69337-85-5

Usage

Uses

Used in Pharmaceutical Industry:
Naproxen is utilized as an analgesic, antipyretic, and anti-inflammatory agent for the treatment of various conditions such as arthritis, menstrual cramps, and acute injuries. Its ability to reduce pain and inflammation, as well as lower fever, makes it a common choice for these applications.
Used in Pain Management:
As a pain reliever, 2-(6-Methoxy-2-naphthyl)-2-methylpropanoic acid is used to alleviate mild to moderate pain, including that associated with headaches, muscle aches, and joint pain.
Used in Inflammation Reduction:
In the context of inflammation reduction, Naproxen is employed to decrease swelling and redness associated with conditions like tendinitis, bursitis, and other inflammatory disorders.
Used in Fever Reduction:
For fever reduction, 2-(6-Methoxy-2-naphthyl)-2-methylpropanoic acid is used to lower elevated body temperatures caused by infections or other illnesses.
However, it is important to note that the use of Naproxen should be under a doctor's supervision due to potential side effects such as gastrointestinal bleeding, cardiovascular problems, and kidney damage. It is available in various forms including tablets, syrups, and injections to cater to different patient needs and preferences.

InChI:InChI=1/C15H16O3/c1-15(2,14(16)17)12-6-4-11-9-13(18-3)7-5-10(11)8-12/h4-9H,1-3H3,(H,16,17)

Upstream product

• 69337-84-4 methyl -2--(6--methoxynaphthalen--2--yl)--2--methylpropanoate 
• 30012-51-2 methyl 2-(6-methoxy-2-naphthyl)propionate 
• 23981-80-8 naproxen 

Relevant academic research and scientific papers

COMPOSITIONS AND METHODS FOR SUBSTRATE-SELECTIVE INHIBITION OF ENDOCANNABINOID OXYGENATION

Methods for selectively inhibiting endocannabinoid oxygenation but not arachidonic acid oxygenation. In some embodiments, the methods include contacting a COX-2 polypeptide with an effective amount of a substrate-selective COX-2 inhibitor. Also provided are methods for elevating a local endogenous cannabinoid concentrations; methods of reducing depletion of an endogenous cannabinoid; methods for inducing analgesia; methods of providing anxiolytic therapy; methods for providing anti-depressant therapy; and compositions for performing the disclosed methods.

Substrate-selective inhibition of cyclooxygenase-2: Development and evaluation of achiral profen probes

Cyclooxygenase-2 (COX-2) oxygenates arachidonic acid and the endocannabinoids 2-arachidonoylglycerol (2-AG) and arachidonoylethanolamide (AEA). We recently reported that (R)-profens selectively inhibit endocannabinoid oxygenation but not arachidonic acid oxygenation. In this work, we synthesized achiral derivatives of five profen scaffolds and evaluated them for substrate-selective inhibition using in vitro and cellular assays. The size of the substituents dictated the inhibitory strength of the analogs, with smaller substituents enabling greater potency but less selectivity. Inhibitors based on the flurbiprofen scaffold possessed the greatest potency and selectivity, with desmethylflurbiprofen (3a) exhibiting an IC50 of 0.11 μM for inhibition of 2-AG oxygenation. The crystal structure of desmethylflurbiprofen complexed to mCOX-2 demonstrated a similar binding mode to other profens. Desmethylflurbiprofen exhibited a half-life in mice comparable to that of ibuprofen. The data presented suggest that achiral profens can act as lead molecules toward in vivo probes of substrate-selective COX-2 inhibition.

The geminal dimethyl analogue of Flurbiprofen as a novel Aβ42 inhibitor and potential Alzheimer's disease modifying agent

The subtle modification of a selection of Aβ42 inhibiting non-steroidal anti-inflammatory drugs (NSAIDs), through synthesis of the geminal dimethyl analogues, was anticipated to ablate their cyclooxygenase activity whilst maintaining Aβ42 inhibition. Methylflurbiprofen 6 exhibited similar in vitro Aβ42 inhibition to its parent NSAID Flurbiprofen and was further evaluated in the Tg2576 mouse model of Alzheimer's disease and an animal model of gastro-intestinal (GI) impairment, but proved unviable for further clinical development.