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 GI tract but likely undergoes significant first pass metabolism with only 60% of the drug reaching systemic circulation unchanged. Many topical formulations are absorbed percutaneous and produce clinically significant plasma concentrations. Absorption is dose proportional over the range of 25-150 mg. Tmax varies between formulations with the oral solution reaching peak plasma concentrations in 10-40min, the enteric coated tablet in 1.5-2h, and the sustained- and extended-release formulations prolonging Tmax even further. Administration with food has no significant effects on AUC but does delay Tmax to 2.5-12h.
Diclofenac is mainly eliminated via metabolism. Of the total dose, 60-70% is eliminated in the urine and 30% is eliminated in the feces. No significant enterohepatic recycling occurs.
Diclofenac has a total volume of distribution of 5-10 L or 0.1-0.2 L/kg. The volume of the central compartment is 0.04 L/kg. Diclofenac distributes to the synovial fluid reaching peak concentration 2-4h after administration. There is limited crossing of the blood brain barrier and cerebrospinal fluid concentrations only reach 8.22% of plasma concentrations. Doses of 50 mg delivered via intramuscular injection produced no detectable diclofenac concentrations in breast milk, however metabolite concentrations were not investigated. Diclofenac has been shown to cross the placenta in mice and rats but human data is unavailable.
Diclofenac has a plasma clearance 16 L/h.
Onset of absorption is delayed when diclofenac sodium is administered orally as delayed-release (enteric-coated) tablets, but the extent of absorption does not appear to be affected. /Diclofenac sodium/
Measurable plasma concentrations of diclofenac have been observed in some fasting individuals within 10 minutes of receiving diclofenac potassium conventional tablets. /Diclofenac potassium/
Diclofenac sodium and diclofenac potassium are almost completely absorbed from the GI tract; however, the drugs undergo extensive first-pass metabolism in the liver, with only about 50-60% of a dose of diclofenac sodium or diclofenac potassium reaching systemic circulation as unchanged drug. Diclofenac also is absorbed into systemic circulation following rectal administration and percutaneously following topical application to the skin as a gel or transdermal system.
Food decreases the rate of absorption of conventional tablets of diclofenac potassium and of delayed-release (enteric-coated) tablets of diclofenac sodium, resulting in delayed and decreased peak plasma concentrations; however, the extent of absorption is not affected substantially. When diclofenac potassium conventional tablets are administered with food, time to achieve peak plasma concentrations of the drug is increased and peak plasma concentrations of the drug are decreased by approximately 30%. When single doses of diclofenac sodium delayed-release (enteric-coated) tablets are taken with food, the onset of absorption usually is delayed by 1-4.5 hours but may be delayed up to 12 hours in some patients. These food-induced alterations in GI absorption of the drug result from delayed transit of the delayed-release (enteric-coated) tablets to the small intestine, the site of dissolution. When diclofenac sodium extended-release tablets are taken with food, onset of absorption is delayed 1-2 hours and peak plasma concentrations are increased two-fold; however, extent of absorption is not substantially affected. Absorption of diclofenac does not appear to be affected substantially by the presence of food following continuous dosing of the drug. Antacids also may decrease the rate but not the extent of absorption of diclofenac.
For more Absorption, Distribution and Excretion (Complete) data for DICLOFENAC (11 total), please visit the HSDB record page.

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Metabolism / Metabolites
Diclofenac undergoes oxidative metabolism to hydroxy metabolites as well as conjugation to glucuronic acid, sulfate, and taurine. The primary metabolite is 4'-hydroxy diclofenac which is generated by CYP2C9. This metabolite is very weakly active with one thirtieth the activity of diclofenac. Other metabolites include 3'-hydroxy diclofenac, 3'-hydroxy-4'methoxy diclofenac, 4',5-dihydroxy diclofenac, an acylglucuronide conjugate, and other conjugate metabolites.
