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Triflusal COX inhibitor

Cat.No.S3200

Triflusal (UR1501) irreversibly inhibits the production of thromboxane-B2 in platelets by acetylating cycloxygenase-1.
Triflusal COX inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 248.16

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Quality Control

Batch: S320001 DMSO]50 mg/mL]false]Ethanol]50 mg/mL]false]Water]Insoluble]false Purity: 99.70%
99.70

Chemical Information, Storage & Stability

Molecular Weight 248.16 Formula

C10H7F3O4

 Storage (From the date of receipt)
CAS No. 322-79-2 Download SDF Storage of Stock Solutions

Synonyms UR1501 Smiles CC(=O)OC1=C(C=CC(=C1)C(F)(F)F)C(=O)O

Solubility

In vitro
Batch:

DMSO : 50 mg/mL ( (201.48 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 50 mg/mL

Water : Insoluble

Molarity Calculator

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

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Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

Targets/IC50/Ki
COX-1 [1]
In vitro
The main Triflusal metabolite, HTB, preserves 6-keto-PGF1α synthesis in porcine aortic endothelial cells (PAEC) cells without a significant decline for up to 24 h even at the higher concentration. [1] This compound at 10 mM, 100 mM and 1 M decreases LDH efflux in rat brain slices after anoxia/reoxygenation by 24%, 35% and 49% respectively. It also reduces inducible NO synthase activity by 18%, 21% and 30%. [2]
In vivo
Triflusal (10 mg/kg i.v.) reduces platelet deposition on subendothelium-induced primary thrombus by about 68% in rabbits. This compound reduces platelet deposition on a fresh thrombus formed over tunica media by about 48% in rabbits. It (40 mg/kg p.o.) reduces platelet deposition on a primary thrombus triggered by subendothelium and tunica media by 53% in rabbits. This chemical significantly reduces Cox-2 mRNA levels and protein levels without influence Cox-1 mRNA levels on the vascular wall in rabbits. [1] It (600 mg/day for 5 days) results in an increase in NO production by neutrophils and an increase in endothelial nitric oxide synthase (eNOS) protein expression in neutrophils in healthy volunteers. [3] This compound (300 mg, twice-daily orally) shows a more important increase in total walking distance and in pain-free walking distance over the basal values than those treated with placebo, together with an improvement of the symptomatology correlated with claudication in patients with chronic peripheral arteriopathy. It shows an increase in the peak-flow recorded through strain-gauge plethysmography in patients with chronic peripheral arteriopathy. [4] This chemical (30 mg/kg) strongly decreases iNOS immunolabeling at both survival times analyzed, attenuating iNOS immunoreactivity in astroglial cells and infiltrated neutrophils in rats. It decreases neuronal and microglial COX-2 expression at 10 and 24 hours after lesion and microglial and astroglial expression of IL-1beta and TNF-alpha at 24 hours after lesion in rats. [5]
References
  • https://pubmed.ncbi.nlm.nih.gov/8593974/
  • https://pubmed.ncbi.nlm.nih.gov/12364744/

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