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Diclofenac Sodium



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Diclofenac Sodium

15307-79-6; Sodium diclofenac; Diclofenac sodium salt; Voltaren; Solaraze

Molecular Formula: C14H10Cl2NNaO2
Molecular Weight: 318.129 g/mol

Diclofenac, sold under the trade names Voltaren among others, is a nonsteroidal anti-inflammatory drug (NSAID) used to treat pain and inflammatory diseases such as gout.[3] It is taken by mouth or applied to the skin.[3] Improvements in pain typically occur within half an hour and last for as much as eight hours.[3] It is also available in combination with misoprostol in an effort to decrease stomach problems.[4]

Common side effects include abdominal paingastrointestinal bleeding, nausea, dizziness, headache, and swelling.[3] Serious side effects may include heart diseasestrokekidney problems, and stomach ulceration.[4][3] Use is not recommended in the third trimester of pregnancy.[3] It is likely safe during breastfeeding.[4] It is believed to work by decreasing the production of prostaglandin.[5] It blocks both cycloxygenase-1 (COX-1) and cycloxygenase-2 (COX-2).[3]

Diclofenac was patented in 1965 by Ciba-Geigy and came into medical use in the United States in 1988.[3][6] It is available as a generic medication.[3] In the United States the wholesale cost per dose is less than US$0.15 as of 2018.[7] In 2016 it was the 78th most prescribed medication in the United States with more than 9 million prescriptions.[8] It is available as both a sodium and a potassium salt.[4]

Medical uses

Diclofenac is used to treat pain, inflammatory disorders, and dysmenorrhea.[9]


Inflammatory disorders may include musculoskeletal complaints, especially arthritisrheumatoid arthritispolymyositisdermatomyositisosteoarthritis, dental pain, temporomandibular joint (TMJ) pain, spondylarthritisankylosing spondylitisgout attacks,[10] and pain management in cases of kidney stones and gallstones. An additional indication is the treatment of acute migraines.[11] Diclofenac is used commonly to treat mild to moderate postoperative or post-traumatic pain, in particular when inflammation is also present,[10] and is effective against menstrual pain and endometriosis.

Diclofenac is also available in topical forms and has been found to be useful for osteoarthritis but not other types of long-term musculoskeletal pain.[12]

It may also help with actinic keratosis, and acute pain caused by minor strains, sprains, and contusions (bruises).[13]

In many countries,[14] eye drops are sold to treat acute and chronic nonbacterial inflammation of the anterior part of the eyes (e.g., postoperative states). Diclofenac eye drops have also been used to manage pain for traumatic corneal abrasion.[15]

Diclofenac is often used to treat chronic pain associated with cancer, in particular if inflammation is also present (Step I of the World Health Organization (WHO) scheme for treatment of chronic pain).[16] Diclofenac can be combined with opioids if needed such as a fixed combination of diclofenac and codeine.


Adverse effects

Diclofenac consumption has been associated with significantly increased vascular and coronary risk in a study including coxib, diclofenac, ibuprofen and naproxen.[18] Upper gastrointestinal complications were also reported.[18] Major adverse cardiovascular events (MACE) were increased by about a third by diclofenac, chiefly due to an increase in major coronary events.[18] Compared with placebo, of 1000 patients allocated to diclofenac for a year, three more had major vascular events, one of which was fatal.[18] Vascular death was increased significantly by diclofenac.[18]


In 2013, a study found major vascular events were increased by about a third by diclofenac, chiefly due to an increase in major coronary events.[18] Compared with placebo, of 1000 people allocated to diclofenac for a year, three more had major vascular events, one of which was fatal.[18] Vascular death was increased by diclofenac (1·65).[18]