The extent of metabolism of diclofenac sodium in excised viable human skin was investigated using combination HPLC and radioactivity assay. In an earlier diffusion experiment using an in vitro flow-through diffusion system, radiolabelled diclofenac sodium in either lotion (Pennsaid) or aqueous solution was applied to viable human skin, either as single dose or multiple dose (8 times over 2 days). In this study, the receptor fluid samples from the diffusion experiment were subjected to extraction and the aliquot was analysed using HPLC to separate diclofenac and authentic metabolites. Based on the radioactivity of each HPLC fraction, the collection time of the fractions was compared with the retention time of diclofenac and metabolites in standard solutions. The samples from a single or multiple dose application of lotion showed radioactivity in mainly one fraction, whose retention time corresponded with diclofenac. Other HPLC fractions showed none or only small amounts of radioactivity within the error range of the assay. The same results were obtained with the pooled samples from the application of the lotion or of aqueous solution. The results suggest that diclofenac sodium does not undergo metabolism in viable human epidermis during percutaneous absorption in vitro. Hence, with topical application to human skin in vivo, diclofenac will be delivered with minimal, if any, metabolism. /Diclofenac sodium/
In humans, metabolism of the commonly used nonsteroidal antiinflammatory drug diclofenac /compound/ 1 yields principally the 4'-hydroxy /compound/ 2, 5-hydroxy /compound/ 3, and acyl glucuronide /compound/ 4 metabolites. All three metabolites have been implicated in rare idiosyncratic adverse reactions associated with this widely used drug. Therefore, for mechanistic toxicological studies of /compound/ 1, substantial quantities of 2-4 are required and their syntheses and characterization are described here. Key steps were a convenient two-step preparation of aniline /compound/ 5 from phenol, efficient and selective 6-iodination of amide /compound/ 18, and high-yielding Ullmann couplings to generate diarylamines /compound/ 11 and /compound/ 21. The acyl glucuronide /compound/ 4 was obtained by Mitsunobu reaction of /compound/ 1 (free acid) with allyl glucuronate /compound/ 23 followed by Pd(0) deprotection, using a modification of a published procedure. /Investigators/ report full characterization of /compound/ 4 ... /Investigators/ report also the metabolic fates of the synthetic metabolites: /compound/ 2 and /compound/ 3 were glucuronidated in rats, but only /compound/ 3 formed glutathione adducts in vivo and by enzymatic synthesis via a quinoneimine intermediate. A previously undescribed glutathione adduct of /compound/ 3 was obtained by enzymatic synthesis. Compound /compound/ 4 formed an imine-linked protein conjugate as evinced by sodium cyanoborohydride trapping.
Diclofenac is eliminated predominantly (approximately 50%) as its 4'-hydroxylated metabolite in humans, whereas the acyl glucuronide (AG) pathway appears more important in rats (approximately 50%) and dogs (>80-90%). However, previous studies of diclofenac oxidative metabolism in human liver microsomes (HLMs) have yielded pronounced underprediction of human in vivo clearance. We determined the relative quantitative importance of 4'-hydroxy and AG pathways of diclofenac metabolism in rat, dog, and human liver microsomes. Microsomal intrinsic clearance values (CL(int) = V(max)/K(m)) were determined and used to extrapolate the in vivo blood clearance of diclofenac in these species. Clearance of diclofenac was accurately predicted from microsomal data only when both the AG and the 4'-hydroxy pathways were considered. However, the fact that the AG pathway in HLMs accounted for ~75% of the estimated hepatic CL(int) of diclofenac is apparently inconsistent with the 4'-hydroxy diclofenac excretion data in humans. Interestingly, upon incubation with HLMs, significant oxidative metabolism of diclofenac AG, directly to 4'-hydroxy diclofenac AG, was observed. The estimated hepatic CL(int) of this pathway suggested that a significant fraction of the intrahepatically formed diclofenac AG may be converted to its 4'-hydroxy derivative in vivo. Further experiments indicated that this novel oxidative reaction was catalyzed by CYP2C8, as opposed to CYP2C9-catalyzed 4'-hydroxylation of diclofenac. These findings may have general implications in the use of total (free + conjugated) oxidative metabolite excretion for determining primary routes of drug clearance and may question the utility of diclofenac as a probe for phenotyping human CYP2C9 activity in vivo via measurement of its pharmacokinetics and total 4'-hydroxy diclofenac urinary excretion.
The metabolism of (14)C-diclofenac in mice was investigated following a single oral dose of 10 mg/kg. The majority of the drug-related material was excreted in the urine within 24 hr of administration (49.7%). Liquid chromatographic analysis of urine and fecal extracts revealed extensive metabolism to at least 37 components, with little unchanged diclofenac excreted. Metabolites were identified using a hybrid linear ion-trap mass spectrometer via exact mass determinations of molecular ions and subsequent multi-stage fragmentation. The major routes of metabolism identified included: 1) conjugation with taurine; and 2) hydroxylation (probably at the 4'-and 5-arene positions) followed by conjugation to taurine, glucuronic acid or glucose. Ether, rather than acyl glucuronidation, predominated. There was no evidence for p-benzoquinone-imine formation (i.e. no glutathione or mercapturic acid conjugates were detected). A myriad of novel minor drug-related 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, glucuronide and taurine) or N-linked sulfation or glucosidation were also observed. Acyl- or amide-linked-conjugates of benzoic acid metabolites and several indolinone derivatives with further hydroxylated and conjugated moieties were also evident. The mechanisms involved in the generation of benzoic acid and indolinone products indicate the formation reactive intermediates in vivo that may possibly contribute to hepatotoxicity.
