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  3. Sodium acetate trihydrate, 99.5%

Sodium acetate trihydrate, 99.5% is a short-chain fatty acid salt with multiple biological activities. Sodium acetate trihydrate, 99.5% serves as a direct precursor of acetyl-CoA, and it extensively affects gene expression by promoting histone acetylation. Sodium acetate trihydrate, 99.5% can activate the p38 MAPK pathway to induce cancer cell apoptosis. Sodium acetate trihydrate, 99.5% can activate the Wnt/β-catenin signaling pathway to stimulate the proliferation and migration of cecal epithelial cells, thereby improving intestinal health. Sodium acetate trihydrate, 99.5% alleviates lead accumulation and oxidative damage by upregulating the testosterone-dependent eNOS/NO/cGMP signaling pathway, as well as activating the Nrf2/HO-1 pathway and its downstream antioxidant enzymes.

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Sodium acetate trihydrate, 99.5%

Sodium acetate trihydrate, 99.5% Chemical Structure

CAS No. : 6131-90-4

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Description

Sodium acetate trihydrate, 99.5% is a short-chain fatty acid salt with multiple biological activities. Sodium acetate trihydrate, 99.5% serves as a direct precursor of acetyl-CoA, and it extensively affects gene expression by promoting histone acetylation. Sodium acetate trihydrate, 99.5% can activate the p38 MAPK pathway to induce cancer cell apoptosis. Sodium acetate trihydrate, 99.5% can activate the Wnt/β-catenin signaling pathway to stimulate the proliferation and migration of cecal epithelial cells, thereby improving intestinal health. Sodium acetate trihydrate, 99.5% alleviates lead accumulation and oxidative damage by upregulating the testosterone-dependent eNOS/NO/cGMP signaling pathway, as well as activating the Nrf2/HO-1 pathway and its downstream antioxidant enzymes[1][2][3][4][5].

In Vitro

Sodium acetate trihydrate (1-5%; 1 h) exerts concentration- and time-dependent anti-tumor effects on MKN1-Luc and MKN45-Luc gastric cancer cells[1].
Sodium acetate trihydrate (3%; 1 h) induces apoptosis in MKN1-Luc and MKN45-Luc gastric cancer cells in a plasma exposure time-dependent manner, with MKN45-Luc cells showing higher sensitivity, while it has no effect on normal human peritoneal mesothelial cells[1].
Sodium acetate trihydrate (3%; 12 h) induces morphological changes associated with apoptosis in MKN45-Luc gastric cancer cells, including the formation of blebs, and these changes emerge as early as 1.5 h post-treatment[1].
Sodium acetate trihydrate (3%; 1 h) activates the p38 MAPK pathway by increasing the levels of phosphorylated MKK3/MKK6 and phosphorylated p38 MAPK in MKN1-Luc and MKN45-Luc gastric cancer cells[1].
Exposure to sodium acetate trihydrate (1-5%; 1-10 min) causes time-dependent increases in the concentrations of H2O2, NO2, Na+, glucose and lactate in plasma, while the K+ level remains unchanged[1].
Sodium acetate trihydrate (2 mM; 24-48 h) promotes the proliferation and migration of primary rabbit cecal epithelial cells by activating the Wnt/β-catenin pathway. This conclusion is supported by enhanced cell proliferation, reduced scratch area, upregulated expression of proliferation-related genes, as well as changes in the phosphorylation level and nuclear localization of β-catenin[3].
Sodium acetate (10 mM; 16-24 h) trihydrate enhances NOX-independent neutrophil extracellular trap formation (NETosis) induced by the calcium ionophore A23187 in DMSO-differentiated neutrophil-like HL-60 cells, and this effect strengthens with prolonged incubation time[4].
Sodium acetate (10 mM; 24 h) trihydrate enhances extracellular DNA release in DMSO-differentiated neutrophil-like HL-60 cells induced by A23187, and this effect depends on the activity of intracellular ACSS2[4].
Sodium acetate (1-10 mM; 1-24 h) trihydrate upregulates the global histone acetylation level in DMSO-differentiated neutrophil-like HL-60 cells in a concentration- and time-dependent manner, with significant acetylation observed after treatment with 10 mM for 24 h[4].
Sodium acetate (10 mM; 24 h) trihydrate significantly increases the acetylation levels of histone H3 at H3K9 and H3K14, decreases the acetylation level at H3K18, and exerts no significant effect on the acetylation at H3K27 in DMSO-differentiated neutrophil-like HL-60 cells[4].
Sodium acetate (10 mM; 24 h) trihydrate increases histone acetylation levels in DMSO-differentiated neutrophil-like HL-60 cells, and these levels decrease rapidly within 0.5 h of stimulation with 10 μM A23187[4].
Sodium acetate (10 mM; 24 h) trihydrate enhances A23187-induced histone H3 citrullination without altering PAD4 expression in DMSO-differentiated neutrophil-like HL-60 cells[4].

