At an IC50 of 7±3 nM, diclofenac efficiently explodes COX-1-mediated microsomal formation in U937 cells[1]. Neural stem cells (NSCs) are killed by diclofenac (1–60 μM; 1 day) in a concentration-dependent way. Every six days, caspase-3 expression is increased by diclofenac (10–60 μM; 1).

Squirrel monkeys administered 1 mg/kg twice daily for 4 days likewise showed a substantial increase in fecal Cr excretion following treatment with diclofenac (3 mg/kg, bid) for 5 days [1]. Wistar rats treated with diclofenac (10 mg/kg; administered prior to triggering factors passing via the route medication) show anti-inflammatory action [1].

Cell Viability Assay[3]
Cell Types: Neural Stem cells (NSCs)
Tested Concentrations: 1, 3, 10, 30, 60 μM
Incubation Duration: 1 day
Experimental Results: Induction of cell death is concentration-dependent and occurs at concentrations up to 60 μM The effect is not saturated.

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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.

Animal/Disease Models: Male SD (SD (Sprague-Dawley)) rats (150±200 g) [1]
Doses: 3 mg/kg
Route of Administration: Oral administration, bid, for 5 days
Experimental Results: Caused a significant increase in fecal 51Cr excretion.

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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))).

Absorption, Distribution and Excretion
Diclofenac is completely absorbed from the gastrointestinal tract, but may undergo significant first-pass metabolism, with only 60% of the drug entering systemic circulation unchanged. Many topical formulations are absorbed through the skin and produce clinically significant plasma concentrations. Absorption is dose-proportional within the dose range of 25–150 mg. Time to peak concentration (Tmax) varies depending on the formulation; oral solutions reach peak plasma concentration within 10–40 minutes, enteric-coated tablets within 1.5–2 hours, while sustained-release and controlled-release formulations further prolong Tmax. Co-administration with food has no significant effect on AUC, but delays Tmax to 2.5–12 hours. Diclofenac is primarily excreted through metabolism. Of the total dose, 60–70% is excreted in the urine and 30% in the feces. There is no significant enterohepatic circulation. The total volume of distribution of diclofenac is 5–10 liters or 0.1–0.2 liters/kg. The central chamber volume is 0.04 L/kg. Diclofenac distributes to the synovial fluid, reaching peak concentration 2–4 hours after administration. Its ability to cross the blood-brain barrier is limited; cerebrospinal fluid concentrations are only 8.22% of plasma concentrations. Diclofenac was not detected in breast milk after an intramuscular 50 mg dose, but metabolite concentrations were not detected. Diclofenac has been shown to cross the placenta in mice and rats, but human data are lacking. The plasma clearance of diclofenac is 16 L/h. Oral administration of diclofenac sodium extended-release (enteric-coated) tablets delays the onset of absorption, but the extent of absorption appears unaffected. Diclofenac sodium: In some fasting subjects, plasma diclofenac concentrations were detectable within 10 minutes of taking a regular diclofenac potassium tablet. Diclofenac potassium: Diclofenac sodium and diclofenac potassium are almost completely absorbed from the gastrointestinal tract; however, these drugs undergo extensive first-pass metabolism in the liver, with only about 50-60% of diclofenac sodium or diclofenac potassium entering systemic circulation unchanged. Diclofenac can also enter systemic circulation via rectal or transdermal administration (gel or transdermal patch). Food reduces the absorption rate of immediate-release diclofenac potassium tablets and extended-release (enteric-coated) diclofenac sodium tablets, leading to a delayed and reduced peak plasma concentration; however, the extent of absorption is largely unaffected. When immediate-release diclofenac potassium tablets are taken with food, the time to reach peak plasma concentration is prolonged, and the peak plasma concentration is reduced by approximately 30%. When a single dose of enteric-coated diclofenac sodium tablets is taken, drug absorption is typically delayed by 1-4.5 hours, but in some