|Accession Number||DB00026 (BIOD00060, BTD00060)|
Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Display: 3D Structure
|Protein chemical formula||C759H1186N208O232S10|
|Protein average weight||17257.6000|
>DB00026 sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLG IHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGW FLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE
|Brand mixtures||Not Available|
|Indication||For the treatment of adult rheumatoid arthritis and treatment of Neonatal-Onset Multisystem Inflammatory Disease (NOMID).|
|Pharmacodynamics||Used to treat rheumatoid arthritis, Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.|
|Mechanism of action||Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.|
|Absorption||When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once daily, NOMID patients = 3628 ng/mL.|
|Volume of distribution||Not Available|
|Protein binding||Not Available|
|Route of elimination||Not Available|
|Half life||Healthy subjects = 4 - 6 hours; NOMID patients = 5.7 hours (range of 3.1 - 28.2 hours).|
Clearance is variable and increases with increasing creatinine clearance and body weight. However, gender and age were not significant factors.
|Toxicity||Most common adverse reactions (incidence ≥ 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used in RA patients. In NOMID patients, the most common AEs during the first 6 months of treatment (incidence >10%) are injection site reaction, headache, vomiting, arthralgia, pyrexia, and nasopharyngitis.|
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|Synthesis Reference||Not Available|
|FDA label||show (62.3 KB)|
|Food Interactions||Not Available|
Receptor for interleukin-1 alpha (IL-1A), beta (IL-1B), and interleukin-1 receptor antagonist protein (IL-1RA). Binding to the agonist leads to the activation of NF-kappa-B. Signaling involves formation of a ternary complex containing IL1RAP, TOLLIP, MYD88, and IRAK1 or IRAK2Organism class: human
UniProt ID: P14778
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report
Searched, but no enzymes found.
Searched, but no transporters found.
Searched, but no carriers found.