For more Metabolism/Metabolites (Complete) data for DICLOFENAC (7 total), please visit the HSDB record page.
Diclofenac has known human metabolites that include 4'-hydroxydiclofenac, 5-hydroxydiclofenac, and (2S,3S,4S,5R)-6-[2-[2-(2,6-Dichloroanilino)phenyl]acetyl]oxy-3,4,5-trihydroxyoxane-2-carboxylic acid.
Diclofenac is a known human metabolite of aceclofenac.
Hepatic.
Route of Elimination: Diclofenac is eliminated through metabolism and subsequent urinary and biliary excretion of the glucuronide and the sulfate conjugates of the metabolites. Little or no free unchanged diclofenac is excreted in the urine. Approximately 65% of the dose is excreted in the urine and approximately 35% in the bile as conjugates of unchanged diclofenac plus metabolites.
Half Life: 2 hours

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Biological Half-Life
The terminal half-life of diclofenac is approximately 2 h, however the apparent half-life including all metabolites is 25.8-33 h.
Following application of diclofenac epolamine transdermal system, the elimination half-life of diclofenac is approximately 12 hours. /Diclofenac epolamine/
Following IV administration of diclofenac sodium in healthy adults, the half-life of diclofenac reportedly averages about 3 minutes in the initial distribution phase, about 16 minutes in the intermediate (redistribution) phase, and about 1-2 hours in the terminal (elimination) phase. /Diclofenac sodium/
Elimination: Up to 6 hours

Hepatotoxicity
Elevated serum aminotransferase levels have been reported in up to 15% of patients taking oral diclofenac chronically, but are greater than 3 times the upper limit of normal in only 2% to 4% (Cases 1 and 2). Clinically apparent and symptomatic liver disease with jaundice due to diclofenac is rare (1 to 5 cases per 100,000 prescriptions, occurring in 1 to 5 persons per 10,000 exposed). Nevertheless, more than a hundred instances of clinically apparent liver injury due to diclofenac have been reported in the literature and, in most case series, diclofenac ranks in the top 10 causes of drug induced liver injury. The time to onset of liver injury varies from within a week to over a year after starting. The majority of cases present within 2 to 6 months (Cases 3 and 4), and the more severe cases tend to present earlier. The pattern of injury is almost exclusively hepatocellular, although cases presenting with mixed patterns have been reported. The clinical picture is that of jaundice preceded by anorexia, nausea, vomiting and malaise. Fever and rash occur in 25% of cases and some cases have immunoallergic features, while others resemble chronic hepatitis and have autoimmune features. In most cases, liver histology reveals an acute lobular hepatitis. However, a cases with prolonged latency diclofenac hepatotoxicity can have clinical and histologic features of chronic hepatitis (Case 2). There seems to be greater susceptibility for diclofenac liver injury among women than men. The injury can be severe, and several cases of acute liver failure have been attributed to diclofenac.
Likelihood score: A (well known cause of clinically apparent liver injury).
Topical forms of diclofenac (solutions, gels, creams, patches) have been associated with only a low rate of serum enzyme elevations (generally less than 1%) that may be no greater than occurs with placebo or vehicle application. However, product labels for topical diclofenac mention the possibility of liver injury and at least one case of clinically apparent liver injury attributed to topical diclofenac has been reported in the literature. Nevertheless, clinically apparent liver injury due to topical forms of diclofenac must be exceedingly rare.

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Data on excretion of diclofenac into milk are poor, but the drug has a short half-life and little glucuronide metabolite formation. Levels in milk appear to be quite low. Most reviewers consider diclofenac to be acceptable during breastfeeding. Other agents having more published information may be preferred, especially while nursing a newborn or preterm infant.
Maternal use of diclofenac topical gel or eye drops would not be expected to cause any adverse effects in breastfed infants. To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue.
