Marketing Feasibility on Aceclofenac

What is feasibility study?

The feasibility study is an integral part in developing a business project. This is an analytical tool used during the project planning process shows how a business would operate under a set of assumptions — the technology used (the facilities, equipment, production process, etc.) and the financial aspects (capital needs, volume, cost of goods, wages etc.). The purpose of a feasibility study is to determine if a business opportunity is possible, practical, and viable.

It is an analytical tool that includes recommendations and limitations, which are utilized to assist the decision-makers when determining if the business concept is viable (Drucker 1985; Hoagland, Williamson 2000; Thompson 2003c; Thompson 2003a).

 Why feasibility study is needed?

The process of defining a new business is critical. A feasibility study is an important tool for making the right decisions. A wrong decision at this point often leads to business failure. Only 50% of startups are still in business after 18 months, and only 20% are in business after 5 years. Also feasibility studies can be done before acquiring an existing business and before expanding an existing business. Knowing how to conduct a feasibility study will help many owners make critical quick decisions to select the right opportunities (University of Colorado, January 2000).

It is estimated that only one in fifty business ideas are actually commercially viable. Therefore a business feasibility study is an effective way to safeguard against wastage of further investment or resources (Gofton 1997; Bickerdyke et al. 2000).

A through viability analysis provides an abundance of information that is also necessary for the business plan. For example, a good market analysis is necessary in order to determine the business concept’s feasibility. This information provides the basis for the market section of business plan (Bangs 2000; Hoagland, Williamson 2000; Truitt 2002; Thompson 2003b).

 Objective of feasibility study:

A feasibility study should contain clear supporting evidence for its recommendations. Recommendations will be reliant on mix of numerical data with qualitative, experienced-based documentation. A business feasibility study is heavily dependent on the market research and analysis. A feasibility study provides the share holders with varying degrees of evidence that a business Concept will in fact be viable (Hoagland, Williamson 2000; Thompson 2003c; Thompson 2003a; Wickham 2004).

The Business Feasibility Study places the findings of the Dimensions of Business Viability Model assessment into a formal business report. It also aligns the findings with functional process of an enterprise which an audience can easily understand (Thompson 2003a).

For the purposes of understanding the structure of a business feasibility study the following represents the framework of the Dimensions of Business Viability (Thompson 2003c; Thompson 2003a):

  • Market viability
  • Technical viability
  • Business model viability
  • Management model viability
  • Economic and financial model viability
  • Exit strategy viability

 Why feasibility is needed in Bangladesh?

To launch a new product, in the market, a huge investment of money is required. So, a feasibility study on the desired product is very essential before launching the product into the market. The study gives the decision that the launching of product is fruitful or not. As Bangladesh is a developing country, so before launching a new product we should study the feasibility of that product. Because here a huge investment in involved.

For example, if a pharmaceutical company wants to bring a new product in Bangladesh market than the company will have to study feasibility on different matters. As like as,

  • Factory feasibility / Technical feasibility:
  1. Process machinery
  2. Tablet tools
  3. Change parts for strip packaging
  4. Change parts for blister
  5. Tablet machine capacity
  6. Coating machine capacity
  7. Manufacturing area
  8. Room condition
  9. Quality control facility

In a feasibility study, project plan or project outline plays very important role. By which we can identify the function and responsibility of individual department of the company. The essential components for the project plan of any kind of drug are shown in Table 01.

Table 01: Responsible Departments and different functions of a project outline.



  1. Recipe Preparation

Marketing and R & D

  1. Recipe Submission


  1. Raw Material Sample Collection


  1. Raw Material Vendor Selection


  1. Lab Batch Preparation & Testing

R & D

  1. Stability Study Data Preparation

R & D

  1. Recipe Approval


  1. Sample Approval


  1. Inclusion Preparation


  1. Inclusion Submission


  1. Inclusion Approval


  1. Block List Preparation


  1. Block List Approval


  1. LC Opening


  1. Pricing


  1. Arrival of Raw Materials at Factory


  1. Packaging Material Development


  1. Packaging Material (PM) Printing


  1. Arrival of PM at Factory


  1. Promotional Material Development


  1. Promotional Material Printing


  1. Gift Material Selection


  1. Gift Material Purchase


  1. Pilot Batch Production

R&D and Production

  1. Commercial Production


  1. Product Briefing to Field Force


  1. Launching


So, in a country like Bangladesh, feasibility study in very essential to assess the total cost for launching the new product in the market.

Introduction about NSAIDs


Non-steroidal anti-inflammatory drugs, usually abbreviated to NSAIDs, are drugs with analgesic, antipyretic (fever-reducing) and, in higher doses, with anti-inflammatory effects (reducing inflammation). The term “non-steroidal” is used to distinguish these drugs from steroids, which (among a broad range of other effects) have a similar eicosanoid-depressing, anti-inflammatory action. As analgesics, NSAIDs are unusual in that they are non-narcotic.

Classification of NSAIDs

NSAIDs are drugs which are effective in relieving pain and inflammation (Crofford et al. 2000). They can be classified by following ways:

                         1) COX-1 SELECTIVE INHIBITOR:

                                    – acetylsalicylic acid at low dosage

                         2) NON SELECTIVE  COX  INHIBITORS:

                                    – acetylsalicylic acid at high  dosage

                                     – diclofenac

                                    – ibuprofen

                                    – ketoprofen

                                    – Aceclofenac

                                    – indomethacin

                                    – piroxicam

                                    – naproxen

                         3) MORE COX-2 SELECTIVE INHIBITORS:

                                    – nimesulid

                                    – meloxicam

                         4) COX-2 SELECTIVE INHIBITORS:

                                    – celecoxib

                                    – etoricoxib

Mechanism of action of pain removing by NSAIDs

NSAIDs remove pain by inhibiting prostaglandin mainly. There is a one type of enzyme known as cyclo-oxygenase, which is required to convert arachidonic acid to the unstable intermediates PGG2 and PGH2. The discovery of cyclooxygenase-2 (COX-2) represented an enormous conceptual advance in prostaglandin biology and provided new therapeutic options (FitzGerald, Patrono 2001). There are two types of cyclooxygenases called cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) (Vane, Botting 1987). COX-1 is a constitutive isoform found in most normal cells and tissues, while COX-2 is induced in setting of inflammation by cytokines and inflammatory mediators (Seibert et al. 1997). COX-2 is also available in certain areas of Kidney and Brain (Breder et al. 1995).

Nonaspirin NSAIDs inhibit the activity of both COX-1 andCOX-2 by reversibly blocking the access of arachidonic acid to the active site at the apex of a hydrophobic channel within these enzymes. The pharmacodynamic properties of the different NSAIDs with respect to the COX enzymes vary with their chemical structures (FitzGerald, Patrono 2001).

Since, they inhibit the enzyme COX-1 and COX-2, prostaglandin cannot be synthesized and pain is removed.

