The non-steroidal anti-inflammatory drug naproxen has both analgesic and anti-inflammatory properties.

The main mediators of inflammation, activators (prostaglandins), are specifically inhibited by non-steroidal anti-inflammatory medicines (NSAIDs), such as naproxen. via inhibiting the activity of COX 1 and COX 2 isoenzymes, which are part of cyclooxygenase. NSAIDs function by blocking the formation of prostaglandins by obstructing the COX enzyme at inflammatory sites and in the central nervous system. The signalling pathways are not activated and the increase in pain sensitivity that results from prostaglandin activity is effectively reduced if inhibition of prostaglandin (PGE2 and Pl2) production is achieved. By activating substance P and glutamate receptors in the spinal cord, naproxen impacts pain receptors in the spinal cord and in key CNS centres and reduces pain. Naproxen has been shown to have an impact on IC channels, transient potential receptors, and voltage-gated Na+, Ca+, and K+ channels.

A muscle relaxant created from meprobamate, carisoprodol takes effect quickly and lasts for 4 to 6 hours.

Like other comparable drugs, naproxen prevents the formation of prostaglandins.

A centrally acting muscle relaxant, carisoprodol also indirectly relaxes skeletal muscles. Meprobamate, a carisoprodol metabolite, has sedative and anxiolytic effects.

Following oral treatment, naproxen is quickly and completely absorbed from the digestive tract. Its action is unaffected by concomitant administration with food, albeit its absorption may be delayed. Depending on the amount of food consumed, the peak plasma levels following a dose are attained in 2 to 4 hours.

In a study, 24 healthy people (12 men and 12 women) who received single doses of 350 mg carisoprodol were examined for their pharmacokinetic responses. The meprobamate Cmax was 2.46 mcg/mL (median SD) following the administration of a single 350-mg dosage of carisoprodol, which is almost 25% lower than the meprobamate Cmax (roughly 8 mcg/mL) following the administration of a single 400-mg dose of meprobamate.

Carisoprodol’s absolute bioavailability is still unknown. The mean time to attain plasma concentrations (Tmax) of carisoprodol was between 1.5 and 2 hours after a single 350 mg dose was administered. The pharmacokinetics of carisoprodol were unaffected by the co-administration of a 350 mg high-fat meal.

The volume of distribution for naproxen is 0.16 l/kg. At typical therapeutic concentrations, it is 99% bound to plasma proteins. Due to increased clearance brought on by saturation of its binding to plasma proteins at large dosages, there is no direct correlation between dose and plasma levels at doses greater than 500 mg/day. But in a dose-proportional way, the concentration of non-protein bound naproxen keeps rising. After 3 to 4 days, naproxen plasma levels stabilize. Naproxen passes through synovial fluid, crosses the placenta, and only makes up around 1% of the maternal plasma levels in breast milk.

The liver extensively metabolizes naproxen to yield 6-o-desmethyl-naproxen. Carisoprodol is mostly metabolized in the liver by the enzyme cytochrome CYP2C19 to produce meprobamate. There is genetic variation in this enzyme.

Naproxen is principally eliminated in the urine (less than 1%), followed by 6-o-desmethyl-naproxen (less than 1%), and then their conjugates (66 to 92%). It has been discovered that the rate of excretion closely resembles the pace at which the medication leaves the plasma. Less than 3% is eliminated in the feces in tiny levels. The clearance of naproxen is about 0.13 mL/min/kg. Naproxen has an elimination half-life of 14 hours, regardless of therapeutic form or formulation. Following administration of a single 350 mg dose of carisoprodol, the drug is removed through both renal and non-renal pathways, with a terminal elimination half-life of around 2 hours. Meprobamate has a half-life of about 10 hours following the delivery of a single dose of 350 mg carisoprodol.