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How long does Firazyr take to work?

Medically reviewed by Carmen Fookes, BPharm. Last updated on May 13, 2020.

Official Answer

by Drugs.com
  • In clinical trials, it took an average of 2 to 2.5 hours for Firazyr (icatibant) to relieve symptoms of angioedema in people with HAE.
  • 92.4% of attacks were treated with a single dose of Firazyr.
  • Firazyr is given by subcutaneous injection (under the skin).
  • Firazyr may be administered by a health professional or people can be taught to self-administer it.

Firazyr (icatibant) is a selective B2 bradykinin receptor antagonist indicated for the treatment of acute attacks in adults 18 years and older with hereditary angioedema (HAE).

Hereditary angioedema is a genetic disorder that causes attacks of swelling severe swelling in the limbs, face, intestinal tract, and airway.

Firazyr may be administered by a trained health professional experienced at treating HAE; however, people can also be taught how to administer it themselves. It is administered by subcutaneous (under the skin) injection into the abdominal area.

How long does it take Firazyr to work?

In clinical trials, it took an average of 2 to 2.5 hours for Firazyr to relieve symptoms of angioedema in people with HAE. 92.4% of attacks were treated with a single dose of Firazyr.

When injected under the skin (subcutaneously), 97% of a dose of Firazyr is absorbed into the bloodstream. It takes approximately 45 minutes for Firazyr to reach peak levels in the blood.

Firazyr has a short half-life (approximately 1.4 hours) and most of a dose is eliminated after 5.6 to 7 hours. There is no evidence of accumulation of Firazyr after three 30mg doses administered 6 hours apart. One subcutaneous 30mg dose of Firazyr effectively blocks bradykinin for a least six hours (up to eight hours).

What is the dosage of Firazyr?

The usual dosage to treat an acute attack of angioedema is 30mg. If attack symptoms persist additional doses may be administered at intervals of at least 6 hours.

No more than 3 doses may be administered in any 24 hour period. In clinical trials, not more than eight doses were administered per month.

How does Firazyr work?

People with hereditary angioedema (HAE) have low levels of naturally occurring C1 inhibitory protein (C1-INH) in their blood. C1-INH is a key regulator of the Factor XII/kallikrein cascade that leads to the production of bradykinin.

Bradykinin is thought to be responsible for the characteristic symptoms of angioedema attacks seen in HAE. Firazyr (icatibant) blocks the bradykinin B2 receptor, to the same extent as what bradykinin would. By inhibiting the binding of bradykinin to the B2 receptor it helps treat the symptoms of an acute attack of HAE.

What is hereditary angioedema?

Hereditary angioedema is a genetic disorder characterized by severe swelling in the limbs, face, intestinal tract, and airway. There are three known types: Type I and II caused by mutations in the Serping I gene and Type III which is caused by mutations in the F12 gene.

The Serping I gene provides instructions for making the C1 inhibitor protein, which helps control inflammation. Mutations in this gene can lead to either reduced levels of C1 protein in the blood or the production of a C1 inhibitor that functions abnormally. When levels of this C1 protein are decreased, excessive amounts of another protein fragment, called bradykinin are generated. Bradykinin increases the leakage of fluid through the walls of blood vessels into body tissues, promoting inflammation. This causes fluid to accumulate which causes the swelling characteristic of hereditary angioedema type I and type II.

Some cases of hereditary angioedema type III are associated with mutations in the F12 gene. This gene codes for an important protein that helps our blood to clot, known as coagulation factor XII. Factor XII is also an important stimulator of inflammation and is involved in bradykinin production. Certain F12 mutations produce Factor XII with an increased activity, which generates more bradykinin, leading to blood vessel wall leakage and angioedema. The gene mutations responsible for other types of hereditary angioedema III have not yet been discovered.

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