 Common side effects of NSAIDs:

Studies have shown that NSAIDs are among the most common drugs responsible for adverse drug reactions seen in clinical practice (Doomra, Gupta 2001). Among these adverse effects gastrointestinal disorders are main. It is observed that 13 of every 1,000 patients with rheumatoid arthritis who take NSAIDs for one year have a serious gastrointestinal complication (Simon, Weaver, Graham 1999). The risk in patients with osteoarthritis is as lower as 7.3 per 1,000 patients per year (Singh 1998). Cardiovascular and renal complications have recently assumed importance in the evaluation of their side effects, since the COX enzymes have prominent biologic roles in the vasculature and the kidneys (Catella-Lawson, Crofford 2001). Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor and a diuretic (Thomas Mc 2000).

Here, mechanism of GI ulceration, the most common adverse effect of NSAIDs is given:

Mechanisms of NSAIDs-induced GI ulcerations:

What causes ulceration is precisely not known. It is believed to occur as the result of a complex interplay of aggravating factors and protective factors. Prostaglandins (PGs) have long been known to be mucoprotective and ulcer healing agents. Prostaglandins protect GI mucosa by forming a cytoprotective layer and increasing the secretion of bicarbonate ions that neutralize the gastric acidity. All therapeutically useful NSAIDs act by inhibiting the synthesis of PGs (Tamblyn, Robyn 1997). Cyclooxygenase has two isoforms, one constitutive (COX-1) and another inducible (COX-2). A third isoform (COX-3) has recently been described as well. NSAIDs are now divided into selective (those inhibiting COX-2) and non-selective (inhibiting both COX-1 and COX-2). Conventional NSAIDs cause non-selective inhibition of cyclooxygenase, which leads to reduction in bicarbonate secretion and reduced mucous production (Raskin 1999).Coupled with it is vasoconstriction that occurs due to NSAIDs, which causes hypoxia and consequent formation of ulcer. Most NSAIDs are weak organic acids and have low pKa. Therefore, they remain unionised in stomach and are absorbed appreciably from stomach. However, once they reach the cell membranes of stomach cells and reach within, they encounter a basic pH (e.g., 7.1). This causes so called “trapping” of the drugs inside the cell (Raskin 1999).

This topical effect is considered an important mechanism of gastro-duodenal damage associated with their use. Even short-term (< 1 week) use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can precipitate ulcer-related bleeding. Risk of ulcer development is increased in patients with advanced age, positive family history, female sex, prolonged use of high dose of NSAIDs and concomitant use of other gastrotoxic or anticoagulant drugs, alcoholism, heavy coffee consumption, and poor general health (Simo et al. 1999). Role of H. pylori in the development of NSAID-induced ulcer is not entirely clear. Thus, it can be understood to be the disease of the war between the factors favouring and those opposing the development of ulcers where the former win over the latter. Although NSAID use is primarily associated with upper GI problems, it is also associated with lower gastrointestinal symptoms such as haemorrhage, inflammation, perforation, and stricture formation. The American Rheumatism Association Medical Information System (ARAMIS) data suggested that risk of death from NSAID use is four times more than non-users (Doomra, Gupta 2001).

Over-the-counter (OTC) availability of histamine H2–receptor antagonists for short-term treatment of dyspepsia may lead a patient to delay optimal care for more severe gastrointestinal disease; if the drug is taken on a long-term basis, its use could delay a diagnosis of gastric cancer also (Wilcox 1994).

Product profile


Aceclofenac is a non-steroidal agent with anti-inflammatory and analgesic properties.

IUPAC name

The IUPAC name of Aceclofenac is [[[2-[(2, 6-Dichlorophenyl) amino] phenyl] acetyl] oxy] acetic acid (BP 2009).

 Chemical formula:                                      

The chemical or molecular formula of Aceclofenac is C16H13Cl2NO4(BP 2009).

 International Medical Statistics (IMS) class and sub-class:

According to International Medical Statistics (IMS), the therapeutic classification of Aceclofenac is given below (IMS 2Q/2008):

            Broad therapeutic class:

Musculo-skeletal system (IMS code-M).

             Therapeutic class:

Anti-Rheumatic system (IMS code-M01).

            Therapeutic subclass-l:

Anti-Rheumatics non steroidal (IMS code-M01A).

            Therapeutic subclass-ll:

Anti-Rheumatics non steroidal Plain (IMS code-M01A1).

 Molecular mass

The molecular mass of Aceclofenac is 354.18472 g/mol (BP 2009).


  • Appearance:

White or almost white, crystalline powder (BP 2009).

  • Solubility:

Practically insoluble in water, freely soluble in acetone, soluble in ethanol (96%) (BP 2009).

  • Normal Half-Life:

            3.5 to 6.2 hours. (

  • Volume of Distribution:

            0.36 L/kg. (

  • Protein Binding (%):

             > 99% (

Dosage form

The available dosage form of Acelclofenac is Tablet (BP 2009).


Film coating is used in case of Aceclofenac tablet.

 List of excipients

The following excipients are used to prepare the Aceclofenac tablet (

  • Core:

                                    Microcrystalline cellulose

                                    Croscarmellose Sodium


                                    Glyceryl distearate (type I)

  • Film-coat:


                                    Titanium dioxide (E171)

                                    Macrogol 400


The strength of Aceclofenac tablet found in the market is 100 mg (QIMP 14, 2008).

Pack size

Each box will contain 10 blister strips of 10 tablets.

Shelf life

The shelf life of Aceclofenac is 2 years from the production date (

Pharmacokinetic properties

The properties are given below (

  • After oral administration, aceclofenac is rapidly and completely absorbed as unchanged drug.
  • Peak plasma concentrations are reached approximately 1.25 to 3.00 hours following ingestion.
  • Aceclofenac penetrates into the synovial fluid, where the concentrations reach approximately 57% of those in plasma. The volume of distribution is approximately 25 L.
  • The mean (geometrical) plasma elimination half-life is 2.30 hours.
  • Aceclofenac is highly protein-bound (> 99%).
  • Aceclofenac circulates mainly as unchanged drug. 4′-Hydroxyaceclofenac is the main metabolite detected in plasma.
  • Approximately two-thirds of the administered dose is excreted via the urine, mainly as hydroxymetabolites.
  • No changes in the pharmacokinetics of aceclofenac have been detected in the elderly.


This is indicated for the relief of pain and inflammation in both acute and chronic pain like osteoarthritis, rheumatic arthritis, alkylosing spondy-litis, dental pain, post-operative pain, low back pain, gynaecological pain etc (

 Dosage and Administration

The dosage and administration procedures are given bellow (

  • Adults:

The recommended dose is 200 mg daily, taken as two separate 100 mg doses, one tablet in the morning and one in the evening (BNF 58).

  • Children:

There are no clinical data on the use of Aceclofenac in children.

  • Elderly:

The pharmacokinetics of Aceclofenac is not altered in elderly patients, therefore it is not considered necessary to modify the dose or dose frequency.

  • Renal insufficiency:

There is no evidence that the dosage of Aceclofenac needs to be modified in patients with mild renal impairment, but as with other NSAIDs caution should be exercised.

  • Hepatic insufficiency:

There is some evidence that the dose of Aceclofenac should be reduced in patients with hepatic impairment and it is suggested that an initial daily dose of 100 mg be used.


