 nuclear clearance within 5 h, and restores GSH levels, reduces oxidative stress, prevents cell death, and normalizes TDP‑43 localization and GAPDH expression within 72 h in mouse motor neuron‑like NSC‑34 cells[2].

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

Glutathione monoethyl ester Related Antibodies

Cell Proliferation Assay[1]

Cell Line: third-passage aged rat bone marrow stromal cells (BMSCs)
Concentration: 1 mM; 2 mM; 3 mM
Incubation Time: 24 h
Result: Increased cell count to 43,000 cells at 2 mM concentration compared to untreated control (29,000 cells).
Produced no significant change in cell count at 1 mM and 3 mM concentrations.

Real Time qPCR[1]

Cell Line: aged rat bone marrow stromal cells (BMSCs)
Concentration: 2 mM
Incubation Time: 24 h
Result: Increased absolute telomere length to 628.68 kb per diploid genome compared to untreated control (283.95 kb per diploid genome).
Increased relative TERT gene expression to 0.65.
Decreased relative CTC1 gene expression to 0.76.
Decreased relative TEN1 gene expression to 0.77.
Produced no significant change in relative TERC or STN1 gene expression.

Cell Differentiation Assay[1]

Cell Line: aged rat bone marrow stromal cells (BMSCs)
Concentration: 2 mM
Incubation Time: 24 h
Result: Increased the percentage of nestin-positive neural stem cells.
Increased the percentage of choline acetyltransferase (ChAT)-positive cholinergic neuron-like cells.
Increased the percentage of neurofilament 160 (NF160)-positive cholinergic neuron-like cells.
In Vivo

Glutathione monoethyl ester (1 mmol/h; intracerebroventricular infusion; continuously; 2 hours of ischaemia plus 48 hours of reperfusion) produces significant neuroprotection in a rat model of transient focal cerebral ischaemia[3].
Glutathione monoethyl ester (2 g/kg; i.p.; single dose; 2 hours before mercuric chloride exposure) moderates mercuric chloride-induced acute renal failure in male Sprague-Dawley rats, preserving creatinine clearance, reducing tubular injury markers, and decreasing renal cortical necrosis severity, while altering early tissue mercury distribution[4].
Glutathione monoethyl ester (2 g/kg; i.p.; single dose) significantly elevates renal cortical and hepatic glutathione content in healthy male Sprague-Dawley rats without altering renal function, while inducing prominent proximal tubular vacuolization[4].
Glutathione monoethyl ester (10 mmol/kg; i.p.; 1 hour before lipopolysaccharide, then every 4 hours thereafter) increases hepatic and mitochondrial glutathione levels, reduces lipopolysaccharide-induced liver enzyme elevation, reactive oxygen intermediate production, and mitochondrial dysfunction, and maintains near 100% survival in endotoxemic mice[5].
Glutathione monoethyl ester (i.p.; three doses at timed intervals) significantly blunts pancreatic glutathione depletion, eliminates pancreatic necrosis and inflammation, and reduces serum amylase elevations in a mouse model of Caerulein (HY-A0190)-induced acute pancreatitis[6].

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

Animal Model: Sprague-Dawley (male, 270-300 g)[3]
Dosage: 1 mmol/h
Administration: intracerebroventricular infusion; continuously; 2 hours of ischaemia plus 48 hours of reperfusion
Result: Reduced overall infarct size to 16% of the total ischaemic hemispher.
Reduced striatal infarct size to 10% of total striatal volume.
Reduced cortical infarct size to 26% of total cortical volume.
Animal Model: Sprague-Dawley (male, 200-250 g body weight, mercuric chloride-induced)[4]
Dosage: 2 g/kg
Administration: i.p.; single dose (2 hours before mercuric chloride exposure)
Result: Maintained creatinine clearance and reduced fractional excretion of sodium and lysozyme in time-dependent manners.
Minimized renal tubular necrosis and induced prominent proximal tubular vacuolization in all rats.
Altered tissue mercury distribution at 3 hours but showed no changes at 24 hours post‑treatment.
Animal Model: Sprague-Dawley (male, 200-250 g body weight)[4]
Dosage: 2 g/kg
Administration: i.p.; single dose
Result: Elevated renal cortical glutathione levels in a time-dependent manner and restored hepatic glutathione to baseline rapidly.
Showed no alterations in renal function indicators relative to control rats.
Induced marked proximal tubular vacuolization of varying degrees in all rats at 24 hours post-treatment.
Animal Model: ICR mice (5-week-old, female)[5]
Dosage: 10 mmol/kg
Administration: i.p.; 1 hour before lipopolysaccharide, then every 4 hours thereafter
Result: Boosted hepatic total and mitochondrial glutathione levels at 3 hours post-lipopolysaccharide injection.
Lowered plasma liver enzyme levels and reduced reactive oxygen intermediate production while preserving mitochondrial membrane potential at 6 hours.
Attenuated mitochondrial permeability transition and maintained nearly 100% survival at 48 hours under high-dose lipopolysaccharide challenge.
Animal Model: Swiss Webster (female, 12-14 g)[6]
Dosage: 20 mmol/kg (1 h before first caerulein dose); 10 mmol/kg (3 h after first caerulein dose); 10 mmol/kg (7 h after first caerulein dose)
Administration: i.p.; three doses at timed intervals
Result: Blunted caerulein-induced pancreatic glutathione depletion and maintained a higher glutathione level at 4 hours.
Prevented pancreatic necrosis and inflammation with only mild histopathological changes at 8 hours.
Significantly reduced serum amylase levels across all time points after caerulein injection.
Molecular Weight

335.38

Formula

C12H21N3O6S
CAS No.
SMILES

OC(CNC([C@H](CS)NC(CC[C@H](N)C(O)=O)=O)=O)=O.CCO
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Storage

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References
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Glutathione monoethyl ester Related Classifications

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  • 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:

Glutathione monoethyl ester118421-50-4Drug DerivativeReactive Oxygen Species (ROS)Drug derivativemercuric chloridelipopolysaccharidemotor neuronal cellsTEN1TERTglutathionebone marrow stromal cellsrat transient focal cerebral ischaemiacholinergic neuronCTC1Inhibitorinhibitorinhibit

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