Following the identification of increased risks of heart attacks with the selective COX-2 inhibitor rofecoxib in 2004, attention has focused on all the other members of the NSAIDs group, including diclofenac. Research results are mixed, with a meta-analysis of papers and reports up to April 2006 suggesting a relative increased rate of heart disease of 1.63 compared to nonusers.[19] Professor Peter Weissberg, Medical Director of the British Heart Foundation said, “However, the increased risk is small, and many patients with chronic debilitating pain may well feel that this small risk is worth taking to relieve their symptoms”. Only aspirin was found not to increase the risk of heart disease; however, this is known to have a higher rate of gastric ulceration than diclofenac. In Britain the Medicines and Healthcare Products Regulatory Agency (MHRA) said in June 2013 that the drug should not be used by people with serious underlying heart conditions—people who had suffered heart failure, heart disease or a stroke were advised to stop using it completely.[20] As of January 15, 2015 the MHRA announced that diclofenac will be reclassified as a prescription-only medicine (POM) due to the risk of cardiovascular adverse events.[21]

A subsequent large study of 74,838 Danish users of NSAIDs or coxibs found no additional cardiovascular risk from diclofenac use.[22] A very large study of 1,028,437 Danish users of various NSAIDs or coxibs found the “Use of the nonselective NSAID diclofenac and the selective cyclooxygenase-2 inhibitor rofecoxib was associated with an increased risk of cardiovascular death (odds ratio, 1.91; 95% confidence interval, 1.62 to 2.42; and odds ratio, 1.66; 95% confidence interval, 1.06 to 2.59, respectively), with a dose-dependent increase in risk.”[23]

Diclofenac is similar in COX-2 selectivity to celecoxib.[24]


  • Gastrointestinal complaints are most often noted. The development of ulceration and/or bleeding requires immediate termination of treatment with diclofenac. Most patients receive a gastro-protective drug as prophylaxis during long-term treatment (misoprostolranitidine 150 mg at bedtime or omeprazole 20 mg at bedtime).


  • Liver damage occurs infrequently, and is usually reversible. Hepatitis may occur rarely without any warning symptoms and may be fatal. Patients with osteoarthritis more often develop symptomatic liver disease than patients with rheumatoid arthritis. Liver function should be monitored regularly during long-term treatment. If used for the short-term treatment of pain or fever, diclofenac has not been found more hepatotoxic than other NSAIDs.
  • As of December 2009, Endo, Novartis, and the US FDA notified healthcare professionals to add new warnings and precautions about the potential for elevation in liver function tests during treatment with all products containing diclofenac sodium.[25]
  • Cases of drug-induced hepatotoxicity have been reported in the first month, but can occur at any time during treatment with diclofenac. Postmarketing surveillance has reported cases of severe hepatic reactions, including liver necrosis, jaundice, fulminant hepatitis with and without jaundice, and liver failure. Some of these reported cases resulted in fatalities or liver transplantation.
  • Physicians should measure transaminases periodically in patients receiving long-term therapy with diclofenac. Based on clinical trial data and postmarketing experiences, transaminases should be monitored within 4 to 8 week after initiating treatment with diclofenac.


  • NSAIDs “are associated with adverse renal [kidney] effects caused by the reduction in synthesis of renal prostaglandins[26] in sensitive persons or animal species, and potentially during long-term use in nonsensitive persons if resistance to side effects decreases with age. However, this side effect cannot be avoided merely by using a COX-2 selective inhibitor because, “Both isoforms of COX, COX-1 and COX-2, are expressed in the kidney… Consequently, the same precautions regarding renal risk that are followed for nonselective NSAIDs should be used when selective COX-2 inhibitors are administered.”[26] However, diclofenac appears to have a different mechanism of renal toxicity.[citation needed]
  • Studies in Pakistan showed diclofenac caused acute kidney failure in vultures when they ate the carcasses of animals that had recently been treated with it. Drug-sensitive species and individual humans are initially assumed to lack genes expressing specific drug detoxification enzymes.[27]

Mental health

  • Mental health side effects have been reported. These symptoms are rare, but exist in significant enough numbers to include as potential side effects. These include depression, anxiety, irritability, nightmares, and psychotic reactions.[28]