The contraindications of Aceclofenac are (

  • Hypersensitivity to any of the constituents.
  • NSAIDs are contraindicated in patients who have previously shown hypersensitivity reactions (e.g. asthma, rhinitis, angioedema or urticaria) in response to ibuprofen, aspirin, or other non-steroidal anti-inflammatory drugs.
  • Severe hepatic and cardiac failure.
  • Moderate to severe renal failure.
  • During the last trimester of pregnancy.
  • Active or previous peptic ulcer.
  • History of upper gastrointestinal bleeding or perforation, related to previous NSAIDs therapy.
  • Use with concomitant NSAIDs including cyclooxygenase-2 specific inhibitors.

Special warnings and precautions for use

Undesirable effects may be minimized by using the lowest effective dose for the shortest duration necessary to control symptoms. Special warnings and precautions are given below (

  • Elderly:

The elderly have an increased frequency of adverse reactions to Aceclofenac especially gastrointestinal bleeding and perforation which may be fatal.

  • Respiratory disorders:

Caution is required if administered to patients suffering from, or with a previous history of, bronchial asthma since Aceclofenac has been reported to precipitate bronco-spasm in such patients.

  • Cardiovascular, Renal and Hepatic Impairment:

The administration of Aceclofenac may cause a dose dependent reduction in prostaglandin formation and precipitate renal failure.

Patients at greatest risk of this reaction are those with impaired renal function, cardiac impairment, liver dysfunction, those taking diuretics and the elderly. Renal function should be monitored in these patients. Effects on renal function are usually reversible on withdrawal of Aceclofenac.

If abnormal liver function tests persist or worsen, clinical signs or symptoms consistent with liver disease develop or if other manifestations occur (eosinophilia, rash), Aceclofenac should be discontinued. Hepatitis may occur without prodromal symptoms.

Use of Aceclofenac in patients with hepatic porphyria may trigger an attack.

  • Gastrointestinal bleeding, ulceration and perforation:

GI bleeding, ulceration or perforation, which can be fatal, has been reported with all NSAIDs at anytime during treatment, with or without warning symptoms or a previous history of serious GI events.

The risk of GI bleeding, ulceration or perforation is higher with increasing Aceclofenac doses, in patients with a history of ulcers, particularly if complicated with hemorrhage or perforation, and in the elderly. These patients should commence treatment on the lowest dose available. Combination therapy with protective agents (e.g. misoprostol or proton pump inhibitors) should be considered for these patients, and also for patients requiring concomitant low dose aspirin, or other drugs likely to increase gastrointestinal risk.

Patients with a history of GI toxicity, particularly when elderly, should report any unusual abdominal symptoms (especially GI bleeding) particularly in the initial stages of treatment.

  • Cardiovascular and cerebro-vascular effects:

Appropriate monitoring and advice are required for patients with a history of hypertension and/or mild to moderate congestive heart failure as fluid retention and edema have been reported in association with Aceclofenac therapy.

Clinical trial and epidemiological data suggest that use of some NSAIDs (particularly at high doses and in long term treatment) may be associated with a small increased risk of arterial thrombotic events (for example myocardial infarction or stroke). There are insufficient data to exclude such a risk for Aceclofenac.

Patients with uncontrolled hypertension, congestive heart failure, established ischemic heart disease, peripheral arterial disease, and/or cerebrovascular disease should only be treated with Aceclofenac after careful consideration. Similar consideration should be made before initiating longer-term treatment of patients with risk factors for cardiovascular disease (e.g. hypertension, hyper-lipidaemia, diabetes mellitus, and smoking).

Caution should be advised in patients receiving concomitant medications which could increase the risk of gastro toxicity or bleeding, such as corticosteroids, or anticoagulants such as warfarin, selective serotonin-reuptake inhibitors or anti-platelet agents such as aspirin.

When GI bleeding or ulceration occurs in patients receiving Aceclofenac the treatment should be withdrawn.

Aceclofenac should be given with care to patients with a history of gastrointestinal disease (ulcerative colitis, Crohn’s disease) as these conditions may be exacerbated.

Close medical surveillance is imperative in patients with bleeding diathesis or hematological abnormalities.

  • SLE and mixed connective tissue disease:

In patients with systemic lupus erythematosus (SLE) and mixed connective tissue disorders there may be an increased risk of aseptic meningitis.

  • Dermatological:

Serious skin reactions, some of them fatal, including exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis, have been reported very rarely in association with the use of NSAIDs. Patients appear to be at highest risk for these reactions early in the course of therapy: the onset of the reaction occurring in the majority of cases within the first month of treatment. Aceclofenac should be discontinued at the first appearance of skin rash, mucosal lesions, or any other sign of hypersensitivity.

  • Female fertility:

The use of Aceclofenac may impair female fertility and is not recommended in women attempting to conceive. In women who have difficulties conceiving or who are undergoing investigation of infertility, withdrawal of Aceclofenac should be considered.

  • Hypersensitivity reactions:

As with other NSAIDs, allergic reactions, including anaphylactic/anaphylactoid reactions, can also occur without earlier exposure to the drug.

  • Hematological:

Aceclofenac may reversibly inhibit platelet aggregation.

  • Long-term treatment:

All patients who are receiving NSAIDs as well as Aceclofenac should be monitored as a precautionary measure e.g. renal function, hepatic function (elevation of liver enzymes may occur) and blood counts.

Drug Interactions

Drug Interactions related with Aceclofenac are (

  • Lithium:

Aceclofenac, like many NSAIDs, may increase plasma concentrations of lithium.

  • Cardiac Glycosides:

Through their renal effects, NSAIDs may increase plasma glycoside (including digoxin) levels, exacerbate cardiac failure       and reduce the glomerular filtration rate in patients receiving glycosides.

  • Diuretics:

Aceclofenac, like other NSAIDs, may inhibit the activity of diuretics. Although it was not shown to affect blood pressure control when co-administered with bendroflumethiazide, interactions with other diuretics cannot be ruled out. When concomitant administration with potassium-sparing diuretics is employed, serum potassium should be monitored.

Diuretics can increase the risk of nephrotoxicity of NSAIDs.

  • Anti-coagulants:

Like other NSAIDs, Aceclofenac may enhance the activity of anticoagulants such as warfarin. Close monitoring of patients on combined anticoagulant and Aceclofenac therapy should be undertaken.

  • Anti-diabetic agents:

Clinical studies have shown that diclofenac can be given together with oral antidiabetic agents without influencing their clinical effect. However, there have been isolated reports of hypo-glycaemic and hyper-glycaemic effects. Thus with Aceclofenac, consideration should be given to adjustment of the dosage of hypo-glycaemic agents.

  • Methotrexate:

Caution should be exercised if Aceclofenac and methotrexate are administered within 24 hours of each other, since this may increase methotrexate plasma levels, resulting in increased toxicity.

  • Mifepristone:

Aceclofenac should not be used for 8-12 days after mifepristone administration as this can reduce the effect of mifepristone.

  • Ciclosporin:

Ciclosporin nephrotoxicity may be increased by the effect of NSAIDs on renal prostaglandins.

