Aceclofenac is a nonsteroidal anti-inflammatory drug (NSAID) commonly used to relieve pain and inflammation associated with conditions such as osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and other musculoskeletal disorders. It works primarily by inhibiting the cyclooxygenase (COX) enzymes—specifically COX-2 more selectively than COX-1—which play a key role in the synthesis of prostaglandins, substances that mediate pain, inflammation, and fever.
Aceclofenac was developed as a chemical analog of diclofenac in 1991, with structural modifications aimed at reducing gastrointestinal side effects often associated with traditional NSAIDs. These modifications allow for better tolerability in the stomach and intestines, making it a preferred choice in patients who require long-term NSAID therapy. It has anti-inflammatory, analgesic, and antipyretic properties and is typically administered orally in tablet form, with a common dose of 100 mg twice daily.
Aceclofenac, developed in Spain in the late 1980s as a derivative of diclofenac, was designed to offer better gastrointestinal tolerability. It was patented in 1983 and received approval for medical use in 1992.
Brand Names:
Aceclofenac is marketed under various brand names, including Hifenac, Zerodol, Aceclo. These formulations may also be combined with other active ingredients such as paracetamol, serratiopeptidase, or chlorzoxazone to enhance therapeutic effects. Brand names can vary depending on the manufacturer and region—for example, it is sold as Acecgen in the UK and Airtal in certain European countries.
Zerodol-SP: Aceclofenac, paracetamol, and serratiopeptidase.
Hifenac-MR: Aceclofenac with a muscle relaxant.
Aceclo Sera: Aceclofenac and serratiopeptidase
Mechanism of Action:
Aceclofenac exerts its anti-inflammatory effects primarily through COX-2 inhibition, leading to reduced production of key inflammatory mediators such as prostaglandin E2 (PGE2), interleukin-1β (IL-1β), and tumor necrosis factor (TNF) via the arachidonic acid (AA) pathway. The suppression of interleukin-6 (IL-6) is believed to result from the conversion of aceclofenac into diclofenac. By downregulating these pro-inflammatory cytokines, aceclofenac also reduces the generation of reactive oxygen species (ROS).
PHARMACOKINETICS
Absorption:
Aceclofenac is rapidly absorbed through the gastrointestinal tract after oral administration.
Distribution:
Aceclofenac has a volume of distribution of about 25 liters, suggesting that it is distributed throughout the body but does not accumulate significantly in peripheral tissues.
Metabolism:
The metabolism of aceclofenac is primarily mediated by the cytochrome P450 (CYP) enzyme system, specifically the CYP2C9 isoenzyme.
Excretion:
Approximately 70–80% of aceclofenac and its metabolites are cleared via the kidneys, with the majority excreted in the urine as hydroxylated and glucuronidated forms.
PHARMACODYNAMICS
Aceclofenac is a non-steroidal anti-inflammatory drug (NSAID) whose pharmacodynamics are primarily driven by its potent inhibition of the cyclooxygenase (COX) enzyme. This inhibition blocks the synthesis of prostaglandins, which are key chemical messengers responsible for causing pain, inflammation, swelling, and fever.
ADMINISTRATION
Aceclofenac is a nonsteroidal anti-inflammatory drug (NSAID) used to relieve pain and inflammation. It is available in multiple formulations, such as oral tablets, dispersible tablets, mouth-dissolving tablets, topical gels, and injectable forms. The route of administration and dosage vary depending on the specific formulation being used.
DOSAGE AND STRENGTH
Aceclofenac is available in a variety of formulations, including:
Standard tablets: The most common form of aceclofenac, typically taken orally.
Sustained-release tablets: Designed for extended action, allowing for less frequent dosing.
Topical gel: Used for external application to relieve localized pain and inflammation.
Injectable form: Administered in clinical settings for more immediate or controlled effects.
Combination tablets: Often combined with other active ingredients such as paracetamol (acetaminophen) or serratiopeptidase to enhance analgesic and anti-inflammatory effects.
DRUG INTERACTIONS
Here are some key drug interactions of aceclofenac:
Anticoagulants (e.g., warfarin): Increased risk of bleeding due to enhanced anticoagulant effects.
Other NSAIDs or corticosteroids: Increased risk of gastrointestinal irritation or ulcers.
ACE inhibitors and ARBs: Reduced antihypertensive effect and potential kidney function impairment.
FOOD INTERACTIONS
When using aceclofenac, it is important to avoid alcohol and certain supplements because they can increase the risk of stomach bleeding and other side effects. To help reduce stomach irritation, aceclofenac should be taken with food or milk.
CONTRAINDICATIONS
Aceclofenac is contraindicated in active gastro-intestinal bleeding, active gastro- intestinal ulceration, cerebrovascular disease, history of gastro-intestinal bleeding related to previous NSAID therapy, history of gastro-intestinal perforation related to previous NSAID therapy, history of recurrent gastro-intestinal.
SIDE EFFECTS
Feeling dizzy
Nausea and vomiting
Diarrhea
Skin rashes
Heartburn
Indigestion
Blurred or altered vision
Drowsiness
TOXICITY
Aceclofenac is a nonsteroidal anti-inflammatory drug (NSAID) that primarily affects the gastrointestinal, renal, hepatic, and cardiovascular systems in cases of toxicity. While its safety profile is comparable to other NSAIDs, clinical evidence indicates it may cause fewer gastrointestinal side effects than older drugs like diclofenac. To reduce the risk of adverse effects, it should always be used at the lowest effective dose for the shortest possible duration.