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

Apoptosis Analysis[1]

Cell Line: human gastric cancer cell lines MKN1-Luc, MKN45-Luc; normal human peritoneal mesothelial cells
Concentration: 3% PASA
Incubation Time: 1 h (treatment); plasma exposure times 0, 1, 3, 5, 10 min
Result: Increased percentages of apoptotic plus dead MKN1-Luc and MKN45-Luc cells significantly at 3 min plasma exposure.
Induced ~70% apoptotic plus dead cells in MKN45-Luc cells at plasma exposure times ≥3 min, showing higher sensitivity to 3% PASA than MKN1-Luc cells.
Caused no significant change in the percentage of apoptotic and dead cells in normal peritoneal mesothelial cells at plasma exposure times ≥3 min.

Western Blot Analysis[1]

Cell Line: human gastric cancer cell lines MKN1-Luc, MKN45-Luc
Concentration: 3% PASA
Incubation Time: 10 min (plasma exposure); 1 h (treatment)
Result: Increased phosphorylated MKK3/MKK6 protein expression levels significantly in both MKN1-Luc and MKN45-Luc cells compared with control.
Increased phosphorylated p38 MAPK protein expression levels significantly in both MKN1-Luc and MKN45-Luc cells compared with control.

Western Blot Analysis[4]

Cell Line: DMSO-differentiated neutrophil-like HL-60 (nHL-60) cells
Concentration: 1 mM, 10 mM
Incubation Time: 24 h
Result: Did not alter the expression levels of ACSS2, MCT-1, or MCT-4 proteins compared to untreated controls.

Western Blot Analysis[4]

Cell Line: DMSO-differentiated neutrophil-like HL-60 (nHL-60) cells
Concentration: 1 mM, 10 mM
Incubation Time: 1 h, 24 h
Result: Increased global histone acetylation in a concentration- and time-dependent manner: minimal acetylation was observed after 1 h, while marked acetylation was detected after 24 h, with a greater effect at 10 mM compared to 1 mM.

Western Blot Analysis[4]

Cell Line: DMSO-differentiated neutrophil-like HL-60 (nHL-60) cells
Concentration: 10 mM
Incubation Time: 24 h
Result: Significantly increased acetylation at histone H3 residues H3K9 and H3K14.
Decreased acetylation at H3K18, and did not significantly alter acetylation at H3K27.

Western Blot Analysis[4]

Cell Line: DMSO-differentiated neutrophil-like HL-60 (nHL-60) cells
Concentration: 10 mM (sodium acetate); 10 μM (A23187 stimulation)
Incubation Time: 24 h (sodium acetate); 0.5 h, 1 h, 2 h (A23187 stimulation)
Result: Increased histone acetylation in nHL-60 cells, but this acetylation was rapidly reduced after A23187 stimulation, with levels dropping significantly within 0.5 h of stimulation.

