What advantages would tavapadon bring to the PD landscape?
It really speaks to the gap that exists in the treatment paradigm. If you look at the MAO-B inhibitors again, efficacy is compromised. They’re minimally efficacious and the D2 and D3 agonists have side effects that are prohibitive, such as somnolence, impulsivity, hallucinations, and hypertension. Within 2 years of having these medications prescribed, they’re either discontinued or something else is added to them, most of the time levodopa. The challenge is the earlier you introduce levodopa, the sooner you start exacerbating the dopamine receptor. As you go up on the dose, that exacerbation of the dopamine receptor causes the desensitization that you see which causes the dyskinesias that patient’s experience. Our hope is that by having a therapy that can actually have good efficacy with a tolerable safety profile, that it can be prescribed at the inception of diagnosis and be continued throughout the progression of the disease. Even when it’s introduced as an adjunct treatment to levodopa, given its long half-life and partial agonist mechanism of action, that it can sustain motor control, allow practitioners to reduce the levodopa dose, reduce the dyskinesia burden, and still have the needed motor control. In fact, our non-human primate trial showed just that.
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