◉ Effects in Breastfed Infants
In one study, 30 mothers undergoing elective cesarean section were allowed to use 25 mg diclofenac suppositories along with either spinal or spinal and epidural anesthesia with a local anesthetic after delivery. The spinal anesthetic group used an average of 56 mg of diclofenac on the day of delivery and 33 mg on the next day whereas the women receiving both spinal and epidural anesthesia used 21 and 18 mg. No mention was made of adverse effects on the breastfed infants.
A breastfed infant developed urticaria on day 15 of life. Her mother had been taking diclofenac (dosage unspecified) for pain since her cesarean section delivery. Diclofenac is a possible cause of the urticaria; however, the infant had also received hepatitis B vaccination 7 days before and the authors thought that it was a more likely cause of the reaction.
◉ Effects on Lactation and Breastmilk
A randomized, double-blind study was performed in pregnant women scheduled for cesarean section under spinal anesthesia with bupivacaine and fentanyl. Patients received either 100 mg diclofenac (n = 100), 100 mg tramadol (n = 100) or placebo (glycerin suppositories) n = 100, all given as rectal suppositories every 8 hours for the first 24 hours after surgery. The time to initiate breastfeeding was significantly shorter among mothers who received diclofenac than a placebo, 1.5 vs 4.1 hours with breastfeeding support and 3.5 vs 6.2 hours without support. Diclofenac was slightly more effective than tramadol among mothers who received no support (3.5 vs 3.7 hours).

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Protein Binding
Diclofenac is over 99.7% bound to serum proteins, primarily albumin. It is undergoes limited binding to lipoproteins as well with 1.1% bound 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 consisting of phenylacetic acid having a (2,6-dichlorophenyl)amino group at the 2-position. It has a role as a non-narcotic analgesic, an antipyretic, an EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor, a xenobiotic, an environmental contaminant, a drug allergen and a non-steroidal anti-inflammatory drug. It is a secondary amino compound, an amino acid, a dichlorobenzene, an aromatic amine and a monocarboxylic acid. It is functionally related to a phenylacetic acid and a diphenylamine. It is a conjugate acid of a diclofenac(1-).
Diclofenac is a phenylacetic acid derivative and non-steroidal anti-inflammatory drug (NSAID). NSAIDs inhibit cyclooxygenase (COX)-1 and-2 which are the enzyme responsible for producing prostaglandins (PGs). PGs contribute to inflammation and pain signalling. Diclofenac, like other NSAIDs, is often used as first line therapy for acute and chronic pain and inflammation from a variety of causes. Diclofenac was the product of rational drug design based on the structures of [phenylbutazone], [mefenamic acid], and [indomethacin]. The addition of two chlorine groups in the ortho position of the phenyl ring locks the ring in maximal torsion which appears to be related to increased potency. It is often used in combination with [misoprostol] to prevent NSAID-induced gastric ulcers. Diclofenac was first approved by the FDA in July 1988 under the trade name Voltaren, marketed by Novartis (previously Ciba-Geigy).
Diclofenac is a Nonsteroidal Anti-inflammatory Drug. The mechanism of action of diclofenac is as a Cyclooxygenase Inhibitor. The physiologic effect of diclofenac is by means of Decreased Prostaglandin Production.
Diclofenac is a commonly used nonsteroidal antiinflammatory drug (NSAID) used for the therapy of chronic forms of arthritis and mild-to-moderate acute pain. Therapy with diclofenac in full doses is frequently associated with mild serum aminotransferase elevations and, in rare instances, can lead to serious clinically apparent, acute or chronic liver disease.
Diclofenac is a nonsteroidal benzeneacetic acid derivative with anti-inflammatory activity. As a nonsteroidal anti-inflammatory drug (NSAID), diclofenac binds and chelates both isoforms of cyclooxygenase (COX-1 and-2), thereby blocking the conversion of arachidonic acid to pro-inflammatory-proprostaglandins. This agent also may inhibit COX-2-mediated tumor angiogenesis. When inhibiting COX-2, diclofenac may be effective in relieving pain and inflammation; when inhibiting COX-1, it may produce unacceptable gastrointestinal side effects. This agent may be more active against COX-2 than several other carboxylic acid-containing NSAIDs. (NCI04)
A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.
A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.

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Drug Indication
Diclofenac is indicated for use in the treatment of pain and inflammation from varying sources including inflammatory conditions such as osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis, as well as injury-related inflammation due to surgery and physical trauma. It is often used in combination with [misoprostol] as a gastro-protective agent in patients with high risk of developing NSAID-induced ulcers.