Mechanism of action

The primary mechanism responsible for its anti-inflammatoryantipyretic, and analgesic action is thought to be inhibition of prostaglandin synthesis by inhibition of the transiently expressed prostaglandin-endoperoxide synthase-2 (PGES-2) also known as cycloxygenase-2 (COX-2). It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis.[29]

Inhibition of prostaglandin synthesis occurs systemically resulting in undesirable symptoms such as irritation of the gastric epithelium.[citation needed] This is the main side effect of diclofenac. Diclofenac inhibits COX-2 with 20 times greater potency than the constitutively expressed isoenzyme COX-1[30] and has, therefore, a somewhat lower incidence of gastrointestinal complaints than noted with aspirin which inhibits COX-1 to a greater extent.

The action of one single dose is much longer (6 to 8 hr) than the very short 1.2–2 hr half-life of the drug would indicate. This could be partly because it persists for over 11 hours in synovial fluids.[31]

Diclofenac may also be a unique member of the NSAIDs. Some evidence indicates it inhibits the lipoxygenase pathways, thus reducing formation of the leukotrienes(also pro-inflammatory autacoids). It also may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain its high potency – it is the most potent NSAID on a broad basis.[32]

Marked differences exist among NSAIDs in their selective inhibition of the two subtypes of cyclooxygenase, COX-1 and COX-2. Much pharmaceutical drug design has attempted to focus on selective COX-2 inhibition as a way to minimize the gastrointestinal side effects of NSAIDs such as aspirin. In practice, use of some COX-2 inhibitors with their adverse effects has led to massive numbers of patient family lawsuits alleging wrongful death by heart attack, yet other significantly COX-selective NSAIDs, such as diclofenac, have been well tolerated by most of the population.\

Besides the COX-inhibition, a number of other molecular targets of diclofenac possibly contributing to its pain-relieving actions have recently been identified. These include:

  • Blockage of voltage-dependent sodium channels (after activation of the channel, diclofenac inhibits its reactivation also known as phase inhibition)[citation needed]
  • Blockage of acid-sensing ion channels (ASICs)[33]
  • Positive allosteric modulation of KCNQ- and BK-potassium channels (diclofenac opens these channels, leading to hyperpolarization of the cell membrane)

Ecological effects

Use of diclofenac for animals is controversial due to toxicity when eaten by scavenging birds that eat dead animals; the drug has been banned for veterinary use in many countries.

Use of diclofenac in animals has been reported to have led to a sharp decline in the vulture population in the Indian subcontinent – a 95% decline by 2003[34] and a 99.9% decline by 2008. The mechanism is presumed to be renal failure;[35] however, toxicity may be due to direct inhibition of uric acid secretion in vultures.[36] Vultures eat the carcasses of livestockthat have been administered veterinary diclofenac, and are poisoned by the accumulated chemical,[37] as vultures do not have a particular enzyme to break down diclofenac. At a meeting of the National Wildlife Board in March 2005, the Government of India announced it intended to phase out the veterinary use of diclofenac.[38] Meloxicam is a safer alternative to replace use of diclofenac.[39] It is more expensive than diclofenac, but the price is coming down as more pharmaceutical companies begin to manufacture it.

Steppe eagles have the same vulnerability to diclofenac as vultures and may also fall victim to it.[40] Diclofenac has been shown also to harm freshwater fish species such as rainbow trout.[41][42][43][44] In contrast, New World vultures, such as the turkey vulture, can tolerate at least 100 times the level of diclofenac that is lethal to Gyps species.[45]

“The loss of tens of millions of vultures over the last decade has had major ecological consequences across the Indian Subcontinent that pose a potential threat to human health. In many places, populations of feral dogs (Canis familiaris) have increased sharply from the disappearance of Gyps vultures as the main scavenger of wild and domestic ungulatecarcasses. Associated with the rise in dog numbers is an increased risk of rabies[39] and casualties of almost 50,000 people.[46] The Government of India cites this as one of the major consequences of a vulture species extinction.[38] A major shift in the transfer of corpse pathogens from vultures to feral dogs and rats could lead to a disease pandemic, causing millions of deaths in a crowded country like India, whereas vultures’ digestive systems safely destroy many species of such pathogens. Vultures are long-lived and slow to breed. They start breeding only at the age of six and only 50% of young survive. Even if the government ban is fully implemented, it will take several years to revive the vulture population.[47]

