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<p>Bradykinin-mediated angioedema, particularly hereditary angioedema due to C1 esterase inhibitor deficiency or dysfunction (HAE-C1INH), is caused by dysregulation of the kallikrein–kinin system with excessive bradykinin generation and subsequent increased vascular permeability. Modern HAE management is based on three major therapeutic strategies: on-demand treatment, short-term prophylaxis (STP), and long-term prophylaxis (LTP). On-demand treatment options include plasma-derived and recombinant C1&#xa0;inhibitor (C1INH) concentrates, the bradykinin B2 receptor antagonist icatibant, and, more recently, the first orally available plasma kallikrein inhibitor, sebetralstat. Short-term prophylaxis prior to invasive medical procedures is performed as replacement therapy by intravenous administration of C1INH concentrates. The goal of long-term prophylaxis is complete disease control with reduction of attack frequency and/or severity and improvement of quality of life. LTP therapies include subcutaneous and intravenous C1INH preparations, the oral kallikrein inhibitor berotralstat, the anti-kallikrein monoclonal antibody lanadelumab, the factor&#xa0;XIIa inhibitor garadacimab, and the antisense oligonucleotide donidalorsen. Currently under development are the oral bradykinin B2 receptor antagonist deucrictibant, which is intended for both on-demand treatment and long-term prophylaxis in different formulations, long-acting antibodies, such as navenibart, and CRISPR/Cas9-based gene-editing therapies, such as NTLA-2002 with potential functional curative properties. In particular, orally available and long-acting therapies are expected to improve adherence, self-management, and quality of life in affected patients.</p>

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Aktuelle und zukünftige Therapien von bradykininvermittelten Angioödemen

  • 期刊论文

  • 发表日期：

    2026年8月4日

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  • Maria Fasshauer,
  • Nina Dominas

摘要

Bradykinin-mediated angioedema, particularly hereditary angioedema due to C1 esterase inhibitor deficiency or dysfunction (HAE-C1INH), is caused by dysregulation of the kallikrein–kinin system with excessive bradykinin generation and subsequent increased vascular permeability. Modern HAE management is based on three major therapeutic strategies: on-demand treatment, short-term prophylaxis (STP), and long-term prophylaxis (LTP). On-demand treatment options include plasma-derived and recombinant C1 inhibitor (C1INH) concentrates, the bradykinin B2 receptor antagonist icatibant, and, more recently, the first orally available plasma kallikrein inhibitor, sebetralstat. Short-term prophylaxis prior to invasive medical procedures is performed as replacement therapy by intravenous administration of C1INH concentrates. The goal of long-term prophylaxis is complete disease control with reduction of attack frequency and/or severity and improvement of quality of life. LTP therapies include subcutaneous and intravenous C1INH preparations, the oral kallikrein inhibitor berotralstat, the anti-kallikrein monoclonal antibody lanadelumab, the factor XIIa inhibitor garadacimab, and the antisense oligonucleotide donidalorsen. Currently under development are the oral bradykinin B2 receptor antagonist deucrictibant, which is intended for both on-demand treatment and long-term prophylaxis in different formulations, long-acting antibodies, such as navenibart, and CRISPR/Cas9-based gene-editing therapies, such as NTLA-2002 with potential functional curative properties. In particular, orally available and long-acting therapies are expected to improve adherence, self-management, and quality of life in affected patients.