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Drug ReportsC1 esterase inhibitor
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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Commercial
Therapeutic Areas
Therapeutic Area
MeSH
cardiovascular diseasesD002318
hereditary congenital and neonatal diseases and abnormalitiesD009358
skin and connective tissue diseasesD017437
immune system diseasesD007154
Trade Name
FDA
EMA
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Drug Products
FDA
EMA
New Drug Application (NDA)
New Drug Application (NDA)
Abbreviated New Drug Application (ANDA)
Abbreviated New Drug Application (ANDA)
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Labels
FDA
EMA
Brand Name
Status
Last Update
berinertBiologic Licensing Application2009-11-10
cinryzeBiologic Licensing Application2010-11-01
ruconestBiologic Licensing Application2020-04-30
Indications
FDA
EMA
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Agency Specific
FDA
EMA
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Patent Expiration
No data
ATC Codes
B: Blood and blood forming organ drugs
B06: Other hematological agents in atc
B06A: Other hematological agents in atc
B06AC: Drugs used in hereditary angioedema
B06AC04: Conestat alfa
HCPCS
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Clinical
Clinical Trials
93 clinical trials
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Indications Phases 4
Indication
MeSH
Ontology
ICD-10
Ph 1
Ph 2
Ph 3
Ph 4
Other
Total
Hereditary angioedemasD054179EFO_00041313351110
AngioedemaD000799EFO_0005532T78.3225119
Hereditary angioedema types i and iiD05682921215
Indications Phases 3
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Indications Phases 2
Indication
MeSH
Ontology
ICD-10
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Kidney transplantationD016030111
Indications Phases 1
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Indications Without Phase
No data
Epidemiology
Epidemiological information for investigational and approved indications
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Drug
General
Drug common nameConestat alfa
INNconestat 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.
Classification
Protein
Drug classenzyme inhibitors
Image (chem structure or protein)Loading
Structure (InChI/SMILES or Protein Sequence)
Identifiers
PDB
CAS-ID
RxCUI
ChEMBL IDCHEMBL2108350
ChEBI ID
PubChem CID
DrugBankDB06404
UNII ID5QS67N4551 (ChemIDplus, GSRS)
Target
No data
Variants
No data
Financial
Revenue by drug
$
£
Ruconest Pharming
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Safety
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4,737 adverse events reported
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