The loss of vultures has had a social impact on the Indian Zoroastrian Parsi community, who traditionally use vultures to dispose of human corpses in Towers of Silence, but are now compelled to seek alternative methods of disposal.[39]

Despite the vulture crisis, diclofenac remains available in other countries including many in Europe.[48] It was controversially approved for veterinary use in Spain in 2013 and continues to be available, despite Spain being home to around 90% of the European vulture population and an independent simulation showing that the drug could reduce the population of vultures by 1-8% annually. Spain’s medicine agency presented simulations suggesting that the number of deaths would be quite small.[49][50]

Formulations and trade names

The name “diclofenac” derives from its chemical name: 2-(2,6-dichloranilino) phenylacetic acid. Diclofenac was first synthesized by Alfred Sallmann and Rudolf Pfister and introduced as Voltaren by Ciba-Geigy (now Novartis) in 1973, now by Glaxo SmithKline.[51]

In the United Kingdom, United States, India, and Brazil diclofenac may be supplied as either the sodium or potassium salt; in China, it is most often supplied as the sodium salt, while in some other countries it is only available as the potassium salt.

Pennsaid is a minimally systemic prescription topical lotion formulation of 1.5% w/w diclofenac sodium, which is approved in the US, Canada and other countries for osteoarthritis of the knee.

Flector Patch, a minimally systemic topical patch formulation of diclofenac, is indicated for acute pain due to minor sprains, strains, and contusions. The patch has been approved in many other countries outside the US under different brand names.

Voltaren and Voltarol contain the sodium salt of diclofenac. In the United Kingdom, Voltarol can be supplied with either the sodium salt or the potassium salt, while Cataflam, sold in some other countries, is the potassium salt only. However, Voltarol Emulgel contains diclofenac diethylammonium, in which a 1.16% concentration is equivalent to a 1% concentration of the sodium salt. In 2016 Voltarol was one of the biggest selling branded over-the-counter medications sold in Great Britain, with sales of £39.3 million.[52]

Diclofenac is available in stomach acid-resistant formulations (25 and 50 mg), fast-disintegrating oral formulations (25 and 50 mg), powder for oral solution (50 mg), slow- and controlled-release forms (75, 100 or 150 mg), suppositories (50 and 100 mg), and injectable forms (50 and 75 mg).

Diclofenac is also available over-the-counter in some countries: 12.5 mg diclofenac as potassium salt in Switzerland (Voltaren dolo), the Netherlands (Voltaren K), and preparations containing 25 mg diclofenac as the potassium salt in Germany (various trade names), New ZealandAustraliaJapan, (Voltaren Rapid), and Sweden (Voltaren T and Diclofenac T). Diclofenac as potassium salt can be found throughout the Middle East in 25 mg and 50 mg doses (Cataflam).

Solaraze (3% diclofenac sodium gel) is topically applied, twice a day for three months, to manage the skin condition known as actinic or solar keratosis. Parazone-DP is a combination of diclofenac potassium and paracetamol, manufactured and supplied by Ozone Pharmaceuticals and Chemicals, Gujarat, India. It is sold in Uruguay alone or, in combination with orphenadrine to treat muscle spasms/pain due to injuries (Dicloflex Ion).

