Replies to post #199019 on Biotech Values

[biomaven0]

>> If CGRP “really is a fundamental mechanism, you would expect a much higher proportion of patients to be completely free of attacks,” Ferrari says.

That's a stupid statement. There are multiple different migraine subtypes and no particular reason to assume they will all respond the same way to any intervention. Or the PK can be different in different patients.

On long-term safety, who knows. CGRP knockout mice basically do OK, but the protein is involved in blood pressure regulation, bone formation and assorted other disparate things.

Peter

[biotech jim]

Yep, that is a concern I would have for patients susceptible to or a family hostory of transient ischemic attacks (TIAs), or those at risk for similar thromboembolic events. CGRP sensory neurotransmission is complex, but I wonder how much peptide is sopped up by an antibody if there is synaptic release and direct post-synaptic receptor activation?

To understand the issue pharmacologically, we really need data in humans, as the animal models for both are neither good or have been shown to be predictive in my opinion.