COX Inhibitor

[lemonman]

I think I remember reading somewhere that COX inhibitor's are not good for you, because cyclooxygenase-2 does something to heal your effected area. Same with histamine,etc.
Is this true?.

 

[Tzcatlipoca]

I couldn't testify to this. I would give it potential, though. Inhibition results in negative bodily response. I would just throw substrate at COX like nsaids and potentiate with cannabis?

 

[clubcard]

Well, NSAIDs are all COX inhibitors. If you refer to the more recent, COX-2 inhibitors, a lot have been pulled from the market because of their tendency to increase 'vascular events' and strokes. I remember them arriving and as usual, every other group went into the 'me too' mode they are famous for. Rofecoxib was pulled in 2004 and valdecoxib in 2007. I don't know how many were removed from the US market but in the UK, only 5 got licensed in the first place. I'm sure lists are scattered around the web. It is an interesting one for students to study. Like the more dubious statins, you can actually identify the moieties that appear to be common to all.

For comparison, I got beta-blockers to study. Pronethalol had the unhappy metabolism issue. The naphthalene ends up being epoxidized. Liver damage results. Over the last 50 odd years they have come and gone as the meta-analyses show new problems. I'm pretty sure that the benefits of the COX-2 inhibitors will see new ones come and go.

It is certainly an excellent class of drug to understand rational design. The statins, alpha and beta blockers also. It shows the scales we need to reach to discover such issues (because I've never seen an honest study later than 1080).

If you are being prescribed a COX-2 inhibitor, it isn't a clear-cut risk, certain groups are at risk. A decent doctor will do a decent job but never underestimate a good pharmacist. There is no such thing as a totally safe drug but it's the risk/benefit we look for. If you are in pain, they do seem very effective (hence initial popularity). I trust you will feel better soon.

Edit:

I'm going to make an informed guess that the lactone moiety in rofecoxib interacts with thromboxane A2 forming a mixed anhydride. An alpha ether confirs stability on what is usually a reactive species. Heck, the anhdride could go on to do the damage but amazingly, nobody has actually researched the detailed mechanism. Once it's an orphan drug, who is going to put in the work on it's ADMA?

 

[sekio]

this is not nspd material