On 14 January 2015, diclofenac oral preparations were reclassified as prescription-only medicines in the UK. The topical preparations are still available without prescription.[53]

Diclofenac formulations are available worldwide under many different trade names.[1]

Title: Diclofenac
CAS Registry Number: 15307-86-5
CAS Name: 2-[(2,6-Dichlorophenyl)amino]benzeneacetic acid
Additional Names: [o-(2,6-dichloroanilino)phenyl]acetic acid
Trademarks: Motifene (Sankyo)
Molecular Formula: C14H11Cl2NO2
Molecular Weight: 296.15
Percent Composition: C 56.78%, H 3.74%, Cl 23.94%, N 4.73%, O 10.80%
Literature References: Prepn: NL 6604752; A. Sallmann, R. Pfister, US 3558690 (1966, 1971 both to Geigy). Pharmacology: Renaud, Lecompte, Thromb. Diath. Haemorrh. 24, 577 (1970), C.A. 74, 86215m (1971); Krupp et al., Experientia 29, 450 (1973). HPLC determn in plasma and urine: J. Godbillon et al., J. Chromatogr. 338, 151 (1985). Symposium on pharmacology and clinical experience: Semin. Arthritis Rheum. 15, Suppl. 1, 57-110 (1985); on pharmacology, efficacy and safety: Am. J. Med. 80, Suppl. 4B, 1-87 (1986). Comprehensive description: C. M. Adeyeye, P-K. Li, Anal. Profiles Drug Subs. 19, 123-144 (1990). Review of clinical trials in actinic keratosis: D. C. Peters, R. H. Foster, Drugs Aging 14, 313-319 (1999).
Properties: Crystals from ether-petr ether, mp 156-158°.
Melting point: mp 156-158°
Derivative Type: Diethylammonium salt
CAS Registry Number: 78213-16-8
Trademarks: Voltarol (Novartis)
Molecular Formula: C14H11Cl2NO2.C4H11N
Molecular Weight: 369.29
Percent Composition: C 58.54%, H 6.00%, Cl 19.20%, N 7.59%, O 8.66%
Derivative Type: Sodium salt
CAS Registry Number: 15307-79-6
Manufacturers’ Codes: GP-45840
Trademarks: Allvoran (TAD); Benfofen (Sanofi-Synthelabo); Dealgic (Pharmacia); Deflamat (Sankyo); Delphinac (Riemser); Dicloflex (Dexcel); Diclomax (Provalis); Diclophlogont (Azupharma); Dicloreum (Alfa); Duravolten (Dura); Ecofenac (Ecosol); Effekton (Teofarma); Lexobene (Merckle); Neriodin (Nagase); Novapirina (Novartis); Primofenac (Streuli); Prophenatin (Nipro); Rewodina (AWD); Rhumalgan (Sandoz); Voldal (Novartis); Voltaren (Novartis); Xenid (RPG)
Molecular Formula: C14H10Cl2NNaO2
Molecular Weight: 318.13
Percent Composition: C 52.86%, H 3.17%, Cl 22.29%, N 4.40%, Na 7.23%, O 10.06%
Properties: Crystals from water, mp 283-285°. uv max (methanol) 283 nm (e 1.05 ´ 105); (phosphate buffer, pH 7.2) 276 nm (e1.01 ´ 105). Soly at 25°C (mg/ml): deionized water (pH 5.2) >9; methanol >24; acetone 6; acetonitrile <1; cyclohexane <1; HCl (pH 1.1) <1; phosphate buffer (pH 7.2) 6. pKa 4. Partition coefficient (N-octanol/aq. buffer): 13.4. LD50 in mice, rats (mg/kg): ~390, 150 orally (Krupp).
Melting point: mp 283-285°
pKa: pKa 4
Log P: Partition coefficient (N-octanol/aq. buffer): 13.4
Absorption maximum: uv max (methanol) 283 nm (e 1.05 ´ 105); (phosphate buffer, pH 7.2) 276 nm (e 1.01 ´ 105)
Toxicity data: LD50 in mice, rats (mg/kg): ~390, 150 orally (Krupp)
Derivative Type: Potassium salt
CAS Registry Number: 15307-81-0
Manufacturers’ Codes: CGP-45840B
Trademarks: Cataflam (Novartis)
Molecular Formula: C14H10Cl2KNO2
Molecular Weight: 334.24
Percent Composition: C 50.31%, H 3.02%, Cl 21.21%, K 11.70%, N 4.19%, O 9.57%
Therap-Cat: Anti-inflammatory.
Keywords: Anti-inflammatory (Nonsteroidal); Arylacetic Acid Derivatives.