patients, the delay can be as long as 12 hours. The altered gastrointestinal absorption of the drug due to food is caused by the delayed transport of enteric-coated tablets into the small intestine (the site of drug dissolution). When diclofenac sodium extended-release tablets are taken with food, drug absorption is delayed by 1-2 hours, and peak plasma concentration doubles; however, the extent of absorption is largely unaffected. The presence of food does not appear to significantly affect the absorption of diclofenac after continuous use. Antacids may reduce the rate of diclofenac absorption, but not its extent. For more complete data on the absorption, distribution, and excretion of diclofenac (11 items in total), please visit the HSDB record page. Metabolites/Metabolites Diclofenac is oxidatively metabolized to produce hydroxy metabolites, which are conjugated with glucuronic acid, sulfate, and taurine. The major metabolite is 4'-hydroxydiclofenac, generated by CYP2C9. This metabolite has extremely weak activity, only one-thirtieth the activity of diclofenac. Other metabolites include 3'-hydroxydiclofenac, 3'-hydroxy-4'-methoxydiclofenac, 4',5-dihydroxydiclofenac, acylglucuronide conjugates, and other conjugated metabolites. This study employed high-performance liquid chromatography (HPLC) coupled with radiometric assays to investigate the metabolic extent of diclofenac sodium in ex vivo human skin. In previous in vitro diffusion experiments, radiolabeled diclofenac sodium emulsion (Pennsaid) or aqueous solution was applied to live human skin, either as a single dose or multiple doses (eight times over two days). In this study, receptor fluid samples from the diffusion experiments were extracted, and the extracts were analyzed using HPLC to separate diclofenac and its standard metabolites. The collection time of each HPLC fraction was compared with the retention time of diclofenac and its metabolites in the standard solution based on the radioactivity of each fraction. Samples with single or multiple emulsion applications showed radioactivity primarily in a fraction with a retention time consistent with diclofenac. Other HPLC fractions showed no radioactivity or only minimal radioactivity, within the measurement error range. Similar results were obtained for mixed samples of emulsion applications or aqueous solutions. The results indicate that diclofenac sodium is not metabolized in the live human epidermis during in vitro transdermal absorption. Therefore, when applied topically to human skin in vivo, diclofenac is metabolized to a very low degree, or even not at all. /Diclofenac Sodium/
In the human body, the commonly used nonsteroidal anti-inflammatory drug diclofenac (compound 1) is metabolized primarily to produce 4'-hydroxy (compound 2), 5-hydroxy (compound 3), and acyl glucuronide (compound 4) metabolites. These three metabolites are all associated with rare, specific adverse reactions related to this commonly used drug. Therefore, in order to conduct mechanistic toxicology studies on compound 1, a large number of compounds 2-4 are required, and their synthesis and characterization will be described in this paper. Key steps include: the preparation of aniline compound 5 from phenol via a simple two-step method; the highly efficient and selective 6-iodination of amide compound 18; and the high-yield Ullmann coupling reaction to generate diarylamine compounds 11 and 21. The preparation of acyl glucuronide compound 4 was achieved by reacting compound 1 (free acid) with allyl glucuronide compound 23 via a Mitsunobu reaction followed by Pd(0) deprotection, an improvement on previously published methods. The researchers reported a complete characterization of compound 4… They also reported the metabolic pathways of the anabolic metabolites: compounds 2 and 3 underwent glucuronidation in rats, but only compound 3 formed a glutathione adduct in vivo and via enzymatic synthesis through a quinone imine intermediate. A previously unreported glutathione adduct of compound 3 was obtained via enzymatic synthesis. Compound 4 formed an imine-linked protein conjugate, as confirmed by sodium cyanoborohydride capture experiments. In humans, diclofenac is primarily (approximately 50%) excreted as its 4'-hydroxylated