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| Targets |
The primary targets of Diclofenac potassium are cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), which it inhibits non-selectively, reversibly, and competitively. By inhibiting COX enzymes, the compound blocks the conversion of arachidonic acid to prostaglandins, which are mediators of inflammation, pain, and fever. The compound also inhibits leukocyte migration, contributing to its anti-inflammatory effects. These targets mediate its therapeutic effects in inflammatory conditions.
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| ln Vitro |
Diclofenac, with an IC50 of 7±3 nM, can efficiently inhibit COX-1-mediated prostaglandin synthesis in U937 cell microsomes[1]. Neural stem cell (NSC) mortality is concentration-dependently induced by diclofenac (1-60 μM; 1 day) [3]. The expression of cleaved (activated) caspase-3 is increased by 10–60 μM diclofenac when given for six hours [3].
In vitro, Diclofenac potassium inhibits COX-1 and COX-2 activity, reducing prostaglandin production in cell-based and enzyme-based assays. It demonstrates anti-inflammatory activity by inhibiting prostaglandin synthesis and leukocyte migration. The compound is used in vitro to study the mechanisms of NSAID action, inflammation, and pain signaling. These in vitro activities confirm its mechanism of action and support its clinical use as an NSAID. |
| ln Vivo |
Rats treated with diclofenac (3 mg/kg twice daily for 5 days) had a considerable increase in 51Cr excreted in their feces; squirrel monkeys treated with 1 mg/kg twice daily for 4 days also experienced this effect [1]. In vivo anti-inflammatory efficacy has been seen in Wistar rats treated with 10 mg/kg of diclofenac orally prior to induction of inflammation [1].
In vivo, Diclofenac potassium is used for the symptomatic treatment of pain and inflammatory diseases, including gout, osteoarthritis, and other conditions. It is available in various formulations, including oral tablets and topical gels. Topical formulations are used for joints amenable to topical therapy, such as hands and knees. The compound reduces inflammation and provides analgesia through COX inhibition and prostaglandin suppression. |
| Enzyme Assay |
In vitro enzyme/receptor binding assays for Diclofenac potassium involve COX-1 and COX-2 inhibition assays using purified enzymes and appropriate substrates (arachidonic acid). The compound is incubated with COX enzymes at concentrations ranging from 0.01-100 μM, and enzyme activity is measured by prostaglandin production using ELISA or radiometric assays. IC50 values are determined by plotting percent inhibition versus inhibitor concentration. Selectivity for COX-1 versus COX-2 can be assessed. All assays include appropriate controls and reference compounds (e.g., indomethacin).
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| Cell Assay |
Cell viability assay [3]
Cell Types: Neural stem cells (NSC) Tested Concentrations: 1, 3, 10, 30, 60 μM Incubation Duration: 1 day Experimental Results: The induction of cell death is concentration-dependent, and the effect is not saturated at a certain concentration . Concentrations up to 60 μM. Western Blot Analysis[3] Cell Types: Neural Stem Cells (NSC) Tested Concentrations: 10, 30 or 60 μM Incubation Duration: 6 hrs (hours) Experimental Results: Activation of caspase-3 increased in a concentration-dependent manner. In vitro cell-based assays for Diclofenac potassium are conducted using inflammatory cell models (e.g., macrophages or synoviocytes). Cells are treated with compound concentrations ranging from 0.01-100 μM, followed by stimulation with LPS or other inflammatory inducers. Prostaglandin E2 and other inflammatory mediators are measured by ELISA. Cell viability is assessed using MTT assays. The compound's effects on COX expression and activity are evaluated by Western blot or activity assays. Leukocyte migration is assessed using chemotaxis assays. Experiments include vehicle controls and positive controls. |
| Animal Protocol |
Animal/Disease Models: Male SD (SD (Sprague-Dawley)) rats (150±200 g) [1]
Doses: 3 mg/kg Route of Administration: po (po (oral gavage)) bid, for 5 days Experimental Results: It resulted in a significant increase in 51Cr excretion in feces. Animal/Disease Models: Wistar rat (150-175 g) formalin-induced rat paw edema model [2] Doses: 10 mg/kg Route of Administration: By oral route before inducing inflammation Experimental Results: Shown in vivo Anti-inflammatory activity (% edema inhibition = 29.2 at 1 hour; 22.2 at 3 hrs (hrs (hours)); 20 at 6 hrs (hrs (hours))). In vivo animal studies with Diclofenac potassium are conducted in various animal models of pain and inflammation, including carrageenan-induced paw edema, formalin-induced pain, and adjuvant-induced arthritis. The compound is administered via oral, intraperitoneal, or topical routes at doses ranging from 1-50 mg/kg. Inflammation is assessed by measuring paw edema, pain responses, or joint swelling. Analgesic effects are evaluated using pain behavior tests. Each group consists of 6-10 animals with vehicle-treated and positive control groups. |
| ADME/Pharmacokinetics |
Pharmacokinetic properties of Diclofenac potassium include rapid and complete absorption following oral administration. The potassium salt formulation allows for faster dissolution and absorption compared to the sodium salt. The compound has a plasma half-life of approximately 1-2 hours. It is highly protein-bound (>99%) and distributes widely in tissues, with high concentrations in synovial fluid. Metabolism occurs through hepatic cytochrome P450 enzymes (CYP2C9), with elimination via renal and biliary excretion. The pharmacokinetics are dose-dependent and influenced by the formulation.