Image result for diclofenac synthesis

Last step

Proposed mechanism

enter image description here

The mechanism begins with the condensation of hydrazine onto a ketone (details not shown) to give a hydrazone. Under basic conditions, this hydrazone is deprotonated at nitrogen to give an anionic intermediate. In this case, the negative charge can be delocalized onto oxygen, resulting in an enolate structure. Typically, the negative charge is only shared between a nitrogen and carbon, so this substrate gives a particularly stable intermediate. Protonation of the enolate at carbon gives the first C-H bond necessary to form the product. A second deprotonation at nitrogen gives a similar flow of electrons to form another enolate structure, this time with cleavage of the C-N bond and release of nitrogen gas. Another C-protonation gives the lactam precursor to diclofenac. Cleavage of the amide with hydroxide (details not shown) gives the target.

Manufacturing Process
2, 6-Dichlorophenol is reacted with MMCA, Aniline and Chloro Acetyl Chloride and AlCl3 to yield (2, 6 –
Dichlorophenol) Indolinone is hydrolyzed using isopropyl alcohol and sodium hydroxide to give crude Diclofenac
Sodium. This on purification using deminerlised water and isopropyl alcohol gives the pure Diclofenac Sodium


Image result for diclofenac nmr

Image result for diclofenac nmr


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  35. ^ Swan, Gerry E.; Cuthbert, Richard; Quevedo, Miguel; Green, Rhys E.; Pain, Deborah J.; Bartels, Paul; Cunningham, Andrew A.; Duncan, Neil; Meharg, Andrew A.; Oaks, J. Lindsay; Parry-Jones, Jemima; Shultz, Susanne; Taggart, Mark A.; Verdoorn, Gerhard; Wolter, Kerri (2006-06-22). “Toxicity of diclofenac to Gyps vultures”Biology Letters2 (2): 279–282. doi:10.1098/rsbl.2005.0425ISSN 1744-9561PMC 1618889PMID 17148382.
  36. ^ Naidoo V, Swan GE (August 2008). “Diclofenac toxicity in Gyps vulture is associated with decreased uric acid excretion and not renal portal vasoconstriction”. Comp. Biochem. Physiol. C Toxicol. Pharmacol149 (3): 269–74. doi:10.1016/j.cbpc.2008.07.014PMID 18727958.
  37. ^ “Vet drug ‘killing Asian vulturesBBC News. 2004-02-28.
  38. Jump up to:a b “Saving the Vultures from Extinction” (Press release). Press Information Bureau, Government of India. 2005-05-16. Retrieved 2006-05-12.
  39. Jump up to:a b c Swan G, Naidoo V, Cuthbert R, Green RE, Pain DJ, Swarup D, Prakash V, Taggart M, Bekker L, Das D, Diekmann J, Diekmann M, Killian E, Meharg A, Patra RC, Saini M, Wolter K (2006). “Removing the threat of diclofenac to critically endangered Asian vultures”PLoS Biol4 (3): e66. doi:10.1371/journal.pbio.0040066PMC 1351921PMID 16435886.
  40. ^ Phadnis, Mayuri (May 28, 2014). “Eagles fall prey to vulture-killing chemical”Pune Mirror. Retrieved May 28, 2014.
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External links


    • US 3 558 690 (Geigy; 26.1.1971; CH-prior. 8.4.1965, 25.2.1966, 30.3.1966, 20.12.1967).
    • DAS 1 543 639 (Ciba-Geigy; appl. 7.4.1966; CH-prior. 8.4.1965).
    • DAS 1 793 592 (Ciba-Geigy; appl. 7.4.1966; CH-prior. 8.4.1965).
    • US 3 652 762 (Ciba-Geigy; 28.3.1972; prior. 9.12.1968, 29.9.1969, 14.4.1970).
    • US 3 778 470 (Geigy; 11.12.1973; appl. 2.10.1970; prior. 4.4.1966).
    • CH 492 679 (Geigy; appl. 30.3.1966).
  • Alternative synthesis:

