Description
The Glu³⁰ to Lys³³ lactam bridge constrains astressin in an α-helical conformation which seems to be responsible for its especially high CRF antagonist activity. Astressin is 100 times more potent than α-helical CRF (9-41) at inhibiting ACTH secretion in vitro, and more than 10 times more potent in vivo than any other CRF antagonist reported to date.



