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This content is not meant to replace a conversation with a healthcare provider. A healthcare provider can evaluate your symptoms and make the appropriate clinical decisions.

For healthcare professionals

For people with HAE and caregivers

The Biology of Bradykinin & HAE

Most cases of hereditary angioedema stem from an inherited defect in the SERPING1 gene that controls production of C1-INH proteins. 


C1-INH proteins are the body’s built-in mechanism for properly controlling the pathway that leads to bradykinin production.

Hi, I’m Bradykinin. My friends call me Brady K.

Around here, I’m a regular, and I have an important role to play.
When there’s physical trauma, an injury, or an infection, I’m the one who brings support to the scene. I bind to B2 receptors on blood vessel walls, sending a message for those vessels to widen and get a little more porous. In normal amounts, that’s incredibly useful. This process opens up the vessels and lets essential fluids get to where they’re needed most.
But HAE attacks completely change the story.

C1-INH doesn’t work like it should.

In people with HAE type 1 and type 2, this C1-inhibitor (C1-INH) either is deficient or doesn’t function correctly, meaning the pathway it’s in charge of isn’t controlled properly.

Which means bradykinin is produced in excess.

When C1-INH isn’t working properly, a specific type of enzyme called plasma kallikrein becomes too active, leading to bradykinin levels that are too high.

Excess bradykinin causes HAE attacks.

When there is too much bradykinin, it signals the B2 receptor to start the swelling. This is where HAE attacks are triggered.

Hi! I’m Bradykinin. My friends call me Brady K.

Around here, I’m a regular, and I have an important role to play.

When there’s physical trauma, an injury, or an infection, I’m the one who brings support to the scene. I bind to B2 receptors on blood-vessel walls, sending a message for those vessels to widen and get a little more porous. In normal amounts, that’s incredibly useful. This process opens up the vessels and lets essential fluids get to where they’re needed most.

But HAE attacks completely change the story…

C1-INH doesn’t work like it should.

In people with HAE type 1 and type 2, this C1-inhibitor (C1-INH) either is deficient or doesn’t function correctly, meaning the pathway it’s in charge of isn’t controlled properly.

Which means bradykinin is produced in excess.

When C1-INH isn’t working properly, a specific type of enzyme called plasma kallikrein becomes too active, leading to bradykinin levels that are too high.

Excess bradykinin causes HAE attacks.

When there is too much
bradykinin, it signals the B2
receptor to start the swelling.
This is where HAE attacks
are triggered.
Excess Bradykinin production

= Angioedema

Excess Bradykinin production = Angioedema 

HAE, hereditary angioedema.

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