    • DOS 2 613 838 (Ikeda Mohando; appl. 31.3.1976; J-prior. 31.3.1975).
Diclofenac 3D.png
Clinical data
Trade names Cataflam, Voltaren, others[1]
AHFS/ Monograph
MedlinePlus a689002
  • AU: C
  • US: C (Risk not ruled out) in 1st and 2nd trimester, D in 3rd trimester
Routes of
By mouth, rectal, intramuscularintravenous(renal- and gallstones), topical
ATC code
Legal status
Legal status
  • AU: S2 (Pharmacy only) – S4
  • UK: POM (Prescription only) (P for topical formulation)
  • ℞-only in most preparations/countries, limited OTC in some countries, manufacture and veterinary use is banned in India, Nepal, and Pakistan due to imminent extinction of local vultures
Pharmacokinetic data
Protein binding More than 99%
Metabolism Liver, oxidative, primarily by CYP2C9, also by CYP2C8CYP3A4, as well as conjugative by glucuronidation (UGT2B7) and sulfation;[2] no active metabolites exist
Elimination half-life 1.2–2 hr (35% of the drug enters enterohepatic recirculation)
Excretion 40% biliary 60% urine
CAS Number
PubChem CID
PDB ligand
ECHA InfoCard 100.035.755 Edit this at Wikidata
Chemical and physical data
Formula C14H11Cl2NO2
Molar mass 296.148 g/mol
3D model (JSmol)


    • ATC:M01AB05; M02AA15; S01BC03
  • Use:anti-inflammatory, antirheumatic
  • Chemical name:2-[(2,6-dichlorophenyl)amino]benzeneacetic acid
  • Formula:C14H11Cl2NO2
  • MW:296.15 g/mol
  • CAS-RN:15307-86-5
  • InChI: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)
  • EINECS:239-348-5
  • LD50:170 mg/kg (M, p.o.);
    62.5 mg/kg (R, p.o.)

Monosodium salt

  • Formula:C14H10Cl2NNaO2
  • MW:318.14 g/mol
  • CAS-RN:15307-79-6
  • EINECS:239-346-4
  • LD50:116 mg/kg (M, i.v.); 390 mg/kg (M, p.o.);
    117 mg/kg (R, i.v.); 150 mg/kg (R, p.o.)

//////////////Diclofenac Sodium


Diclofenac Sodium

structure depiction
FDA Orange Book Patent
FDA Orange Book Patents: 1 of 21 (FDA Orange Book Patent ID)
Patent 9339551
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 2 of 21 (FDA Orange Book Patent ID)
Patent 9339552
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 3 of 21 (FDA Orange Book Patent ID)
Patent 9415029
Expiration Jul 10, 2029
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 4 of 21 (FDA Orange Book Patent ID)
Patent 9370501
Expiration Jul 10, 2029
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 5 of 21 (FDA Orange Book Patent ID)
Patent 9375412
Expiration Jul 10, 2029
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 6 of 21 (FDA Orange Book Patent ID)
Patent 8946292
Expiration Mar 22, 2027
Drug Application N022396 (Prescription Drug: DYLOJECT. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 7 of 21 (FDA Orange Book Patent ID)
Patent 9168305
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 8 of 21 (FDA Orange Book Patent ID)
Patent 9168304
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 9 of 21 (FDA Orange Book Patent ID)
Patent 9220784
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 10 of 21 (FDA Orange Book Patent ID)
Patent 6407079
Expiration Jun 18, 2019
Drug Application N022396 (Prescription Drug: DYLOJECT. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 11 of 21 (FDA Orange Book Patent ID)
Patent 8252838
Expiration Apr 21, 2028
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 12 of 21 (FDA Orange Book Patent ID)
Patent 8618164
Expiration Jul 10, 2029
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 13 of 21 (FDA Orange Book Patent ID)
Patent 8546450
Expiration Aug 9, 2030
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 14 of 21 (FDA Orange Book Patent ID)
Patent 8217078
Expiration Jul 10, 2029
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 15 of 21 (FDA Orange Book Patent ID)
Patent 8563613
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 16 of 21 (FDA Orange Book Patent ID)
Patent 8871809
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 17 of 21 (FDA Orange Book Patent ID)
Patent 9066913
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 18 of 21 (FDA Orange Book Patent ID)
Patent 8741956
Expiration Jul 10, 2029
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 19 of 21 (FDA Orange Book Patent ID)
Patent 9101591
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 20 of 21 (FDA Orange Book Patent ID)
Patent 9132110
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)
FDA Orange Book Patents: 21 of 21 (FDA Orange Book Patent ID)
Patent 9539335
Expiration Oct 17, 2027
Applicant HZNP
Drug Application N204623 (Prescription Drug: PENNSAID. Ingredients: DICLOFENAC SODIUM)