  • Quinolone antimicrobials:

Convulsions may occur due to an interaction between quinolones and Aceclofenac. This may occur in patients with or without a previous history of epilepsy or convulsions. Therefore, caution should be exercised when considering the use of a quinolone in patients who are already receiving Aceclofenac.

  • Other analgesics including cyclooxygenase-2 selective inhibitors:

Avoid concomitant use of two or more NSAIDs (including aspirin) as this may increase the risk of adverse effects.

  • Anti-hypertensives:

Reduced anti-hypertensive effect.

  • Corticosteroids:

Increased risk of gastrointestinal ulceration or GI bleeding.

  • Tacrolimus:

Possible increased risk of nephrotoxicity when Aceclofenac is given with tacrolimus.

  • Anti-platelet agents and selective serotonin reuptake inhibitors (SSRIs):

Increased risk of gastrointestinal bleeding.

  • Zidovudine:

Increased risk of haematological toxicity when NSAIDs are given with zidovudine.

There is evidence of an increased risk of haemarthroses and haematoma in HIV (+) haemophiliacs receiving concurrent treatment with zidovudine and ibuprofen.

  • Ritonavir:

Plasma concentration of Aceclofenac possibly increased by ritonavir.

Side Effects

The side effects are (

The majority of side effects observed have been reversible and of minor in nature and include gastrointestinal disorders (dyspepsia, abdominal pain, nausea and diarrhoea) and occasional occurrence of dizziness.

Dermatological complaints including pruritus and rash, abnormal hepatic enzyme and raised serum creatinine levels have occasionally been reported.

Use in Special Populations

The special cases are (

  • Pregnancy:

There is no information on the use of Aceclofenac during pregnancy. Aceclofenac should not be prescribed during pregnancy, unless there are compelling reasons for doing so.

  • Lactation:

There is no information on the secretion of Aceclofenac to breast milk. The use of Aceclofenac should be avoided in lactation unless the potential benefits to the mother outweigh the possible risks to the fetus.

Product status

Aceclofenac is an existing molecule in Bangladesh market.

2. Literature Survey

González et al. made an important study which is related with the upper gastrointestinal bleeding (UGIB) or perforation by the use of NSAIDs. They found that, the risk of UGIB depends on the doses of individual NSAIDs in patients. And drugs with long half-life or slow-release formulation and / or associated with profound and coincident inhibition of both COX-isozymes were associated with a greater risk of UGIB (González et al. 2010).

 An important double-blind, double-dummy, randomized, multicentric, comparative study was done (Pareek et al. 2009) to compare Aceclofenac-Tizanidine combination against Aceclofenac alone in case of acute low back pain. 197 patients of either sex in the age range of 18-70 years with acute low back pain were enrolled in this study. It was observed that Aceclofenac-Tizanidine combination was more effective than Aceclofenac alone and had a favorable safety profile in the treatment of acute low back pain.

A study was made (Moore, Derry and McQuay 2009) to find out the efficacy of single dose oral Aceclofenac in acute post-operative pain. In this study it was found that single dose oral Aceclofenac is not effective in post operative pain.

A research work was done by Qureshi et al. in 2009 to develop and evaluate an oral chronomodulated drug delivery system (CDDS) for the treatment of rheumatoid arthritis. It was found that, a time-specific pulsatile-release tablet of Aceclofenac as a dosage form, for morning pain in rheumatoid arthritis, is possible and also stable (Qureshi et al. 2009.)

To uncover the skin penetration mechanism of aceclofenac using a novel nanoemulsion formulation a study was carried out (Shakeel et al. 2008). After the study it was found that, nanoemulsions can be successfully used to enhance skin penetration of Aceclofenac.

Setty and other three scientists made a research (Setty et al. 2008) to develop the fast dispersible Aceclofenac tablets and to observe the effect of functionality of super-disintegrants. The study showed that tablets containing super-disintegrants were sensitive to high humidity conditions. At the end the scientists said that fast-dispersible Aceclofenac tablets could be prepared by direct compression using super-disintegrants.

A study was done to compare the Aceclofenac and Paracetamol in the treatment of symptomatic osteoarthritis of the Knee in 2007 (Batlle-Gualda et al. 2007). A greater improvement in pain and functional capacity were observed, among the experimental patients, with aceclofenac than paracetamol with no difference in tolerability.

Vargas et al. carried out a study to discover the photodegradation and in vitro phototoxicity of aceclofenac. The interaction of Aceclofenac with human serum albumin (HSA) was studied through fluorescence spectroscopy.So, it was observed that photodegradation and in vitro phototoxicity is not occurred in case of Aceclofenac (Vargas et al. 2007).

In case of primary dysmenorrhoea the efficacy and safety of aceclofenac against placebo and naproxen was observed in a study. The study was run by Letzel et al. in 2006. It was observed that Aceclofenac (100 mg) and naproxen (500 mg) effectively managed the pain associated with primary dysmenorrhoea, and both were more effective than placebo to reduce menstrual pain assessed by various pain relief criteria (Letzel et al. 2006).

An important study was done by some scientists (Pareek et al. 2006) to observe the efficacy and safety of Aceclofenac and Diclofenac in osteoarthritis. It was found that Aceclofenac is more effective and safe drug than Diclofenac in Osteoarthritis.

A comparative study was done between Aceclofenac and Etoricoxib in case of post extraction pain control by two scientists (Chalini, Raman 2005). In this study, it was found that there were no significant differences between Aceclofenac and Etoricoxib.

Legrand made a study to observe the effects of Aceclofenac in the management of inflammatory pain. At the end of the study, it was proved that Aceclofenac is well-tolerated amongst the NSAIDs, with a lower occurrence of gastrointestinal disturbance. This good tolerability profile results in a reduced withdrawal rate and hence greater compliance with treatment (Legrand 2004).

Laporte et al. ran a research work on the newer and older agents of NSAIDs. That study was carried out to estimate the risk of upper gastrointestinal bleeding associated with NSAIDs and analgesics in normal clinical practice. Ketorolac was associated with the highest risk estimate by the study. The risk was significantly increased in patients with a history of peptic ulcer and on concomitant treatments. Last of all the study said that, NSAID-induced upper gastrointestinal bleeding is a common cause of hospital admission (Laporte et al. 2004).

A comparative study was done (Schattenkirchner, Milachowski 2003) between Aceclofenac and Diclofenac resinate in case of acute low back pain. In the study it was found that, Aceclofenac has a better safety and tolerability profile over Diclofenac resinate from a clinical point of view.

Ding made a study to observe the affects of NSAIDs on progression of osteoarthritis. It was observed that Aceclofenac increased the matrix component synthesis and protected the chondrocytes against apoptosis, while others (e.g., piroxicam) had no effects (Ding 2002).

A study was done by Lemmel et al. on the patients and physicians satisfaction on Aceclofenac. It is observed that both the patients and physicians are happy by getting a powerful anti-inflammatory agent with a low occurrence of side-effects (Lemmel et al. 2002).

Maneiro et al. made a study. They showed that, PGE2 production may be modulated by Aceclofenac. For this, Aceclofenac increases the synthesis of interleukin 1 receptor antagonist and decreases the production of nitric oxide in human articular chondrocytes (Maneiro et al. 2001).