metabolite, while the acyl glucuronide (AG) pathway appears to be more significant in rats (approximately 50%) and dogs (>80-90%). However, previous studies on the oxidative metabolism of diclofenac in human liver microsomes (HLMs) have significantly underestimated its clearance in humans. We determined the relative quantitative importance of the 4'-hydroxy and AG pathways in diclofenac metabolism in rat, dog, and human liver microsomes. We determined the intrinsic microsomal clearance (CL(int) = V(max)/K(m)) and used it to infer the plasma clearance of diclofenac in these species. Only by considering both the AG and 4'-hydroxy pathways can the clearance of diclofenac be accurately predicted based on microsomal data. However, the fact that the AG pathway accounts for approximately 75% of the estimated intrinsic liver clearance (CL(int)) of diclofenac in the HLMs is clearly inconsistent with human excretion data for 4'-hydroxydiclofenac. Interestingly, significant oxidative metabolism of diclofenac AG was observed after incubation with human liver microsomes (HLMs), directly converting it to 4'-hydroxydiclofenac AG. The estimated hepatic clearance (CL(int)) of this pathway suggests that a significant portion of the intrahepatic diclofenac AG may be converted in vivo to its 4'-hydroxy derivative. Further experiments indicated that this novel oxidation reaction is catalyzed by CYP2C8, rather than by CYP2C9-catalyzed diclofenac 4'-hydroxylation. These findings may have general implications for determining the primary pathway of drug clearance using total (free + bound) oxidative metabolite excretion and may challenge the effectiveness of using diclofenac as a probe to analyze the in vivo human CYP2C9 activity phenotype by measuring its pharmacokinetics and total urinary excretion of 4'-hydroxydiclofenac. This study investigated the metabolism of diclofenac in mice following a single oral dose of 10 mg/kg (14)C-diclofenac. Most drug-related substances were excreted in the urine within 24 hours of administration (49.7%). Liquid chromatography analysis of urine and fecal extracts showed that diclofenac was extensively metabolized into at least 37 components, with only a small amount of unmetabolized diclofenac excreted. Metabolites were identified using hybrid linear ion trap mass spectrometry via precise molecular ion mass determination and subsequent multi-stage fragmentation. The major metabolic pathways identified included: 1) binding to taurine; and 2) hydroxylation (potentially at the 4'- and 5'-aromatic ring positions), followed by binding to taurine, glucuronic acid, or glucose. Etherification, rather than acyl glucuronidation, was predominant. No formation of p-benzoquinone imines was observed (i.e., no glutathione or thiouric acid conjugates were detected). Numerous novel drug-related minor metabolites were also detected, including ribose, glucose, sulfate, and glucuronide ether-linked conjugates of hydroxylated diclofenac derivatives. Combinations of these hydroxylated derivatives with acyl conjugates (glucose, glucuronic acid, and taurine) or N-linked sulfation or glycosylation were also observed. Acyl or amide-linked conjugates of benzoic acid metabolites, as well as several indololinone derivatives with further hydroxylation and binding moieties, were also evident. The formation mechanisms of benzoic acid and indololinone compounds suggest the formation of reactive intermediates in vivo, which may lead to hepatotoxicity. For more complete data on the metabolism/metabolites of diclofenac (7 metabolites in total), please visit the HSDB record page. Known human metabolites of diclofenac include 4'-hydroxydiclofenac, 5-hydroxydiclofenac, and (2S,3S,4S,5R)-6-[2-[2-(2,6-dichloroaniline)phenyl]acetyl]oxy-3,4,5-trihydroxyoxacyclohexane-2-carboxylic acid. Diclofenac is the known human metabolite of aceclofenac. It is primarily metabolized in the liver. Excretion pathway: Diclofenac is metabolized and subsequently excreted in urine and bile as glucuronide and sulfate conjugates. Almost no free, unmetabolized diclofenac is excreted in urine. Approximately 65% of the dose is excreted in urine as unmetabolized diclofenac and its metabolites in conjugates, and approximately 35% is excreted in bile.
Half-life: 2 hours

