EC Number   |
Inhibitors |
Structure  |
|---|
   3.4.21.47 | more |
the anticoagulogen Ab (14E7) has no effect on the conversion of C3. Abs against coagulation factor G (monoclonal) and the proclotting enzyme (polyclonal) do not inhibit the deposition of C3b on Escherichia coli |
 |
| 3.4.21.47 | more |
eculizumab does not block the activity of the APC C3 convertase |
|
| 3.4.21.47 | more |
the anti-factor B autoantibody binds to factor B and to the alternative pathway C3 convertase and alters the kinetics of complement activation and regulation, the anti-factor B autoantibody does not influence the assembly of the C3 convertase |
|
| 3.4.21.47 | more |
addition of guinea pig serum in 40 mM EDTA initiates lysis of existing convertase complexes and excludes the possibility of de novo convertase formation |
|
| 3.4.21.47 | more |
regulatory proteins inactivate C3/C5 convertases on host surfaces to avoid collateral tissue damage |
|
| 3.4.21.47 | EDTA |
- |
  |
| 3.4.21.47 | hydroxylamine |
inactivates the thioester bond on C3, dramatically decreases the deposition of C3b on microbes |
|
| 3.4.21.47 | thioredoxin 1 |
Trx-1, causes significant inhibition of alternative convertases, mechanism, overview. Trx-1 is capable of inhibiting all classical and alternative convertases but its effect is more pronounced in inhibition of alternative ones |
|
| 3.4.21.47 | diisopropyl phosphate |
- |
|
| 3.4.21.47 | factor H |
mediates decay acceleration of the C3bBb complex |
|