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DR ANTHONY MELVIN CRASTO, Born in Mumbai in 1964 and graduated from Mumbai University, Completed his Ph.D from ICT, 1991,Matunga, Mumbai, India, in Organic Chemistry, The thesis topic was Synthesis of Novel Pyrethroid Analogues, Currently he is working with AFRICURE PHARMA, ROW2TECH, NIPER-G, CLEANCHEM LABS as ADVISOR, earlier assignment was with GLENMARK LIFE SCIENCES LTD, as CONSUlTANT, Retired from GLENMARK in Jan2022 Research Centre as Principal Scientist, Process Research (bulk actives) at Mahape, Navi Mumbai, India. Total Industry exp 32 plus yrs, Prior to joining Glenmark, he has worked with major multinationals like Hoechst Marion Roussel, now Sanofi, Searle India Ltd, now RPG lifesciences, etc. He has worked with notable scientists like Dr K Nagarajan, Dr Ralph Stapel, Prof S Seshadri, etc, He did custom synthesis for major multinationals in his career like BASF, Novartis, Sanofi, etc., He has worked in Discovery, Natural products, Bulk drugs, Generics, Intermediates, Fine chemicals, Neutraceuticals, GMP, Scaleups, etc, he is now helping millions, has 9 million plus hits on Google on all Organic chemistry websites. His friends call him Open superstar worlddrugtracker. His New Drug Approvals, Green Chemistry International, All about drugs, Eurekamoments, Organic spectroscopy international, etc in organic chemistry are some most read blogs He has hands on experience in initiation and developing novel routes for drug molecules and implementation them on commercial scale over a 32 PLUS year tenure till date Feb 2023, Around 35 plus products in his career. He has good knowledge of IPM, GMP, Regulatory aspects, he has several International patents published worldwide . He has good proficiency in Technology transfer, Spectroscopy, Stereochemistry, Synthesis, Polymorphism etc., He suffered a paralytic stroke/ Acute Transverse mylitis in Dec 2007 and is 90 %Paralysed, He is bound to a wheelchair, this seems to have injected feul in him to help chemists all around the world, he is more active than before and is pushing boundaries, He has 100 million plus hits on Google, 2.5 lakh plus connections on all networking sites, 100 Lakh plus views on dozen plus blogs, 227 countries, 7 continents, He makes himself available to all, contact him on +91 9323115463, email, Twitter, @amcrasto , He lives and will die for his family, 90% paralysis cannot kill his soul., Notably he has 38 lakh plus views on New Drug Approvals Blog in 227 countries...... , He appreciates the help he gets from one and all, Friends, Family, Glenmark, Readers, Wellwishers, Doctors, Drug authorities, His Contacts, Physiotherapist, etc He has total of 32 International and Indian awards

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