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| Toxicity/Toxicokinetics |
Toxicological data for Diclofenac potassium indicate that it is generally well-tolerated at therapeutic doses. Common adverse effects include gastrointestinal upset, nausea, and dyspepsia. More serious adverse effects include gastrointestinal bleeding, cardiovascular events, and hepatotoxicity. The compound is contraindicated in patients with active peptic ulcer disease, severe cardiovascular disease, or known hypersensitivity to NSAIDs. Long-term use is associated with increased cardiovascular and gastrointestinal risks. Comprehensive safety data are available from clinical use.
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| References |
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| Additional Infomation |
Diclofenac potassium is the potassium salt of diclofenac. It contains a diclofenac (1-) group. Diclofenac potassium is the potassium salt form of diclofenac, a phenylacetic acid derivative belonging to the nonsteroidal anti-inflammatory drug (NSAID) class, possessing analgesic, antipyretic, and anti-inflammatory effects. Diclofenac potassium is a nonselective, reversible, competitive inhibitor of cyclooxygenase (COX), blocking the conversion of arachidonic acid to prostaglandin precursors. This leads to inhibition of prostaglandin production involved in pain, inflammation, and fever. It is a nonsteroidal anti-inflammatory drug (NSAID) with antipyretic and analgesic effects. It exists primarily as a sodium salt. See also: Diclofenac (containing the active moiety).
Diclofenac potassium is an approved therapeutic agent for the treatment of pain and inflammatory diseases, including gout and osteoarthritis. It is a non-selective, reversible, competitive inhibitor of COX-1 and COX-2. The potassium salt formulation allows for faster absorption compared to other salt forms. Available in various formulations including oral tablets and topical gels. It is a widely used NSAID with established efficacy and safety profile. |
| Molecular Formula |
C14H10CL2KNO2
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|---|---|
| Molecular Weight |
334.2390
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| Exact Mass |
332.972
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| CAS # |
15307-81-0
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| Related CAS # |
Diclofenac;15307-86-5;Diclofenac diethylamine;78213-16-8;Diclofenac Sodium;15307-79-6
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| PubChem CID |
23667642
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| Appearance |
White to off-white solid powder
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| Boiling Point |
412ºC at 760 mmHg
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| Melting Point |
156-158ºC
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| Flash Point |
203ºC
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| Vapour Pressure |
1.59E-07mmHg at 25°C
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| LogP |
3.102
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
20
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| Complexity |
310
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
KXZOIWWTXOCYKR-UHFFFAOYSA-M
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| InChi Code |
InChI=1S/C14H11Cl2NO2.K/c15-10-5-3-6-11(16)14(10)17-12-7-2-1-4-9(12)8-13(18)19;/h1-7,17H,8H2,(H,18,19);/q;+1/p-1
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| Chemical Name |
potassium;2-[2-(2,6-dichloroanilino)phenyl]acetate
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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: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| 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 : ~100 mg/mL (~299.19 mM)
H2O : ~14.29 mg/mL (~42.75 mM) H2O : ~14.29 mg/mL (~42.75 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.48 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% 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 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (7.48 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 25.0 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.48 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9919 mL | 14.9593 mL | 29.9186 mL | |
| 5 mM | 0.5984 mL | 2.9919 mL | 5.9837 mL | |
| 10 mM | 0.2992 mL | 1.4959 mL | 2.9919 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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