A reappraisal was made in 2001 on behalf of Aceclofenac to use in the treatment of pain and rheumatic diseases. After the trials of 2 to 6 months, comparing with several NSAIDs, they came to the decision that Aceclofenac is effective in the management of pain and rheumatic disease (Dooley, Spencer, Dunn 2001).

3. Objective of my study

To evaluate the market condition of Aceclofenac and identify the challenges that are faced by this molecule and by doing this the possibilities of this molecule is tried to be identified.

To determine the existing market of the molecule.

To assume the future market of Aceclofenac in Bangladesh.

To visualize the overall market scenario of Aceclofenac and short comparison with its main direct competitors.

To see the past & present market strategy and the future market expanding ability of the subjected drug.

To find out the prospect of aceclofenac.

To find out the total market picture of aceclofenac for launching.

To assess the suitability of aceclofenac (as a drug) in Bangladesh market.

4. Methodology of my study

In this study, at first I did literature survey of different journals on Aceclofenac that means research works on Aceclofenac were studied from different journals which provided lot of knowledge about Aceclofenac.

Next, my researcher gave me more idea about Aceclofenac. Then I went on searching for the collection of data on Aceclofenac’s pharmacology. After getting the generalized primary knowledge on the molecule as well as NSAIDs, I was motivated to work on this molecule (Aceclofenac).

After that, I worked on the marketing data of Aceclofenac which was solely found from the Information Medical Statistics (IMS). My researcher provided IMS data from the year 2005 to 2007 to me. I collected the IMS data of the year 2008 and 2009 from the Rangs pharmaceuticals ltd and Orion laboratories ltd respectively. Then I put the market values (of last five years up to 2009) of NSAIDs in Microsoft office excel worksheet and prepared an excel sheet as a data bank of NSAIDs market share. After that, I drew some graphs to visualize the marketing status of NSAIDs and compared Aceclofenac with other major NSAIDs by graphical representation.

Then the feasibility of this molecule (Aceclofenac) was checked by the help of different types of books (IMS, QIMP etc) and personal interactions with the experts such as physicians, marketing executives, medical promotion officers etc. I observed physician’s prescriptions also.

After that, I collected the total product feature (chemical formula, chemical structure, molecular mass, characteristics, properties, indications, contraindications etc) of Aceclofenac by the help of British national formulary(BNF)-58, Therapeutic index of Beximco, Square, Opsonin and Somatec pharmaceuticals ltd, Goodman and Gilman’s The pharmacological basis of therapeutics, Quick index of medical products and problems(QIMP)-14, British pharmacopoeia 2009, Physician’s desk reference (PDR) and some literatures on Aceclofenac in different web sites.

After that, I gained the basic knowledge of feasibility study from different literatures of different web sites and correlated this knowledge with Aceclofenac to do feasibility study on Aceclofenac and its major competitors.

Then by the collected recent marketing data, the market strength of Aceclofenac and its competitors were compared and present market condition of Aceclofenac in Bangladesh was shown.

I analyzed all data with Micro-soft Excel and Different types of graphical representations.

Last of all, by analyzing all the data carefully, I prepared the result and discussion part of my research paper.

5. Result & Discussion

 Pharma Market of Bangladesh

Pharmaceutical sector is one of the largest sectors of Bangladesh. According to the IMS 2009/2Q the size of this sector is BDT 511878, 55,873 with growth rate of 18.22%.

The above graph shows the growth trend of Bangladesh pharmaceutical market from the year 2005 to 2009. The most significant feature is that the market is expanding in every year. So, Bangladesh pharma market is maintaining a upward positive trend.

The above graph shows the growth rate of Bangladesh pharmaceutical market from the year 2005 to 2009. In 2005 the growth rate was 6.18% and in 2009 the rate was 16.91%. In the year 2007  a reduction  was occurred.

 Market condition of NSAIDs                                                                                                

Market scenario of NSAIDs in Bangladesh:

The market of NSAIDs, in the year 2009, was BDT 21333, 09,753 with growth rate of 17% and sharing 3.89% of total pharmaceutical market.

The above graph shows the annual growth rate of NSAID market in Bangladesh. It is observed that except in 2007, the NSAID market has always kept a positive growth. Last year (in 2009) its growth rate was 17%. After a great fluctuation, in last two years the curve of growth rate is showing a good positive trend.

The total market size of NSAID drugs in Bangladesh was about 21333, 09,753 BDT in the year 2009. The annual sales of Aceclofenac and its competitors in the last year (2009) have shown in figure 04.

So, we can see that Aceclofenac is in third position in total NSAIDs market according to annual sales of the year-2009. Diclofenac is in first position. Naproxen is in second position and Aceclofenac is standing just after that. Comparing with these three molecules, others are in very low level.

a Diclofenac

Diclofenac originated from Ciba-Geigy (now Novartis) in 1973. It is used to treat pain or inflammation caused by arthritis or ankylosing spondylitis. Diclofenac is available as an immediate-release tablet and an extended-release (long-acting) tablet to take by mouth. Diclofenac immediate-release tablets are usually taken two to four times a day. Diclofenac extended-release tablets are usually taken once a day. Diclofenac is the leading NSAID in Bangladesh market. If we see the yearly growth rate of diclofenac, we will find that it always fluctuates and last year it earns a growth rate of 12.51% and annual sale was about BDT 89, 74, 82,431.

The growth of Diclofenac was very low in the year-2005 and it was increased positively in 2006. But after a fluctuation now it has increased positively in 2009. In last year its growth was 12.51% which is significant.

b Ketoprofen

Ketoprofen is generally prescribed for arthritis-related inflammatory pains or severe toothaches that result in the inflammation of the gums. Ketoprofen can also be used for treatment of some pain, especially nerve pain like post-herpetic neuralgia and referred pain for radiculopathy.

The growth of ketoprofen was low in last few years, but in 2008 it was increased. In last year its growth was -2.57% with total sales of about BDT 10.69 crores. The market position of this molecule is not so good. Because, there are fluctuations in its growth rate curve.

c Indometacin

It is a non-steroidal anti-inflammatory drug commonly used to reduce fever, pain, stiffness, and swelling. In the graph we can see that this drug has got always positive growth. Last year it earns 18.68% growth rate and the total sales was about BDT 8.54 crores.

The growth of Indometacin was low in the year 2005, but it was rapidly increased in 2006.After some fluctuations, in 2009 it was increased. In last year its growth rate was 18.68%.

d Ibuprofen

Ibuprofen was derived from propionic acid by the research arm of Boots Group during the 1960s (Adams SS, 1992). It was discovered by Stewart Adams, with colleagues John Nicholson, Andrew RM Dunlop, Jeffery Bruce Wilson & Colin Burrows and was patented in 1961. The drug was launched as a treatment for rheumatoid arthritis in the United Kingdom in 1969, and in the United States in 1974. The market of Ibuprofen has been fallen in last few years. In last year it earned a negative growth of -6.22% with annual sales of about 7.26crores BDT.

