OH and to those of you have taken the time to read these posts an...

Well, I certainly don't have any answers--just lists and lists of questions.

The Merck literature was so focused on the receptor that I originally went off in that direction trying to locate all cysLT1 receptors. The Merck papers from 2000 clearly say that they believed this receptor only concerned the lungs including airways. Other people had already identified the spleen by that time, then came intestinal mucosa, and brain etc. Hypo-glycemia came out as a big potential issue. When I asked about that on the board, many responded that behavior was in some cases was quite related to hunger.

When I went back to read about the development of montelukast, then the fact that it was a quinoline really stuck out. The quinoline/quinolones are known to cause neurotoxicity. Many of those drugs warn about hypo-glycemia and electrolyte (such as potassium) unbalance.

So for the next week or so, I am going all the way back to 1991 to see what they were thinking when they chose to pursue a quinoline structure.

After that I hope to find something about why montelukast could "come apart" so to speak so that it behaves like a "raw" chloro-quinolin. I don't know what words to use here. But we can all get the point.

We are probably headed for third base in our quest to understand about these side effects. Neurotoxicity of the quinoline/quinolone is accepted. If there is a direct link to quinoline toxicity, then we round for home plate. I hate organic chemistry so I will have to find an expert source for exactly how that could happen to montelukast.