Conestat alfa
Ruconest (conestat alfa) is a protein pharmaceutical. Conestat alfa was first approved as Ruconest on 2010-10-28. It has been approved in Europe to treat hereditary angioedemas.
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Indications Phases 4
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Indications Phases 3
Indication | MeSH | Ontology | ICD-10 | Ph 1 | Ph 2 | Ph 3 | Ph 4 | Other | Total |
|---|---|---|---|---|---|---|---|---|---|
| Hereditary angioedemas | D054179 | EFO_0004131 | — | — | 7 | 4 | — | 2 | 11 |
| Angioedema | D000799 | EFO_0005532 | T78.3 | — | 6 | 4 | — | 2 | 10 |
| Inborn genetic diseases | D030342 | EFO_0000508 | — | — | 3 | 2 | — | — | 4 |
Indications Phases 2
Indication | MeSH | Ontology | ICD-10 | Ph 1 | Ph 2 | Ph 3 | Ph 4 | Other | Total |
|---|---|---|---|---|---|---|---|---|---|
| Acute kidney injury | D058186 | — | N17 | — | 3 | — | — | — | 3 |
| Covid-19 | D000086382 | — | U07.1 | — | 2 | — | — | — | 2 |
| Kidney transplantation | D016030 | — | — | — | 1 | — | — | — | 1 |
| Graft rejection | D006084 | — | — | — | 1 | — | — | — | 1 |
| Myocardial infarction | D009203 | EFO_0000612 | I21 | — | 1 | — | — | — | 1 |
| Non-st elevated myocardial infarction | D000072658 | — | — | — | 1 | — | — | — | 1 |
| Infarction | D007238 | EFO_0009463 | — | — | 1 | — | — | — | 1 |
| Ischemic stroke | D000083242 | — | — | — | 1 | — | — | — | 1 |
| Ischemia | D007511 | EFO_0000556 | — | — | 1 | — | — | — | 1 |
| Infections | D007239 | EFO_0000544 | — | — | 1 | — | — | — | 1 |
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Indications Phases 1
Indication | MeSH | Ontology | ICD-10 | Ph 1 | Ph 2 | Ph 3 | Ph 4 | Other | Total |
|---|---|---|---|---|---|---|---|---|---|
| Renal insufficiency | D051437 | — | N19 | 1 | — | — | — | — | 1 |
| Delayed graft function | D051799 | — | — | 1 | — | — | — | — | 1 |
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Epidemiological information for investigational and approved indications
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Drug
General
| Drug common name | Conestat alfa |
| INN | conestat alfa |
| Description | C1-inhibitor (C1-inh, C1 esterase inhibitor) is a protease inhibitor belonging to the serpin superfamily. Its main function is the inhibition of the complement system to prevent spontaneous activation but also as the major regulator of the contact system. C1-inhibitor is an acute-phase protein that circulates in blood at levels of around 0.25 g/L. The levels rise ~2-fold during inflammation. C1-inhibitor irreversibly binds to and inactivates C1r and C1s proteases in the C1 complex of classical pathway of complement. MASP-1 and MASP-2 proteases in MBL complexes of the lectin pathway are also inactivated. This way, C1-inhibitor prevents the proteolytic cleavage of later complement components C4 and C2 by C1 and MBL. Although named after its complement inhibitory activity, C1-inhibitor also inhibits proteases of the fibrinolytic, clotting, and kinin pathways. Note that C1-inhibitor is the most important physiological inhibitor of plasma kallikrein, FXIa, and FXIIa.
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| Classification | Protein |
| Drug class | enzyme inhibitors |
| Image (chem structure or protein) |  |
| Structure (InChI/SMILES or Protein Sequence) | — |
Identifiers
| PDB | — |
| CAS-ID | — |
| RxCUI | — |
| ChEMBL ID | CHEMBL2108350 |
| ChEBI ID | — |
| PubChem CID | — |
| DrugBank | DB06404 |
| UNII ID | 5QS67N4551 (ChemIDplus, GSRS) |
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Ruconest – Pharming
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4,737 adverse events reported
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