FDA Label

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Mechanism of Action
Diclofenac inhibits cyclooxygenase-1 and -2, the enzymes responsible for production of prostaglandin (PG) G₂ which is the precursor to other PGs. These molecules have broad activity in pain and inflammation and the inhibition of their production is the common mechanism linking each effect of diclofenac. PGE₂ is the primary PG involved in modulation of nociception. It mediates peripheral sensitization through a variety of effects. PGE₂ activates the G_q-coupled EP₁ receptor leading to increased activity of the inositol trisphosphate/phospholipase C pathway. Activation of this pathway releases intracellular stores of calcium which directly reduces action potential threshold and activates protein kinase C (PKC) which contributes to several indirect mechanisms. PGE₂ also activates the EP₄ receptor, coupled to G_s, which activates the adenylyl cyclase/protein kinase A (AC/PKA) signaling pathway. PKA and PKC both contribute to the potentiation of transient receptor potential cation channel subfamily V member 1 (TRPV1) potentiation, which increases sensitivity to heat stimuli. They also activate tetrodotoxin-resistant sodium channels and inhibit inward potassium currents. PKA further contributes to the activation of the P2X3 purine receptor and sensitization of T-type calcium channels. The activation and sensitization of depolarizing ion channels and inhibition of inward potassium currents serve to reduce the intensity of stimulus necessary to generate action potentials in nociceptive sensory afferents. PGE₂ act via EP₃ to increase sensitivity to bradykinin and via EP₂ to further increase heat sensitivity. Central sensitization occurs in the dorsal horn of the spinal cord and is mediated by the EP₂ receptor which couples to G_s. Pre-synaptically, this receptor increases the release of pro-nociceptive neurotransmitters glutamate, CGRP, and substance P. Post-synaptically it increases the activity of AMPA and NMDA receptors and produces inhibition of inhibitory glycinergic neurons. Together these lead to a reduced threshold of activating, allowing low intensity stimuli to generate pain signals. PGI₂ is known to play a role via its G_s-coupled IP receptor although the magnitude of its contribution varies. It has been proposed to be of greater importance in painful inflammatory conditions such as arthritis. By limiting sensitization, both peripheral and central, via these pathways NSAIDs can effectively reduce inflammatory pain. PGI₂ and PGE₂ contribute to acute inflammation via their IP and EP₂ receptors. Similarly to β adrenergic receptors these are G_s-coupled and mediate vasodilation through the AC/PKA pathway. PGE₂ also contributes by increasing leukocyte adhesion to the endothelium and attracts the cells to the site of injury. PGD₂ plays a role in the activation of endothelial cell release of cytokines through its DP₁ receptor. PGI₂ and PGE₂ modulate T-helper cell activation and differentiation through IP, EP₂, and EP₄ receptors which is believed to be an important activity in the pathology of arthritic conditions. By limiting the production of these PGs at the site of injury, NSAIDs can reduce inflammation. PGE₂ can cross the blood-brain barrier and act on excitatory G_q EP₃ receptors on thermoregulatory neurons in the hypothalamus. This activation triggers an increase in heat-generation and a reduction in heat-loss to produce a fever. NSAIDs prevent the generation of PGE₂ thereby reducing the activity of these neurons.
Diclofenac has pharmacologic actions similar to those of other prototypical NSAIAs. The drug exhibits anti-inflammatory, analgesic, and antipyretic activity. The exact mechanisms have not been clearly established, but many of the actions appear to be associated principally with the inhibition of prostaglandin synthesis. Diclofenac inhibits the synthesis of prostaglandins in body tissues by inhibiting cyclooxygenase; at least 2 isoenzymes, cyclooxygenase-1 (COX-1) and -2 (COX-2) (also referred to as prostaglandin G/H synthase-1 (PGHS-10 and -2 (PGHS-2), respectively), have been identified that catalyze the formation of prostaglandins in the arachidonic acid pathway. Diclofenac, like other prototypical NSAIAs, inhibits both COS-1 and COS-2. Although the exact mechanisms have not been clearly established, NSAIAs appear to exert anti-inflammatory, analgesic, and antipyretic activity principally through inhibition of the COS-2 isoenzyme; COX-1 inhibition presumably is responsible for the drugs' unwanted effects on GI mucosa and platelet aggregation.
As for all non-steroidal anti-inflammatory drugs the pharmacodynamic effects of diclofenac sodium are of anti-inflammatory, analgesic and antipyretic character due to the decrease of the prostaglandin synthesis from arachidonic acid by inhibition of the cyclo-oxygenase activity. It also induces deleterious effects on gastric and intestinal mucosa and an inhibition of platelet aggregation. /Diclofenac sodium/

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.)