2. Immunology/Inflammation Metabolic Enzyme/Protease NF-κB GPCR/G Protein
  3. COX Phosphodiesterase (PDE) NF-κB NO Synthase Prostaglandin Receptor
  4. Triflusal

Triflusal is an orally bioavailable, blood-brain barrier-permeable dual Cyclooxygenase-1 (COX-1)/cAMP phosphodiesterase inhibitor. Triflusal inhibits platelet aggregation, NF-κB activation, iNOS activity, and prostaglandin synthesis in ischaemic tissue. Triflusal stimulates neutrophil nitric oxide production, eNOS protein expression, and cNOS activity. Triflusal alleviates cerebral ischemic injury in rats and ameliorates pathological lesions and related gene expression in transgenic Alzheimer’s disease models. Triflusal can be used for the research of thromboembolic/ischemic cardiovascular and cerebrovascular diseases, and Alzheimer’s disease.

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Triflusal

Triflusal Chemical Structure

CAS No. : 322-79-2

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Based on 1 publication(s) in Google Scholar

Other Forms of Triflusal:

Triflusal Related Antibodies

Top Publications Citing Use of Products

View All COX Isoform Specific Products:

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COX COX-1 COX-2 COX-3

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PDE1 PDE2 PDE3 PDE4 PDE5 PDE6 PDE7 PDE9 PDE10 PDE11 PDE12 PDE8 Autotaxin

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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nNOS iNOS eNOS

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DP EP FP IP TXA2/TP TXB2

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Triflusal is an orally bioavailable, blood-brain barrier-permeable dual Cyclooxygenase-1 (COX-1)/cAMP phosphodiesterase inhibitor. Triflusal inhibits platelet aggregation, NF-κB activation, iNOS activity, and prostaglandin synthesis in ischaemic tissue. Triflusal stimulates neutrophil nitric oxide production, eNOS protein expression, and cNOS activity. Triflusal alleviates cerebral ischemic injury in rats and ameliorates pathological lesions and related gene expression in transgenic Alzheimer’s disease models. Triflusal can be used for the research of thromboembolic/ischemic cardiovascular and cerebrovascular diseases, and Alzheimer’s disease[1][2][3][4][5].

IC50 & Target[4]

COX-1

 

NF-κB

 

iNOS

 

eNOS

 

In Vitro

Triflusal (37.5-300 μM; 30 min pre-incubation) does not significantly inhibit endothelial Cox-2 activity or reduce prostacyclin synthesis in Phorbol 12-myristate 13-acetate (HY-18739)-stimulated porcine aortic endothelial cells[2].
Triflusal irreversibly inhibits COX-1 and reduces TXB2 production in human platelets while sparing vascular endothelial cell arachidonic acid metabolism, and exhibits greater anti-aggregant potency in human whole blood than in platelet rich plasma[3].
Triflusal increases NO production by human neutrophils by 150%, inhibits NF-κB activation in human mononuclear cells[3].
Triflusal (3.3 mM) inhibits thrombin-induced platelet activation by 61% in human platelet-rich plasma[4].
Triflusal (1 mM) increases basal cAMP levels by 36% in rat[4].
Triflusal (3 mM) inhibits NF-κB activation in human peripheral blood mononuclear cells[4].
Triflusal potently inhibits cAMP phosphodiesterase, significantly elevates cGMP levels in human platelets and neutrophils: it is ~2-fold more potent at inhibiting TNFα-induced NFκB activation, ~4-10-fold more potent at inhibiting NFAT-mediated transcription, and effective at attenuating anoxia/reperfusion-related injury, iNOS activity and lipid peroxidation in rat brain slices[4].
Triflusal inhibits NF-κB activation and downstream expression of proinflammatory mediators in human peripheral blood mononuclear cells and endothelial cells, and strongly suppresses inflammation-induced COX-2 expression in human cells[5].

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

Triflusal Related Antibodies
In Vivo

Triflusal (40 mg/kg/day; p.o.; daily; 8 days) reduces vascular Cox-2 mRNA and protein expression in normal rabbit aortas while sparing Cox-1 mRNA, with only a 39% reduction in Cox-2 protein levels[2].
Triflusal (40 mg/kg/day; p.o.; daily; 8 days) reduces secondary platelet deposition on preformed primary thrombi in a rabbit model of severe carotid stenosis by 53-63% [2].
Triflusal (10 mg/kg; i.v.; single dose) reduces secondary platelet deposition on preformed primary thrombi in a rabbit model of thrombosis by 48-66%[2].
Triflusal (chronic administration) provides 60% protection against arachidonic acid-induced cerebral ischaemia in rats[3].
Triflusal (30 mg/kg) reduces NMDA (HY-17551)-induced excitotoxic brain lesions in rats[3].
Triflusal inhibits neuronal and glial NF-κB activation, reduces lesion volume by approximately 50%, and dampens the astroglial response in a postnatal rat model of excitotoxic brain injury[4].
Triflusal reduces inflammatory markers and functional deficits in rat models of isolated cerebral ischaemia or isolated Alzheimer's disease-like pathology, but has reduced efficacy in a model of concurrent cerebral ischaemia and Alzheimer's disease-like pathology[4].
Triflusal (30 mg/kg; p.o.; daily; 3-5 consecutive months) rescues cognitive deficits, reduces dense-core amyloid plaque load by up to 64%, lowers neuroinflammatory markers, normalizes axonal curvature, and upregulates memory-related gene expression in Tg2576 Alzheimer's disease transgenic mice[5].

