ArticleClinical, cosmetic and investigational dermatology2011
Ecallantide is a novel treatment for attacks of hereditary angioedema due to C1 inhibitor deficiency.
Article in Clinical, cosmetic and investigational dermatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- A Case of Status Epilepticus in a Patient Experiencing an Acute Attack of Hereditary Angioedema.Clinical practice and cases in emergency medicine · 2025Article
- Article
- A modular map of Bradykinin-mediated inflammatory signaling network.Journal of cell communication and signaling · 2022Article
- The Screen of a Phage Display Library Identifies a Peptide That Binds to the Surface ofFrontiers in microbiology · 2022Article
- Clinical manifestations of hereditary angioedema and a systematic review of treatment options.Laryngoscope investigative otolaryngology · 2021Review
- Proteomic Analysis of the Venom of JellyfishesMarine drugs · 2020Article
- Enhanced Antifibrinolytic Efficacy of a Plasmin-Specific Kunitz-Inhibitor (60-Residue Y11T/L17R with C-Terminal IEK) of Human Tissue Factor Pathway Inhibitor Type-2 Domain1.Journal of clinical medicine · 2020Article
- A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm.eLife · 2020Article
- A hypothesized role for dysregulated bradykinin signaling in COVID-19 respiratory complications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Plant/Bacterial Virus-Based Drug Discovery, Drug Delivery, and Therapeutics.Pharmaceutics · 2019Review
- Discovery, Synthesis, Pharmacological Profiling, and Biological Characterization of Brintonamides A-E, Novel Dual Protease and GPCR Modulators from a Marine Cyanobacterium.Journal of medicinal chemistry · 2018Article
- S2'-subsite variations between human and mouse enzymes (plasmin, factor XIa, kallikrein) elucidate inhibition differences by tissue factor pathway inhibitor -2 domain1-wild-type, Leu17Arg-mutant and aprotinin.Journal of thrombosis and haemostasis : JTH · 2016Article
- Management of acute attacks of hereditary angioedema: role of ecallantide.Journal of blood medicine · 2015Review
- Anaesthesia Management of a Patient with Hereditary Angioedema with Prophylactic Administration of C1 Esterase Inhibitor: Case report and literature review.Sultan Qaboos University medical journal · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary angioedema (HAE) resulting from the deficiency of the C1 inhibitor protein is a rare disease, characterized by paroxysms of edema formation in the subcutis and in the submucosa. Edema can cause obstruction of the upper airway, which may lead to suffocation. Prompt elimination of edema is necessary to save patients from this life-threatening condition. Essentially, these edematous attacks are related to the activation of the kinin-kallikrein system and the consequent release of bradykinin. Ecallantide (known as DX-88 previously), a potent and specific inhibitor of plasma kallikrein is an innovative medicinal product. This is the only agent approved recently by the FDA for all localizations of edematous HAE attacks. Its advantages include no risk of viral contamination, high selectivity, very rapid onset of action, good tolerability, and straightforward subcutaneous administration. Owing to the risk of anaphylaxis, ecallantide should be administered by a health care professional. A postmarketing survey to improve risk-assessment and risk-minimization has been launched. The results of these studies may lead to the approval of ecallantide for self-administration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.