Western Blot Analysis[4]

Cell Line: DMSO-differentiated neutrophil-like HL-60 (nHL-60) cells
Concentration: 10 mM (sodium acetate); 10 μM (A23187 stimulation)
Incubation Time: 24 h (sodium acetate); 3 h (A23187 stimulation for histone citrullination analysis)
Result: Significantly enhanced A23187-induced histone H3 citrullination, but did not alter the expression level of PAD4 (the enzyme responsible for histone citrullination).
In Vivo

Sodium acetate (200 mg/kg; p.o.; once daily; 28 days) trihydrate alleviates lead-induced sexual dysfunction in male Wistar rats by upregulating the testosterone-dependent eNOS/NO/cGMP signaling pathway and activating the Nrf2/HO-1 pathway[2].
Sodium acetate (2 g/kg; p.o.; ad libitum; 10 weeks) trihydrate improves growth performance and intestinal health in male New Zealand white rabbits[3].

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

Animal Model: Wistar (male, 10 weeks old, similar weights, lead acetate-induced sexual dysfunction)[2]
Dosage: 200 mg/kg/day
Administration: p.o.; daily; 28 days
Result: Improved lead-induced reductions in absolute and relative penile weight.
Decreased penile lead concentration.
Shortened prolonged mount, intromission, and ejaculation latency.
Increased reduced mount, intromission, and ejaculation frequency.
Improved reduced motivation to mate and penile reflex.
Restored penile eNOS, NO, and cGMP concentrations.
Attenuated increased penile acetylcholinesterase activity.
Increased reduced plasma LH, FSH, testosterone, and dopamine concentrations.
Blunted lead-induced increases in penile MDA and GSSG concentrations and restored GSH concentrations and GSH/GSSG ratio.
Upregulated reduced penile GR, GPx, GST, SOD, and catalase activities.
Restored reduced penile Nrf2 and HO-1 concentrations.
Minimized penile vascular congestion compared to lead-only treated rats.
Animal Model: New Zealand White (male, 35 days old, 1.70 kg)[3]
Dosage: 2 g/kg
Administration: oral; ad libitum; 10 weeks
Result: Improved growth performance and intestinal health in male New Zealand White rabbits, as evidenced by a 27.12% reduction in feed conversion ratio, decreased diarrhea score, enhanced cecal antioxidant capacity, and activation of the Wnt/β-catenin pathway to support cecal epithelial cell function
Molecular Weight

137.09

Formula

C2H4O2.3H2O.Na

CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C(C)O.[Na].O.O.O

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Store at room temperature, keep dry and cool

In solvent -80°C 1 year
-20°C 6 months
Solvent & Solubility
In Vitro: 

H2O : ≥ 200 mg/mL (1458.90 mM)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 7.2945 mL 36.4724 mL 72.9448 mL
5 mM 1.4589 mL 7.2945 mL 14.5890 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact MedChemExpress (MCE).
Purity & Documentation

Purity: 99.99%

References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
H2O 1 mM 7.2945 mL 36.4724 mL 72.9448 mL 182.3620 mL
5 mM 1.4589 mL 7.2945 mL 14.5890 mL 36.4724 mL
10 mM 0.7294 mL 3.6472 mL 7.2945 mL 18.2362 mL
15 mM 0.4863 mL 2.4315 mL 4.8630 mL 12.1575 mL
20 mM 0.3647 mL 1.8236 mL 3.6472 mL 9.1181 mL
25 mM 0.2918 mL 1.4589 mL 2.9178 mL 7.2945 mL
30 mM 0.2431 mL 1.2157 mL 2.4315 mL 6.0787 mL
40 mM 0.1824 mL 0.9118 mL 1.8236 mL 4.5590 mL
50 mM 0.1459 mL 0.7294 mL 1.4589 mL 3.6472 mL
60 mM 0.1216 mL 0.6079 mL 1.2157 mL 3.0394 mL
80 mM 0.0912 mL 0.4559 mL 0.9118 mL 2.2795 mL
100 mM 0.0729 mL 0.3647 mL 0.7294 mL 1.8236 mL

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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Sodium acetate trihydrate, 99.5%
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