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

Animal Model: New Zealand White (male, 2.8 kg)[2]
Dosage: 40 mg/kg/day
Administration: p.o.; daily; 8 days
Result: Left vascular Cox-1 mRNA levels unchanged relative to placebo.
Reduced Cox-2 mRNA levels.
Reduced Cox-2 protein levels by 39%.
Animal Model: New Zealand White (male, 2.8 kg)[2]
Dosage: 40 mg/kg/day
Administration: p.o.; daily; 8 days
Result: Reduced platelet deposition on subendothelium-induced primary thrombus (severe stenosis, 1690 s-1) by 63% relative to placebo.
Reduced platelet deposition on tunica media-induced primary thrombus (severe stenosis, 1690 s-1) by 53% relative to placebo.
Animal Model: New Zealand White (male, 2.8 kg)[2]
Dosage: 10 mg/kg
Administration: i.v.; single dose
Result: Reduced platelet deposition on subendothelium-induced primary thrombus (mild stenosis, 212 s-1) by 66% relative to placebo.
Reduced platelet deposition on tunica media-induced primary thrombus (mild stenosis, 212 s-1) by 48% relative to placebo.
Animal Model: Tg2576 (gender-matched; starting treatment at 10 or 13 months of age; overexpressing human mutant APP with KM670/671NL on mixed hybrid C57Bl6j/SJL background)[5]
Dosage: 30 mg/kg
Administration: p.o.; daily; 3 or 5 consecutive months
Result: Achieved significantly more platform crossings in Morris water maze probe trials, and restored contextual fear conditioning freezing levels.
Decreased dense-core (Thioflavin-S-reactive) plaque burden by 47% at 13 months and 64% at 18 months, and reduced total Thioflavin-S-positive plaque counts by 37% at 13 months and 57% at 18 months.
Reduced astrocyte counts in the hippocampal CA1 subfield and entorhinal cortex, decreased microglial counts in the CA1 region at both 13 and 18 months, and lowered brain proinflammatory cytokine levels (IL-1β by 70%; TNF-α by 50%) at 13 months.
Ameliorated axonal curvature near plaques (<50 μm) at 13 months and in both peri-plaque and distal regions (>50 μm) at 18 months, and upregulated hippocampal c-fos and BDNF mRNA expression, restoring BDNF levels to those of non-transgenic controls.
Clinical Trial
Molecular Weight

248.16

Formula

C10H7F3O4
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C(O)C1=CC=C(C(F)(F)F)C=C1OC(C)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 2 years
-20°C 1 year
Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (402.97 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 4.0297 mL 20.1483 mL 40.2966 mL
5 mM 0.8059 mL 4.0297 mL 8.0593 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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

  • Molarity Calculator

  • Dilution Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Volume
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Molecular Weight *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start)

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: ≥ 3 mg/mL (12.09 mM); Clear solution

    This protocol yields a clear solution of ≥ 3 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (30.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

    Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
  • Protocol 2

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: ≥ 3 mg/mL (12.09 mM); Clear solution

    This protocol yields a clear solution of ≥ 3 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (30.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

    Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:

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Number of animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO +
% 
+
%
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%
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration: mg/mL
Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).
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).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 4.0297 mL 20.1483 mL 40.2966 mL 100.7415 mL
5 mM 0.8059 mL 4.0297 mL 8.0593 mL 20.1483 mL
10 mM 0.4030 mL 2.0148 mL 4.0297 mL 10.0741 mL
15 mM 0.2686 mL 1.3432 mL 2.6864 mL 6.7161 mL
20 mM 0.2015 mL 1.0074 mL 2.0148 mL 5.0371 mL
25 mM 0.1612 mL 0.8059 mL 1.6119 mL 4.0297 mL
30 mM 0.1343 mL 0.6716 mL 1.3432 mL 3.3580 mL
40 mM 0.1007 mL 0.5037 mL 1.0074 mL 2.5185 mL
50 mM 0.0806 mL 0.4030 mL 0.8059 mL 2.0148 mL
60 mM 0.0672 mL 0.3358 mL 0.6716 mL 1.6790 mL
80 mM 0.0504 mL 0.2519 mL 0.5037 mL 1.2593 mL
100 mM 0.0403 mL 0.2015 mL 0.4030 mL 1.0074 mL
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Triflusal 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:

Triflusal322-79-2COXPhosphodiesterase (PDE)NF-κBNO SynthaseProstaglandin ReceptorCyclooxygenaseNuclear factor-κBNuclear factor-kappaBNitric oxide synthasesNOSeNOSprostaglandin synthesiscyclooxygenasehuman umbilical vein endothelial cellsiNOSBDNFTg2576 Alzheimer's disease transgenic miceplatelet aggregationcAMP phosphodiesteraseInhibitorinhibitorinhibit

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