| Size | Price | Stock | Qty |
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| 50mg |
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| 100mg |
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| 250mg |
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| 500mg |
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| 1g | |||
| Other Sizes |
| Targets |
TRISALICYLIC ACID targets cyclooxygenase-2 (COX-2) (IC50 = 0.8 μM) [1]
TRISALICYLIC ACID targets α-glucosidase (IC50 = 12 μM) [1] TRISALICYLIC ACID targets peroxisome proliferator-activated receptor γ (PPARγ) (EC50 = 5 μM) [1] |
|---|---|
| ln Vitro |
In LPS-stimulated RAW264.7 macrophages, TRISALICYLIC ACID (1–20 μM) dose-dependently inhibited pro-inflammatory cytokine production. At 10 μM, TNF-α and IL-6 secretion decreased by ~72% and ~68%, respectively, and prostaglandin E2 (PGE2) levels (COX-2 product) reduced by ~75% [1]
- For α-glucosidase inhibition, TRISALICYLIC ACID (2–40 μM) suppressed enzyme activity in a dose-dependent manner, with an IC50 of 12 μM. At 20 μM, it inhibited α-glucosidase by ~65% compared to control [1] - In 3T3-L1 adipocytes, TRISALICYLIC ACID (5–25 μM) enhanced insulin-dependent glucose uptake: at 15 μM, glucose uptake increased by ~2.3-fold. It also upregulated PPARγ mRNA expression by ~2.1-fold at 15 μM, promoting adipocyte differentiation and insulin sensitivity [1] - It showed no significant inhibition of COX-1 (IC50 > 100 μM), indicating selective COX-2 inhibition [1] |
| ln Vivo |
In LPS-induced inflammatory C57BL/6 mice, oral administration of TRISALICYLIC ACID (25, 50, 100 mg/kg/day for 3 days) dose-dependently reduced systemic inflammation. At 100 mg/kg, serum TNF-α and IL-6 levels decreased by ~68% and ~62%, respectively, and paw edema (induced by carrageenan) was inhibited by ~70% [1]
- In db/db diabetic mice (type 2 diabetes model), oral administration of TRISALICYLIC ACID (50, 100 mg/kg/day for 4 weeks) improved glucose metabolism. At 100 mg/kg, fasting blood glucose reduced by ~55%, glycated hemoglobin (HbA1c) decreased from ~9.2% to ~6.8%, and insulin sensitivity (HOMA-IR index) improved by ~45% [1] - In high-fat diet (HFD)-induced obese mice, TRISALICYLIC ACID (100 mg/kg/day for 6 weeks) reduced body weight gain by ~30% and visceral fat accumulation by ~35%, with no significant change in food intake [1] |
| Enzyme Assay |
COX-2/COX-1 activity assay: Recombinant COX-2 or COX-1 enzyme was incubated with arachidonic acid and TRISALICYLIC ACID (0.1–200 μM) in reaction buffer at 37°C for 30 minutes. The production of PGE2 (COX product) was quantified by ELISA. The inhibition rate was calculated, and IC50 values for COX-2 and COX-1 were determined from dose-response curves [1]
- α-glucosidase activity assay: α-glucosidase enzyme was mixed with p-nitrophenyl-α-D-glucopyranoside (substrate) and TRISALICYLIC ACID (2–40 μM) in phosphate buffer (pH 6.8) at 37°C for 60 minutes. The reaction was terminated by adding sodium carbonate, and the absorbance of p-nitrophenol (product) was measured at 405 nm to calculate enzyme inhibition rate [1] - PPARγ binding assay: Recombinant PPARγ ligand-binding domain was incubated with a fluorescently labeled PPARγ ligand and TRISALICYLIC ACID (1–50 μM) at 25°C for 1 hour. Fluorescence polarization was measured to assess the binding affinity of the drug to PPARγ, and EC50 was determined based on competitive displacement of the labeled ligand [1] |
| Cell Assay |
Macrophage inflammatory response assay: RAW264.7 cells were seeded in 24-well plates and stimulated with LPS (1 μg/mL) in the presence of TRISALICYLIC ACID (1–20 μM) for 24 hours. Cell culture supernatants were collected, and TNF-α, IL-6, and PGE2 levels were quantified by ELISA [1]
- Adipocyte glucose uptake and PPARγ expression assay: 3T3-L1 pre-adipocytes were differentiated into adipocytes, then treated with TRISALICYLIC ACID (5–25 μM) and insulin (100 nM) for 12 hours. [3H]-2-deoxyglucose was added, and radioactivity was measured to assess glucose uptake. RT-PCR was performed to detect PPARγ mRNA levels [1] |
| Animal Protocol |
LPS-induced inflammation mouse model: Male C57BL/6 mice (6–8 weeks old) were randomly divided into control and treatment groups. TRISALICYLIC ACID was dissolved in 0.5% carboxymethylcellulose sodium (CMC-Na) and administered by oral gavage at 25, 50, or 100 mg/kg/day for 3 days. On day 3, LPS (5 mg/kg) was intraperitoneally injected to induce inflammation. Serum cytokines (TNF-α, IL-6) were measured 6 hours later. For paw edema assessment, carrageenan (1% w/v) was injected into the hind paw after 3 days of drug treatment, and paw thickness was measured at 4 hours [1]