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Biological half-life
The terminal half-life of diclofenac is approximately 2 hours, but the apparent half-life, including all metabolites, is 25.8–33 hours.
After use of diclofenac-epolide transdermal patches, the elimination half-life of diclofenac is approximately 12 hours. /Diclofenac-epolide/
It has been reported that after intravenous injection of diclofenac sodium in healthy adults, the half-life of diclofenac is approximately 3 minutes on average in the initial distribution phase, approximately 16 minutes on average in the intermediate (redistribution) phase, and approximately 1–2 hours on average in the terminal (elimination) phase. Diclofenac sodium/
Elimination: Up to 6 hours

Hepatotoxicity
It has been reported that up to 15% of patients taking diclofenac long-term experience elevated serum transaminase levels, but only 2% to 4% have transaminase levels exceeding three times the upper limit of normal (Case 1 and 2). Clinically significant and symptomatic liver disease (with jaundice) caused by diclofenac is relatively rare (1 to 5 cases per 100,000 prescriptions, 1 to 5 cases per 10,000 exposed individuals). Nevertheless, more than 100 cases of clinically significant liver injury caused by diclofenac have been reported in the literature, and in most case series, diclofenac ranks among the top ten causes of drug-induced liver injury. The onset of liver injury ranges from within one week to more than one year after administration. Most cases develop symptoms within 2 to 6 months (Case 3 and 4), while more severe cases tend to develop symptoms earlier. The injury pattern is almost entirely hepatocellular, but mixed-type injury has also been reported. Clinical manifestations include jaundice, with prodromal symptoms including anorexia, nausea, vomiting, and fatigue. Fever and rash occur in 25% of cases; some cases exhibit immune hypersensitivity features, while others resemble chronic hepatitis with autoimmune features. Liver histology in most cases shows acute lobular hepatitis. However, cases with prolonged incubation of diclofenac hepatotoxicity may present with clinical and histological features of chronic hepatitis (Case 2). Women appear to be more susceptible to diclofenac liver injury than men. Diclofenac-induced liver injury can be severe; several cases of acute liver failure have been attributed to diclofenac. Probability score: A (Known cause of clinically significant liver injury). Topical diclofenac (solution, gel, cream, patch) is associated only with a low rate of serum enzyme elevation (usually less than 1%), and may not be higher than placebo or excipients. However, product labels for topical diclofenac mention the possibility of liver injury, and at least one case of clinically significant liver injury caused by topical diclofenac has been reported in the literature. Nevertheless, clinically significant liver injury caused by topical diclofenac should be extremely rare.

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Effects during pregnancy and lactation
◉ Overview of medication use during lactation
Data on diclofenac excretion in breast milk is limited, but the drug has a short half-life and produces few glucuronide metabolites. Drug concentrations in breast milk appear to be low. Most reviewers consider diclofenac use during lactation acceptable. Other medications may be preferred, especially for breastfeeding newborns or premature infants, as there is more publicly available information on these types of medications.
Maternal use of diclofenac topical gel or eye drops is not expected to have any adverse effects on breastfed infants. To significantly reduce the amount of medication entering breast milk after using eye drops, press your finger against the tear duct near the corner of your eye for at least 1 minute, then wipe away any excess medication with absorbent tissue.
◉ Effects on breastfed infants
In one study, 30 mothers who underwent elective cesarean section were able to use 25 mg diclofenac suppositories postpartum, while receiving spinal anesthesia or a combination of spinal-epidural anesthesia and local anesthesia. In the spinal anesthesia group, the average dose of diclofenac was 56 mg on the day of delivery and 33 mg the following day; while women receiving both spinal and epidural anesthesia received 21 mg and 18 mg, respectively. No adverse reactions were reported in breastfed infants. One breastfed infant developed urticaria on day 15 after birth. The mother had been taking diclofenac (dosage not specified) for pain relief since the cesarean section. Diclofenac may have been one of the triggers for the urticaria; however, the infant had also received a hepatitis B vaccine 7 days prior, which the authors considered more likely to be the cause of the reaction. ◉ Effects on breastfeeding and breast milk: A randomized, double-blind study was conducted in pregnant women scheduled for cesarean section under spinal anesthesia with bupivacaine and fentanyl. Patients received 100 mg diclofenac (n = 100), 100 mg tramadol (n = 100), or placebo (glycerol suppositories, n = 100), all administered as rectal suppositories every 8 hours for 24 hours. Mothers receiving diclofenac had significantly shorter times to initiate breastfeeding compared to those receiving placebo: 1.5 hours vs. 4.1 hours with breastfeeding support, and 3.5 hours vs. 6.2 hours without support. In mothers receiving no support, diclofenac was slightly more effective than tramadol (3.5 hours vs. 3.7 hours). Protein Binding: Diclofenac binds to over 99.7% of serum proteins, primarily albumin. It also binds to lipoproteins to a limited extent, with 1.1% binding to HDL, 0.3% to LDL, and 0.15% to VLDL.

[1]. Biochemical and pharmacological profile of a tetrasubstituted furanone as a highly selective COX-2 inhibitor. Br J Pharmacol. 1997 May;121(1):105-17.

[2]. Design, synthesis of novel isoindoline hybrids as COX-2 inhibitors: Anti-inflammatory, analgesic activities and docking study. Bioorg Chem. 2018 Oct;80:70-80.

[3]. Diclofenac Inhibits Proliferation and Differentiation of Neural Stem Cells. Biochem Pharmacol. 2003 Jul 15;66(2):289-95.

