Dr. Matthew Hill

And I'm sure we'll talk about some of the PTSD stuff and anxiety later. But so that's kind of one of the things. The drug has not really been used that widely yet. It's still... It's one of the frustrations I have as a scientist who does a lot of translational work and with clinical partners like Leah is that getting access to these molecules is not easy when they're not kind of wide.

They're not like out in the market. So you can just go and get them. You really have to. Try and get access from the drug companies to be able to do trials with them. And so we are in the midst of trying to do that. We did just complete a trial that Lee and Marcus ran that I worked with them on as well that was on PTSD. And so there are various potential indications for this.

They're not like out in the market. So you can just go and get them. You really have to. Try and get access from the drug companies to be able to do trials with them. And so we are in the midst of trying to do that. We did just complete a trial that Lee and Marcus ran that I worked with them on as well that was on PTSD. And so there are various potential indications for this.

They're not like out in the market. So you can just go and get them. You really have to. Try and get access from the drug companies to be able to do trials with them. And so we are in the midst of trying to do that. We did just complete a trial that Lee and Marcus ran that I worked with them on as well that was on PTSD. And so there are various potential indications for this.

I mean, Johnson & Johnson developed one as well, and they looked at it in social anxiety disorder. They had some moderate efficacy in their trial. So I'd say the jury's still out on exactly what we're going to do with these, but they have some potential, I think, in certain clinical settings. We just have to figure that out exactly. But I think going back to where we started this from...

I mean, Johnson & Johnson developed one as well, and they looked at it in social anxiety disorder. They had some moderate efficacy in their trial. So I'd say the jury's still out on exactly what we're going to do with these, but they have some potential, I think, in certain clinical settings. We just have to figure that out exactly. But I think going back to where we started this from...

I mean, Johnson & Johnson developed one as well, and they looked at it in social anxiety disorder. They had some moderate efficacy in their trial. So I'd say the jury's still out on exactly what we're going to do with these, but they have some potential, I think, in certain clinical settings. We just have to figure that out exactly. But I think going back to where we started this from...

they're not psychoactive. And so, I mean, when Pfizer first made the drug, they were actually initially concerned that it wasn't getting in the brain because no one could tell they were on the drug. I mean, this was the Wild West at this point. No one had any idea what endocannabinoids were actually gonna do. People were basing it on what we knew about THC.

they're not psychoactive. And so, I mean, when Pfizer first made the drug, they were actually initially concerned that it wasn't getting in the brain because no one could tell they were on the drug. I mean, this was the Wild West at this point. No one had any idea what endocannabinoids were actually gonna do. People were basing it on what we knew about THC.

they're not psychoactive. And so, I mean, when Pfizer first made the drug, they were actually initially concerned that it wasn't getting in the brain because no one could tell they were on the drug. I mean, this was the Wild West at this point. No one had any idea what endocannabinoids were actually gonna do. People were basing it on what we knew about THC.

So the assumption was people would have psychoactivity. But they didn't. Pfizer then actually had to do – they did a sleep study to show that it did have some effects on sleep cycle the same way THC does. And then they also did like an in vivo PET binding study to show that they could displace a radioactive molecule that would bind to the enzyme in the brain.

So the assumption was people would have psychoactivity. But they didn't. Pfizer then actually had to do – they did a sleep study to show that it did have some effects on sleep cycle the same way THC does. And then they also did like an in vivo PET binding study to show that they could displace a radioactive molecule that would bind to the enzyme in the brain.

So the assumption was people would have psychoactivity. But they didn't. Pfizer then actually had to do – they did a sleep study to show that it did have some effects on sleep cycle the same way THC does. And then they also did like an in vivo PET binding study to show that they could displace a radioactive molecule that would bind to the enzyme in the brain.

So what's it doing?

So what's it doing?

So what's it doing?

Yeah, I mean, I think I would say the main way that we think about this is the difference between endocannabinoids and THC is endocannabinoids are going to be released in a very specific spatial and temporal manner. They evolve to do that. Yeah, so there's going to be, and I think it's very clear that anandamide, for example, is not active at every synapse that has CB1.

Yeah, I mean, I think I would say the main way that we think about this is the difference between endocannabinoids and THC is endocannabinoids are going to be released in a very specific spatial and temporal manner. They evolve to do that. Yeah, so there's going to be, and I think it's very clear that anandamide, for example, is not active at every synapse that has CB1.

Yeah, I mean, I think I would say the main way that we think about this is the difference between endocannabinoids and THC is endocannabinoids are going to be released in a very specific spatial and temporal manner. They evolve to do that. Yeah, so there's going to be, and I think it's very clear that anandamide, for example, is not active at every synapse that has CB1.

And so when we boost anandamide signaling by inhibiting its metabolism, all we're doing is amplifying anandamide signaling at the synapses it already exists. Whereas THC, when you consume it orally or inhalation-wise and it gets into your blood and into your brain, it's just blanket activation. You're just carpet bombing the whole system indiscriminately.