- db/db diabetic mouse model: Male db/db mice (8 weeks old) were divided into control and treatment groups. TRISALICYLIC ACID (50, 100 mg/kg/day) was administered orally in 0.5% CMC-Na for 4 weeks. Fasting blood glucose was measured weekly, and HbA1c and insulin levels were detected at the end of treatment. HOMA-IR index was calculated to evaluate insulin sensitivity [1] - HFD-induced obese mouse model: Male C57BL/6 mice were fed a high-fat diet for 4 weeks to induce obesity, then treated with TRISALICYLIC ACID (100 mg/kg/day, oral gavage) for 6 weeks. Body weight was recorded weekly, and visceral fat mass was measured after sacrifice [1] |
| ADME/Pharmacokinetics |
Oral pharmacokinetics in rats: After oral administration of trisalicylic acid (100 mg/kg), the plasma concentration (Cmax) reached a maximum of ~8.5 μg/mL at 1.5 hours (Tmax), and the elimination half-life (t1/2) was approximately 6.2 hours. The oral bioavailability was approximately 45% [1]
- Tissue distribution: After oral administration, trisalicylic acid was widely distributed in various tissues. The highest concentrations were found in the liver (approximately 22 μg/g), pancreas (approximately 18 μg/g), and adipose tissue (approximately 15 μg/g) 2 hours after administration [1] - Metabolism and excretion: Approximately 60% of the administered dose was excreted in the urine (mainly as glucuronide conjugates) within 24 hours, and approximately 30% was excreted in the feces. Only trace amounts of the parent drug were detected [1] |
| Toxicity/Toxicokinetics |
Acute toxicity: No deaths or obvious toxic symptoms (e.g., lethargy, diarrhea) were observed in mice after oral administration of trisalicylic acid at doses up to 2000 mg/kg. LD50 > 2000 mg/kg [1] - Subchronic toxicity: No significant changes in body weight, serum ALT, AST, creatinine, or urea nitrogen levels were observed in rats after oral administration of trisalicylic acid (50–200 mg/kg/day for 12 weeks). Histological examination of the liver, kidneys, and pancreas showed no abnormal lesions [1] - Plasma protein binding: Trisalicylic acid binds to human plasma proteins at a rate of approximately 82%, and the binding affinity does not change in a dose-dependent manner [1]
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| References | |
| Additional Infomation |
Trisalicylic acid is a synthetic salicylic acid derivative designed for dual-action therapy against inflammation and diabetes [1]. Its anti-inflammatory mechanism involves selectively inhibiting COX-2 (without affecting COX-1), thereby reducing the levels of PGE2 and pro-inflammatory cytokines (TNF-α, IL-6) [1]. Its anti-diabetic effect is achieved through two pathways: 1) inhibiting α-glucosidase, delaying carbohydrate digestion and glucose absorption; 2) activating PPARγ, improving insulin sensitivity and regulating lipid metabolism [1]. Due to its good bioavailability and tolerability, oral administration is the preferred route for treating inflammatory diseases such as rheumatoid arthritis and type 2 diabetes [1].
|
| Molecular Formula |
C21H14O7
|
|---|---|
| Molecular Weight |
378.33166
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| Exact Mass |
378.074
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| CAS # |
85531-17-5
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| PubChem CID |
57871430
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| Appearance |
White to off-white solid powder
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| LogP |
3.528
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
28
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| Complexity |
575
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
YVJQWLQBUBZFTE-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C21H14O7/c22-16-10-4-1-7-13(16)20(25)28-18-12-6-3-9-15(18)21(26)27-17-11-5-2-8-14(17)19(23)24/h1-12,22H,(H,23,24)
|
| Chemical Name |
2-[2-(2-hydroxybenzoyl)oxybenzoyl]oxybenzoic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~250 mg/mL (~660.80 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.50 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (5.50 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.6432 mL | 13.2160 mL | 26.4320 mL | |
| 5 mM | 0.5286 mL | 2.6432 mL | 5.2864 mL | |
| 10 mM | 0.2643 mL | 1.3216 mL | 2.6432 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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