The growth of Ibuprofen was very low in the year 2005, but it was rapidly increased in 2006. After some great fluctuations, in 2008 it was increased though it was negative. In last year (2009) its growth was -6.22%. From the curve, we can predict that the market situation of this molecule is very bad.

e Naproxen

Naproxen Sodium is a non-steroidal anti-inflammatory drug (NSAID) commonly used for the reduction of mild to moderate pain, fever, inflammation and stiffness caused by conditions such as osteoarthritis, rheumatoid arthritis, psoriatic arthritis, gout, ankylosing spondylitis, menstrual cramps, tendinitis, bursitis, and the treatment of primary dysmenorrhea. Last year Naproxen got an annual growth of 24.64% by achieving the 35.17 crores BDT annual sale.

The growth of Naproxen was very high in the year 2005, but it was decreased in 2006 till 1st half of 2007. From 2nd half of 2007 to 2009 its growth rate increased significantly. In last year (2009) its growth was 24.64%.

 Market scenario of Aceclofenac in Bangladesh:

Since Aceclofenac is a very good and potential molecule, so it was decided to study the market and opportunity of Aceclofenac.

a Aceclofenac:

Aceclofenac has been shown to exert effects on a variety of mediators of inflammation. The drug inhibits synthesis of the inflammatory cytokines like interleukin (IL) –1β and tumor necrosis factor (TNF), and inhibits prostaglandin E2 (PGE2) production. In vitro data indicate inhibition of COX-1 and COX-2 by Aceclofenac in whole blood assays, with selectivity for COX‑2 being evident (Gonzalez, de la Cruz, de Nicolas 1994). It has been suggested that Aceclofenac blocks PGE2 production via COX-1 and COX-2 inhibition after intracellular metabolism to 4´-hydroxyaceclofenac and diclofenac in human rheumatoid synovial and other inflammatory cells (Yamazaki, Kawai, Matsumoto 1999). IC50 values for COX-1 and COX-2, respectively, were > 100 and 0.8 μmol/L for aceclofenac and > 100 and 36 μmol/L for 4´-hydroxyaceclofenac.

The mode of action of Aceclofenac has been recently clarified in that the compound was shown to elicit preferential inhibition of COX-2 as a result of limited but sustained biotransformation to diclofenac (Hinz, Brune 2004).

Aceclofenac has also shown stimulatory effects on cartilage matrix synthesis that may be linked to the ability of the drug to inhibit IL-1β. IL-1β suppresses various growth factors. Inhibition of IL-1β thus stimulates synthesis of cartilage matrix. In vitro data show stimulation by aceclofenac of glycosaminoglycan synthesis in human osteoarthritic cartilage. There is also evidence that Aceclofenac stimulates the synthesis of IL‑1 receptor antagonist in human articular chondrocytes subjected to inflammatory stimuli (Maneiro, Lopez-Armada, Fernandez-Sueiro 2001) and that 4’‑hydroxyaceclofenac has chondroprotective properties attributable to suppression of IL‑1β-mediated promatrix metalloproteinase production and proteoglycan release (Yamazaki, Kawai, Mizushima 2000).

Thus aceclofenac may prevent the degradation of articular connective tissue in patients with rheumatoid arthritis and osteoarthritis, and should be classified as a unique NSAID.

b Market of Aceclofenac

The total market of Aceclofenac in Bangladesh is BDT 334,187,771. Its Growth rate is 22.53%. And Market share is 0.65% (IMS 2Q/2009).

c Illustration of Aceclofenac’s market growth

Aceclofenac is one of the leading NSAIDs in Bangladesh market in terms of sales and growth. In last year the sales of aceclofenac exceeded 33 crores BDT (exact value: 33, 41, 87,771 BDT) and took the 0.65% share of total market. The graph of yearly sales of Aceclofenac (from the year 2005 to 2009) is given below as figure 10.

From the above graph we can say that, the sale of Aceclofenac is generally increasing in every year except in 2007. Comparing with the sales of 2005, the sales of 2009 is very excellent. So the market of Aceclofenac is expanding.

The growth of Aceclofenac is quite good from its entering in the market. In the year 2005 it earned an enormous growth of 57.81%. From then it has kept a good record of growing. Only exception was year 2007. In that year market of Aceclofenac fall a little bit. The yearly growth of Aceclofenac  has shown in figure 11.

d Number of direct competitor

Brand wise Aceclofenac has 51 direct competitors (IMS 2Q/2009).

List of direct competitors of Aceclofenac

The list has given in the following table 02 (IMS 2Q/2009):

Brand name

Company name


Brand name

Company name

FlexiSquare CelofenACI
ReservixIncepta  NoakOrion
MervanAristopharma ArosGlobe
VaxtinSandoz AcebidBeacon
ApecloApex PankilEverest pharma
AcloAclo AcenacMedicon
ZolfinBeximco PainexChemist
XerifenPeoples TuffoxSK+F
MovexOpsonin AlonaChemical
CeclofenRenata ClofentaAmico
ClofBio pharma Ac-prPacific
ApitacAcme RheumaMystic
TernillaHealthcare AcecolZiska
AcefenacGeneral SyclofenSyntho
OstoflexSomatec EcenaEdruc
PreservinIbn-sina MotifenPharmadesh
NofenacDrug int. ZerodolNavana
OrifenSilva AcecloraMarks Man
AcflamApollo AcelockBristol
XpainGaco XeriflamKumudini
AclovixAexim CasynEthical drugs lab
SapcloSAPL AclofenGlobe
EnaAsiatic ClasifenOasis
QripSanofi Aventis XefastDesh Pharma
UacWhite horse SilfeenacSilco pharma

   Table 02: Market wise list of Aceclofenac’s brand names by the year-2009 in Bangladesh

f Number of indirect competitors

Brand wise Aceclofenac has 393 indirect competitors.

.g List of indirect competitors (QIMP 14)

          Table 03: List of indirect competitors of Aceclofenac and their number of brands.

Serial number

Generic name of NSAIDs

Number of brands from different companies



09 brands



03 brands


Diclofenac sodium

164 brands


Diclofenac free acid

02 brands


Diclofenac diethylammonium salt

06 brands



07 brands



39 brands



25 brands



25 brands


Mefenamic acid

14 brands



01 brand



45 brands



02 brands



04 brands



02 brands



03 brands



17 brands


Diclofenac sodium and misoprostol

13 brands

h Comparison of Aceclofenac with its competitors

If we compare the growth rate of Aceclofenac with its competitors, we will see that Aceclofenac was in top position in 2005 and 2006. But in 2007, suddenly the growth rate fall down, because of syndication the price of most of the NSAIDs were decreased. However, the collapse was recovered very quickly by increasing the sales volume of the drug. Now Aceclofenac is in second position among the competitors according to the growth rate and in a stable situation.

The comparison will be clearer if we do it for the individual drug. That thing is done below:

Aceclofenac Vs Diclofenac:

If we see the annual sales of last year, Diclofenac is clearly ahead than Aceclofenac. But if we discuss the growth rate, Aceclofenac has been doing well for last few years except 2007. The Market of Diclofenac was much larger than Aceclofenac in 2009. And from the growth rate curve we can say that market of Aceclofenac is increasing and the growth curve is in positive trend.

