klevertree

We're still prototyping and testing, but you'll probably have to eat it twice a day to get complete coverage. It needs to be in the gut at the same time as the plasticizer to have any effect.

Not a bad idea for your health, but it won't trap plasticizers. We're modifying the beta glucan to have many tiny, "sticky" pores to trap the chemicals in the gut, so they go out with the rest of the beta glucan. Pure beta glucan, whether from oats or barley, won't have much effect.

Yes, what do you think the pk trials and liver experiments would involve if not people who have a variety of phenotypes?

Author here. Thanks! I'm pretty sure most of the negative effects of SSRIs were discovered in phase 2 trials, though. Pk trials aren't usually powered to find adverse effects in subpopulations like teenage patients. Same thing with GLP-1 agonists and their effects on addictions (which I think were actually discovered post approval).

That being said, we'd still have to do dose escalation studies for toxicology even if we had great pbpk models. Not denying that.

Author here. As someone who works in pharma, organ on a chip models are not even close to being relevant to providing accurate PK curves for oral absorption. The state of the art is trying to make it work for cutaneous absorption and that's still not great/commercially useful.

My whole point is that there needs to be way more open data on pharmacokinetics. That's the only way we're going to solve this.

Author here. That's not what I said. Please don't be a jerk on the Internet.

Cyclosporine and tacrolimus, if you look at the range in any of their pk trials you'll easily see 10 fold variability.

Author here. Enzyme polymorphisms are tricky and would require a whole different blog post. Some drugs they matter a lot for, some drugs they do not. I actually have not found any drugs with 10-fold variability that could be ascribed solely (or even mainly) to polymorphisms, although it doesn't seem impossible.