Système complémentaire

Iptacopan (LNP023) is an inhibitor with high affinity to factor B, with a KD value of 7.9 nM and an IC50 value of 10 nM. Cost-effective and quality-assured.

Refinicopan is a complement factor D inhibitor with an IC50 of 10 nM, demonstrating an inhibition activity on rabbit erythrocyte hemolysis with an IC50 of 41 nM. It possesses excellent pharmacokinetic and pharmacodynamic properties.

Pelecopan (BCX9930), an oral complement factor D inhibitor, prevents hemolysis in PNH (IC50=14.3 nM).

Factor B-IN-3 is a potent inhibitor of complement factor B. Factor B-IN-3 can be used to study inflammatory and immune-related diseases.

Factor B-IN-4 is a potent inhibitor (IC50: 1 μM) of complement factor B. Factor B-IN-4 can be used to study inflammatory and immune-related diseases.

C5aR-IN-3, a potent C5aR inhibitor, may treat autoimmune and inflammatory diseases.

Izicopan (INF056) is an antagonist of the complement factor C5a receptor. It inhibits C5a-induced calcium mobilization with an IC50 ranging from 10 to 100 nM.

Factor B-IN-6 is an orally bioavailable inhibitor of Factor B. It exhibits significant inhibitory activity on the activation of the human serum alternative pathway. In model animals, Factor B-IN-6 can improve kidney lesions and function, reducing urinary protein levels. Factor B-IN-6 is applicable for kidney disease research.

(Rel)-Factor B-IN-5 is a complement factor B inhibitor that can be used to study diseases associated with activation of the alternative complement pathway.

Bisphenol S disulfate disodium acts as a complement inhibitor (IC₅₀ = 660 μM).

4-Octylphenol is an endocrine disruptor with gender-specific effects on male germ cells, significantly reducing the mitotic index and the number of spermatogonia. It also causes inflammatory damage in the gills of carp by activating the complement system through the C3a/C3a receptor (C3a/C3aR) axis and C5a/C5a receptor 1 (C5a/C5aR1) axis. Furthermore, 4-Octylphenol induces immune suppression by disrupting the balance between helper T (Th) cells 1/Th2 and regulatory T (Treg)/Th17 cells, and triggers inflammatory damage through the Toll-like receptor 7 (Toll-like Receptor (TLR))/inhibitor κBα/nuclear factor κB (TLR7/IκBα/NF-κB) pathway.