Aceclofenac Vs Ibuprofen:

Aceclofenac is clearly ahead than ibuprofen now. Last year Aceclofenac achieve 3 times more sales than Ibuprofen. And the growth rate of Aceclofenac is always better than Ibuprofen. The growth condition of Ibuprofen is not so good compared with Aceclofenac; figure 16 visualize this statement very clearly. And figure 15 shows the market condition of the molecules in 2009.

Aceclofenac Vs Naproxen:

Naproxen earned a little bit more sales last year. The growth of Aceclofenac was always better than the Naproxen but in last year Naproxen did better than the Aceclofenac. Figure 17 shows the market condition of Aceclofenac and Naproxen in 2009. And figure 18 is showing the growth rate of last few years of the two molecules.

Aceclofenac Vs Indomethacin:

Aceclofenac did always better than Indometacin. Except the 2007, Aceclofenac’s growth rate is always better than the Indometacin and last year Aceclofenac earned more than three times revenue of Indometacin. Last year the growth rate of Aceclofenac was higher than that of Indometacin. So Aceclofenac is clearly ahead than Indometacin.

Aceclofenac Vs Ketoprofen:

Aceclofenac is a clear ahead molecule than ketoprofen. The growth rate of Aceclofenac is very high from 2005 to 2009. It earned almost three times more revenue than ketoprofen and its growth rate is also much higher than that of ketoprofen. The below given illustrations bear the evidence of the above acclamation.

Table 04: Brand wise market analysis (IMS 2Q/2009).



Brand name

Name of Company

Dosage form


MRP / Unit price in BDT

Value in BDT



Growth rate (%)



















Aristo pharma
























Alco pharma












0 3.59

– 4.42








– 10.79

















i Top ten direct competitor’s (of Aceclofenac) market analysis

j Illustration on top 10 brands of Aceclofenac in terms of sales:

The illustration says that top 3 brands in 2009 are respectively Flexi (growth rate 18.85%), Reservix (growth rate 19.5%) and Mervan (growth rate 35.39%). Ceclofen was in 10th position.

k Illustration on market shares of various brands of Aceclofenac

The above illustration shows that Flexi occupied the highest market share among the all other brands of Aceclofenac in the year 2009. The other positions were occupied by Reservix, Mervan, Vaxtin etc. The top four brands are the main share holders of the market of Aceclofenac.

6. Conclusion

By the analysis of indications, contraindications, side-effects and other information of Aceclofenac, it can be said that, Aceclofenac is safer as well as active than any other NSAIDs found in Bangladesh. It causes less gastro-intestinal disturbance than any other NSAIDs. Now it is used for long term therapy.

By the analysis of its marketing related data, it can be said that, it is a potential molecule for Bangladesh pharmaceutical market. As its price is reasonable as well as potent and safe than other NSAIDs, so in recent future its market will increase significantly and it will lead the market of NSAIDs in Bangladesh.

So, at the end of the feasibility study on Aceclofenac & its major competitors, it can be said that Aceclofenac is very much viable in Bangladesh pharmaceutical market.

7. Limitations of my study

It is important to critically evaluate the whole study. The present study has certain limitations that need to be taken into account when considering the study and its contributions.

This study has focused on a phenomenon that is a very extensive and major one, i.e. the market scenario of Aceclofenac in Bangladesh market. Clearly, this represents a challenging task for research regardless of the more specific interests that the study may have. This study represents idea about Aceclofenac. By understanding something about this particular molecule more in depth, we might eventually also learn something about more general phenomena.

In this study, detailed pharmacology, more therapeutic uses, new dosage form, new route of administration, etc of Aceclofenac could be discussed but I have focused mainly on market status.

Detailed pharmacological information of NSAIDs and more analysis on NSAIDs could be included in this study. Individually NSAIDs have not been studied and the market scenario of individual NSAIDs has not been analyzed.

More graphical representations on the market strategy of Aceclofenac could be included and more research work on market scenario of Aceclofenac could be done. More detailed comparison between Aceclofenac and other NSAIDs could be studied but because of time limitation it was not possible to extend the study more.

Data used here have been produced by someone else. I have just collected them. Directly I did not produce any data.

I did not arrange any clinical study to produce the pharmacological data for my research work. I just collected them from different sources.

Last of all it can be said that, Limitations of any study produce avenues for future research.


Adams SS. The propionic acids: a personal perspective. J Clin Pharmaco. 1992; 32 (4): 317–23.

Bangs D. The Australlian Business Planning Guide. Warriewood, Woodslane Pty Ltd. 2000.

Batlle-Gualda E, Román Ivorra J, Martín-Mola E, Carbonell Abelló J, Linares Ferrando LF, Tornero Molina J, Raber Béjar A, Fortea Busquets J. Aceclofenac vs paracetamol in the management of symptomatic osteoarthritis of the knee: a double-blind 6-week randomized controlled trial. Osteoarthritis Cartilage. 2007; Aug;15(8):900-8.

Bickerdyke I, Lattimore R, Madge A. Business Failure and Change: An Australian Perspective. Canberra, Productivity Commission Research Paper. 2000

BNF 58, September 2009, BMJ Groups & RPS Publishing, London.

BP (British Pharmacopoeia) 2009, Volume I & II, Monographs: Medicinal and Pharmaceutical Substances, Aceclofenac.

Breder CD, Dewitt D, Kraig RP. Characterization of inducible cyclooxygenage in rat brain. J. Comp. Neurol. 1995; 355:296-315.

Catella-Lawson F, Crofford LJ. Cyclooxygenase inhibition and thrombogenicity. Am J Med 2001; 110:Suppl 3A:28S-32S.

 Chalini S, Raman U. Comparative efficacy of aceclofenac and etoricoxib in post extraction pain control: randomized control trial. Indian J Dent Res. 2005; Apr-Jun; 16(2):47-50.

Crofford LJ, Lipsky PE, Brooks P, Abramson SB, Simon LS, van de Putte LBA. Basic biology and clinical application of specific cyclooxygenase-2 inhibitors. Arthritis Rheum 2000;43:4-13.

 Ding C. Do NSAIDs affect the progression of osteoarthritis? Inflammation. 2002; Jun;26(3):139-42

 Dooley M, Spencer CM, Dunn CJ. Aceclofenac: a reappraisal of its use in the management of pain and rheumatic disease. J Drugs. 2001; 61(9):1351-78.

Doomra R, Gupta SK. Intensive adverse drug reaction monitoring in various specialty clinics of a Tertiary Care Hospital In North India. Intern J Med Toxicol. 2001; 4 (1): 1-4.

Drucker PF. Innovation & Entrepreneurship. New York, Harper-Trade. 1985

FitzGerald GA, Patrono C. The coxibs, selective inhibitors of cyclooxygenase-2. N Engl J Med. 2001;345:433-42.