Diclofenac is a monocarboxylic acid composed of phenylacetic acid with a (2,6-dichlorophenyl) amino group linked at the 2-position. It has multiple functions, including non-narcotic analgesia, antipyretic, EC 1.14.99.1 (prostaglandin intraperoxidase) inhibitor, xenobiotic, environmental pollutant, drug allergen, and nonsteroidal anti-inflammatory drug (NSAID). It is a secondary amino compound, amino acid, dichlorobenzene, aromatic amine, and monocarboxylic acid. Its structure is related to phenylacetic acid and diphenylamine. It is the conjugate acid of diclofenac (1-). Diclofenac is a phenylacetic acid derivative and also a NSAID. NSAIDs inhibit cyclooxygenase (COX)-1 and -2, which are enzymes responsible for the production of prostaglandins (PGs). Prostaglandins (PGs) are involved in inflammation and pain signaling. Diclofenac, like other NSAIDs, is commonly used as a first-line treatment for acute and chronic pain and inflammation of various causes. Diclofenac is a drug developed through rational drug design based on the structures of phenazorone, mefenamic acid, and indomethacin. The introduction of two chlorine atoms at the ortho position of the benzene ring puts the benzene ring in a maximally torsional state, which appears to be related to enhanced efficacy. It is often used in combination with misoprostol to prevent gastric ulcers induced by nonsteroidal anti-inflammatory drugs (NSAIDs). Diclofenac was first approved by the U.S. Food and Drug Administration (FDA) in July 1988, marketed under the brand name Voltaren, and sold by Novartis (formerly Ciba-Geigy). Diclofenac is a nonsteroidal anti-inflammatory drug. Its mechanism of action is as a cyclooxygenase inhibitor. The physiological effect of diclofenac is achieved by reducing prostaglandin production. Diclofenac is a commonly used NSAID for the treatment of chronic arthritis and mild to moderate acute pain. Full-dose diclofenac treatment typically results in a mild elevation of serum transaminases, and in rare cases, can lead to severe, clinically significant acute or chronic liver disease. Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) of phenylacetic acid. As an NSAID, diclofenac binds to and chelates two isoenzymes of cyclooxygenase (COX-1 and COX-2), thereby blocking the conversion of arachidonic acid to pro-inflammatory prostaglandins. It may also inhibit COX-2-mediated tumor angiogenesis. By inhibiting COX-2, diclofenac effectively relieves pain and inflammation; inhibition of COX-1 may produce unacceptable gastrointestinal side effects. Its activity against COX-2 may be higher than several other carboxylic acid-containing NSAIDs. (NCI04) A nonsteroidal anti-inflammatory drug (NSAID) with antipyretic and analgesic effects. It exists primarily in sodium salt form.
A nonsteroidal anti-inflammatory drug (NSAID) with antipyretic and analgesic effects. It exists primarily in sodium form.
Drug Indications

Diclofenac is indicated for the treatment of pain and inflammation from various causes, including inflammatory diseases such as osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis, as well as injury-related inflammation caused by surgery and physical trauma. Diclofenac is often used in combination with misoprostol as a gastric protectant in patients with high-risk NSAID-induced ulcers.
FDA Label
Mechanism of Action

