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.
Reports like this on the dangers of DEHP is exactly why I started work on NeutraOat (https://neutraoat.com/), a modified oat fiber supplement designed to trap plasticizers in your gut before they can get into your bloodstream. The idea is to give people an easy, safe way to avoid absorbing plasticizers that you've ingested.
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. 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.
The corporate attorney agreed not to require me to pay any of their invoices until I closed a seed round, while the patent attorney let me pay their invoices a full year after I received them. These sorts of arrangements are common with attorneys who work with startups.
Unfortunately, the reality of trying to cure animals is that sometimes you accidentally hurt animals. That's also the reality of trying to cure humans.
This is the exact same issue vets face when they perform surgery on your cat, and it's the exact same issue that surgeons face when they perform surgery on you. The difference is that vets don't have to pay tons of money for malpractice insurance in case they get sued by the owner, which is one of the big reasons why veterinary surgery is so much cheaper (i.e. affordable to ordinary people) than human surgery.
Trying to cure a disease that gives cats such bad mouth sores that they sometimes can't even drink water isn't exactly "pushing crap".
We're trying to make it to profitability so we can get to the point where we can test the solution in humans who have neurodegeneration. When you're dealing with incredibly complex regulatory environments and millions of dollars in development costs, it's not always easy to make it from point A to point B. That's the point of this post.
To add to what everyone else said: it's not just an immunosuppressant, it's an immunosuppressant with unpredictable, severe side effects. It's really interesting, and I hope to reformulate it to make it possible for healthy people to use, but you will cause severe damage to yourself if you self-administer.
I thought it'd be too much in the weeds. The UTexas paper goes into their prescribing data and comes out with the conclusion that calcineurin inhibitors are the only common factor in their patients who don't get dementia.
Rapamycin also does not have any evidence of efficacy on neurodegeneration, while there's evidence for CNI on other forms of neurodegeneration.
Sorry, didn't mean that it was obvious scientifically. I meant obvious in terms of pharmaceutical progress. They built a mouse model to mimic muscular dystrophy and cured the mouse model of muscular dystrophy, which is why they felt confident spending their millions on human muscular dystrophy. Unfortunately, it was not a good model, in the same way that most most mouse models are not good models.
In this analogy, I meant to indicate all the wooden beams were rotten to the core, in the same way that muscles die in Duchenne muscular dystrophy. Quadrupling up the beams just means that you've spent a lot more resources on something that's fundamentally unusable.