Gofton L. Business Market Research. London, Kogan Page. 1997

Gonzalez E, de la Cruz C, de Nicolas R. Long-term effect of nonsteroidal anti inflammatory drugs on the production of cytokines and other inflammatory mediators by blood cells of patients with osteoarthritis. Agents Actions. 1994; 41:171-8

González EL, Patrignani P, Tacconelli S, Rodríguez LA. Variability of risk of upper gastrointestinal bleeding among nonsteroidal anti-inflammatory drugs. Arthritis Rheum. 2010 Feb 22.

Hinz B, Brune K. Pain and osteoarthritis: new drugs and mechanisms. Curr Opin Rheumatol. 2004; 16:628-33

Hoagland H, Williamson L. Feasibility Studies. Kentucky, University of Kentucky. 2000.

IMS-2008, 1st quadrant, managed from Rangs Pharmaceutical Ltd.

IMS-2009, 2nd quadrant, managed from Orion Laboratories Ltd.

 Laporte JR, Ibáñez L, Vidal X, Vendrell L, Leone R. Upper gastrointestinal bleeding associated with the use of NSAIDs: newer versus older agents. Drug Saf. 2004; 27(6):411-20.

 Legrand E. Aceclofenac in the management of inflammatory pain. Expert Opin Pharmacother. 2004 Jun;5(6):1347-57

 Lemmel EM, Leeb B, De Bast J, Aslanidis S.Patient and physician satisfaction with aceclofenac: results of the European Observational Cohort Study (experience with aceclofenac for inflammatory pain in daily practice). Aceclofenac is the treatment of choice for patients and physicians in the management of inflammatory pain. Curr Med Res Opin. 2002; 18(3):146-53.

Letzel H, Mégard Y, Lamarca R, Raber A, Fortea J. The efficacy and safety of aceclofenac versus placebo and naproxen in women with primary dysmenorrhoea. Eur J Obstet Gynecol Reprod Biol. 2006 Dec; 129(2):162-8.

Maneiro E, Lopez-Armada MJ, Fernandez-Sueiro JL. Aceclofenac increases the synthesis of interleukin 1 receptor antagonist and decreases the production of nitric oxide in human articular chondrocytes. J Rheumatol 2001;28:2692-9.

 Maneiro E, López-Armada MJ, Fernández-Sueiro JL, Lema B, Galdo F, Blanco FJ. Aceclofenac increases the synthesis of interleukin 1 receptor antagonist and decreases the production of nitric oxide in human articular chondrocytes. J Rheumatol. 2001; Dec; 28(12):2692-9.

Moore RA, Derry S, McQuay HJ. Single dose oral aceclofenac for postoperative pain in adults. Cochrane Database Syst Rev. 2009; Jul 8 ;( 3):CD007588.

 Pareek A, Chandanwale AS, Oak J, Jain UK, Kapoor S. Efficacy and safety of aceclofenac in the treatment of osteoarthritis: a randomized double-blind comparative clinical trial versus diclofenac – an Indian experience. Curr Med Res Opin. 2006; May; 22(5):977-88.

Pareek A, Chandurkar N, Chandanwale AS, Ambade R, Gupta A, Bartakke G. Aceclofenac-tizanidine in the treatment of acute low back pain: a double-blind, double-dummy, randomized, multicentric, comparative study against aceclofenac alone. Eur Spine J. 2009; Dec; 18(12):1836-42. Epub 2009 May 7.

QIMP-14, July 2007, Dhaka,

Qureshi J, Ahuja A, Baboota S, Chutani K, Jain S, Ali J. Development and evaluation of a time-specific pulsatile-release tablet of aceclofenac: a solution for morning pain in rheumatoid arthritis. Methods Find Exp Clin Pharmacol. 2009; Jan-Feb; 31(1):15-23.

Raskin JB. Gastrointestinal effects of NSAID therapy. Am J Med 1999; 106 (S 5B): 3-12.

Roth SH, Bennet RE. Nonsteroidal anti-inflammatory drug gastropathy. Arch Intern Med 1987; 147: 2093-2100.

 Schattenkirchner M, Milachowski KA. A double-blind, multicentre, randomised clinical trial comparing the efficacy and tolerability of aceclofenac with diclofenac resinate in patients with acute low back pain. Clin Rheumatol. 2003; May; 22(2):127-35.

Seibert K, Zhang Y, Leahy K, Hauser S, Masferrer J, Isakson P. Distribution of COX-1 and COX-2 in normal tissue and inflamed tissue. Adv. Exp. Med. Biol. 199; 400A:167-170.

Setty CM, Prasad DV, Gupta VR, Sa B.Development of fast dispersible aceclofenac tablets: effect of functionality of superdisintegrants. Indian J Pharm Sci. 2008; Mar-Apr; 70(2):180-5.

Shakeel F, Baboota S, Ahuja A, All J, Shafiq S. Skin permeation mechanism of aceclofenac using novel nanoemulsion formulation. Pharmazie. 2008; Aug; 63(8):580-4.

Simon LS, Weaver AL, Graham DY. Anti-inflammatory and upper gastrointestinal effects of celecoxib in rheumatoid arthritis: a randomised controlled trial. JAMA 1999; 282 (20):1921-8.

Singh G. Recent considerations in non-steroidal anti-inflammatory drug gastropathy. Am J Med 1998; 105 (1B):31S-38S.

Tamblyn, Robyn. Unnecessary prescribing of NSAIDs and the management of NSAID-related gastropathy in medical practice. Ann Intern Med 1997; 127: 429-38.

Thomas, Mc. “Diuretics, ACE inhibitors and NSAIDs–the triple whammy”. The Medical journal of Australia.  2000; 172 (4): 184–5.

Thompson A. Business Feasibility Studies: Dimensions of Business Viability. Perth, Best Entrepreneur. 2003a

Thompson A. Overview of a Business Plan. Perth, Best Entrepreneur. 2003b

Thompson A. Understanding the Proof of Business Concept. Perth, Best Entrepreneur. 2003c

Truitt W. Business Planning: A Comprehensive framework and Process. London, Quorum Books. 2002

University of Colorado at Denver, NXLevel Guide for Entrepreneurs, January 2000

Vane J, Botting R. Inflammation and mechanism of action of anti-inflammatory drugs. FASEB J , 1987; 1:89-96.

Vargas F, Rivas C, Zoltan T, Fuentes A, Padrón L, Díaz Y, Izzo C. Photodegradation and in vitro phototoxicity of aceclofenac. Pharmazie. 2007; May; 62(5):337-41.

Wickham P. Strategic Entrepreneurship. Essex, Pearson Education. 2004

Wilcox CM. Striking prevalence of over-the-counter non-steroidal anti-inflammatory drug use in patients with upper gastrointestinal hemorrhage. Arch Intern Med. 1994;154: 42-46.

Yamazaki R, Kawai S, Matsumoto T, et al. Hydrolytic activity is essential for aceclofenac to inhibit cyclooxygenase in rheumatoid synovial cells. J Pharmacol Exp Ther 1999; 289:676-81.

Yamazaki R, Kawai S, Mizushima Y. A major metabolite of aceclofenac, 4´‑hydroxyaceclofenac, suppresses the production of interstitial pro-collagenase/proMMP‑1 and prostromelysin‑1/proMMP‑3 by human rheumatoid synovial cells. Inflamm Res 2000; 49:133-8