Diclofenac inhibits cyclooxygenase-1 and -2, two enzymes responsible for the production of prostaglandin (PG) G2, a precursor to other PGs. These molecules have broad activity in pain and inflammation, and inhibiting their production is the common mechanism of all diclofenac's effects. PGE2 is a major PG involved in nociceptive modulation. It mediates peripheral sensitization through multiple mechanisms. PGE2 activates the Gq-coupled EP1 receptor, leading to enhanced activity of the inositol triphosphate/phospholipase C pathway. Activation of this pathway releases intracellular calcium ions, directly lowering the action potential threshold and activating protein kinase C (PKC), which is involved in various indirect mechanisms. Prostaglandin E2 (PGE2) also activates the Gs-coupled EP4 receptor, thereby activating the adenylate cyclase/protein kinase A (AC/PKA) signaling pathway. Both PKA and PKC enhance the activity of transient receptor potential cation channel V subfamily member 1 (TRPV1), thereby increasing sensitivity to thermal stimuli. They also activate tetrodotoxin-resistant sodium channels and inhibit inward potassium currents. Furthermore, PKA is involved in activating P2X3 purine receptors and sensitizing T-type calcium channels. Activation and sensitization of depolarized ion channels, along with inhibition of inward potassium currents, collectively reduce the stimulus intensity required for nociceptive afferent neurons to generate action potentials. Prostaglandin E2 (PGE2) increases sensitivity to bradykinin via the EP3 receptor and further increases sensitivity to heat via the EP2 receptor. Central sensitization occurs in the dorsal horn of the spinal cord and is mediated by the EP2 receptor, which is coupled to the Gs protein. Presynaptically, this receptor increases the release of the nociceptive neurotransmitters glutamate, calcitonin gene-related peptide (CGRP), and substance P. Postsynaptically, it increases the activity of AMPA and NMDA receptors and inhibits inhibitory glycinergic neurons. These effects collectively lead to a lower activation threshold, allowing pain signals to be generated from low-intensity stimuli. PGI₂ is known to act through its Gs-coupled IP receptor, but the extent of its effect varies from person to person. Some studies suggest that PGI₂ is more important in painful inflammatory diseases such as arthritis. Nonsteroidal anti-inflammatory drugs (NSAIDs) effectively reduce inflammatory pain by limiting peripheral and central sensitization through these pathways. PGI₂ and PGE₂ participate in acute inflammation through their IP and EP₂ receptors. Similar to β-adrenergic receptors, these receptors are also Gs-coupled and mediate vasodilation through the AC/PKA pathway. PGE₂ also functions by increasing the adhesion of leukocytes to endothelial cells and attracting cells to the site of injury. PGD₂ participates in activating endothelial cells to release cytokines via its DP1 receptor. Prostaglandin I₂ (PGI₂) and prostaglandin E₂ (PGE₂) regulate the activation and differentiation of helper T cells through IP, EP₂, and EP₄ receptors, which are thought to play an important role in the pathogenesis of arthritis. Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce inflammation by limiting the production of these prostaglandins at the site of injury. PGE₂ can cross the blood-brain barrier and act on excitatory Gq and EP₃ receptors on hypothalamic thermoregulatory neurons. This activation triggers increased thermogenesis and decreased heat dissipation, resulting in fever. NSAIDs inhibit the production of PGE₂, thereby reducing the activity of these neurons. The pharmacological effects of diclofenac are similar to other typical NSAIDs. This drug has anti-inflammatory, analgesic, and antipyretic effects. The exact mechanism is not fully elucidated, but many of its effects appear to be primarily related to the inhibition of prostaglandin synthesis. Diclofenac inhibits prostaglandin synthesis in tissues by inhibiting cyclooxygenases; at least two isoenzymes, cyclooxygenase-1 (COX-1) and -2 (COX-2) (also known as prostaglandin G/H synthase-1 (PGHS-1) and -2 (PGHS-2), have been identified, catalyzing the production of prostaglandins in the arachidonic acid pathway. Like other typical nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac inhibits both COX-1 and COX-2. Although the exact mechanism is not fully understood, NSAIDs appear to exert their anti-inflammatory, analgesic, and antipyretic effects primarily through the inhibition of the COX-2 isoenzyme; COX-1 inhibition may contribute to the adverse effects of the drug on the gastrointestinal mucosa and platelet aggregation. Like all nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac sodium exhibits anti-inflammatory, analgesic, and antipyretic properties due to its reduction of COX-1 and COX-2 activity. Diclofenac sodium inhibits the synthesis of prostaglandins from arachidonic acid by inhibiting cyclooxygenase activity. It also damages the gastrointestinal mucosa and inhibits platelet aggregation.

C14H11CL2NO2

296.15

295.016

15307-86-5

Diclofenac diethylamine;78213-16-8;Diclofenac-d4;153466-65-0;Diclofenac Sodium;15307-79-6;Diclofenac potassium;15307-81-0;Diclofenac-13C6;1261393-71-8

3033

White to light yellow solid powder

1.4±0.1 g/cm3

412.0±45.0 °C at 760 mmHg

156-158ºC

203.0±28.7 °C

0.0±1.0 mmHg at 25°C

1.662

4.06

2

3

4

19

304

0

DCOPUUMXTXDBNB-UHFFFAOYSA-N

InChI=1S/C14H11Cl2NO2/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)

2-[2-(2,6-dichloroanilino)phenyl]acetic acid

Diclofenac acid Dichlofenac Voltarol Voltaren

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~125 mg/mL (~422.08 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (7.02 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 20.8 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.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (7.02 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.

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 (Please use freshly prepared in vivo formulations for optimal results.)