EC Number   |
Inhibitors  |
Structure |
|---|
   3.4.21.41 | 3-alkoxy-4-chloro-7-guanidinoisocoumarin |
- |
   |
| 3.4.21.41 | 4-chloro-3-(3-isothiureidopropoxy)isocoumarin |
- |
|
| 3.4.21.41 | 4-Nitrophenyl-4-guanidinobenzoate |
- |
|
| 3.4.21.41 | C1 inhibitor |
during complex formation, C1 inhibitor dissociates C1r and C1s from the activated C1 macromolecule, a process that is determined primarily by the interaction with C1r |
|
| 3.4.21.41 | C1 inhibitor |
- |
|
| 3.4.21.41 | C1-inhibitor |
regulates the classical and the lectin complement pathway inhibiting complement components C1r and C1s, and MASP-2, factor XIa, Factor XIIa, and plasma kallikrein, mechanism, overview |
|
| 3.4.21.41 | C1bar-inhibitor |
Ca2+ decreases the rate at which C1rbar complexes with C1bar-inhibitor. C1rbar-(C1bar-inhibitor) interaction is accelerated by heparin. Flufenamic acid inhibits the action of the inhibitor |
|
| 3.4.21.41 | C1bar-inhibitor |
irreversible |
|
| 3.4.21.41 | C1bar-inhibitor |
kinetics of the reaction between inhibitor and enzyme |
|
| 3.4.21.41 | C1INH |
sole inhibitor of the activated proteases C1r and C1s. Hereditary angioedema results from functional deficiency of the C1 inhibitor (C1INH) protein, which plays a key role in the classical pathway of complement activation |
|
