Owen McCarty: Targeting FXI and FXII to Reduce Device-Associated Thrombosis and Inflammation
Owen McCarty, Professor and Chair at Oregon Health and Science University, shared Vumedi Oncology’s post on LinkedIn:
”Had a chance to share our recent work on FXI and FXII in medical device-associated thrombosis and inflammation.”
Vumedi Oncology shared a post on LinkedIn:
”Could targeting factor XI or factor XII reduce both device-associated thrombosis and inflammation?
Blood-contacting devices such as ECMO oxygenators and catheters activate the contact pathway at their surfaces. That same pathway appears to drive inflammation and organ injury, not only clot formation.
In this presentation, a recap of his talk at ISTH this summer, Dr. Owen McCarty of Oregon Health & Science University traces this work from mechanism to nonhuman primate models to early clinical data.
Key insights include:
- In a catheter thrombosis study, the share of patients with catheter clots fell from about 40 percent in controls to 12 percent with AB023
- After a single dose of AB023, CRP was lower at 2 weeks, an early sign of a systemic anti-inflammatory effect
- In a baboon S. aureus sepsis model, blocking FXI/FXII activation improved survival and lowered IL-6, IL-8 and IFN-γ
McCarty also makes a broader point: targeting FXII activation or FXI activity may do more than reduce thrombin generation, and could help protect organs in the setting of infection.
Watch the full video on Vumedi.”
Proceed to the video attached to the post.
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