2. Signaling Pathways
  3. Immunology/Inflammation
  4. Complement System

Complement System

Complement System

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The complement system, composed of more than 30 serum and cell surface components, is collaborating in recognition and elimination of pathogens as a part of both the innate and acquired immune systems. Once the complement system is activated, a chain of reactions involving proteolysis and assembly occurs, resulting in cleavage of the third complement component (C3). The cascade up to C3 cleavage is called the activation pathway. There are three activation pathways: the classical, lectin, and alternative pathways.

The complement cascade is a dual-edged sword, causing protection against bacterial and viral invasion by promoting phagocytosis and inflammation. Pathologically, complement can cause substantial damage to blood vessels (vasculitis), kidney basement membrane and attached endothelial and epithelial cells (nephritis), joint synovium (arthritis), and erythrocytes (hemolysis) if it is not adequately controlled.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-117992
    BR103
    		99.75%
    BR103 is a C3aR-specific small molecule ligand. BR103 can be used to measure ligand affinity for a G protein-coupled receptor for saturation and competitive binding.
    BR103
  • HY-110136
    PMX 205
    		Antagonist 99.78%
    PMX 205 is a potent complement C5a receptor (C5aR; CD88) antagonist.
    PMX 205
  • HY-147297
    Pelecopan
    		Inhibitor 98.13%
    Pelecopan (BCX9930) is a potent, selective, orally active inhibitor of complement factor D with an IC50 value of 14.3 nM. Pelecopan can target factor D to prevent both intravascular and extravascular hemolysis in PNH. Pelecopan also be used for other alternative pathway (AP) mediated diseases.
    Pelecopan
  • HY-P1505A
    C3a (70-77) TFA
    		99.79%
    C3a (70-77) TFA (Complement 3a (70-77) TFA) is an octapeptide corresponding to the COOH terminus of C3a, exhibits the specificity and 1 to 2% biologic activities of C3a.
    C3a (70-77) TFA
  • HY-B0579R
    Cyclosporin A (Standard)
    		Inhibitor
    Cyclosporin A (Standard) is the analytical standard of Cyclosporin A. This product is intended for research and analytical applications. Cyclosporin A (Cyclosporine A) is an immunosuppressant which binds to the cyclophilin and inhibits phosphatase activity of protein phosphatase 2B (PP2B/calcineurin) with an IC50 of 5 nM. Cyclosporin A also inhibits CD11a/CD18 adhesion.
    Cyclosporin A (Standard)
  • HY-122700
    Factor D inhibitor 6
    		Inhibitor 99.18%
    Factor D inhibitor 6 is a potent, highly selective and orally active factor D (FD) inhibitor with an IC50 of 30 nM and a Kd of 6 nM. Factor D inhibitor 6 is inactive against factor B, lassical and lectin complement-pathway activation, and a broad assay panel of receptors, ion channels, kinases and proteases.
    Factor D inhibitor 6
  • HY-P990025
    Empasiprubart
    		99.99%
    Empasiprubar (ARGX-117) is a humanized inhibitory monoclonal antibody targeting complement C2. Empasiprubar binds to the Sushi-2 domain of C2, preventing the formation of C3 pre convertase and inhibiting the activation of classical and lectin pathways upstream of C3 activation. Empasiprubar can prevent complement mediated autoimmune hemolytic anemia and antibody mediated organ transplant rejection. Empasiprubar can prevent neuroglial lymphoconjunctival injury in GM1 antibody mediated mouse models.
    Empasiprubart
  • HY-147762
    NRP1 antagonist 2
    		Antagonist 99.05%
    NRP1 antagonist 2 (Compound 1) is an NRP1 antagonist.
    NRP1 antagonist 2
  • HY-P5506
    C5a Receptor agonist, W5Cha
    		Agonist 99.50%
    C5a Receptor agonist, W5Cha (Peptide 1) is a selective complement C5a receptor (C5aR) agonist (EC50=0.2 μM), a hexapeptide derived from the C-terminus of C5a with specific amino acid modifications. C5a Receptor agonist, W5Cha is able to interact with the Arg-206 site of the C5a receptor through its C-terminal arginine, thereby activating the receptor.
    C5a Receptor agonist, W5Cha
  • HY-P99298
    Lampalizumab
    		Inhibitor 99.46%
    Lampalizumab (RG 7417) is a humanised monoclonal antibody targeting complement Factor D in the alternative complement pathway. Lampalizumab binds an exosite and sterically blocks Factor B access to the active site. Lampalizumab can be used for age-related macular degeneration (AMD) research.
    Lampalizumab
  • HY-P99786
    Pozelimab
    		Inhibitor 99.42%
    Pozelimab (REGN3918) is a fully human IgG4 anti-C5 monoclonal antibody. Pozelimab binds to C5 and C5 variants with high affinity and blocks complement-mediated hemolysis. Pozelimab can be used for the research of complement-mediated diseases.
    Pozelimab
  • HY-W371165
    C1s-IN-1 trihydrochloride
    		Inhibitor 99.73%
    C1s-IN-1 trihydrochloride (Compound A1) is the selective inhibitor for C1s protease with the Ki of 5.8 μM. C1s-IN-1 trihydrochloride inhibits cleavage of C2 by C1s with an IC50 of 85 μM, inhibits the activation of classic pathway with an IC50 of 22 μM. C1s-IN-1 trihydrochloride is the competitive inhibitor for thrombin with the Ki of 51.2 μM.
    C1s-IN-1 trihydrochloride
  • HY-P10639
    C5aR2 agonist P32
    		Agonist 99.82%
    C5aR2 agonist P32 (Ac-RHYPYWR-OH) is a C5aR2-selective agonist. C5aR2 agonist P32 has been shown to elicit multiple immunomodulatory activities, both by down-regulating the C5aR1-mediated cell signalling, and acting in a C5aR1-independent fashion, in vitro and in vivo.
    C5aR2 agonist P32
  • HY-102034
    Complement factor D-IN-1
    		98.85%
    Complement factor D-IN-1 is a potent and selective small-molecule reversible factor d inhibitor, with IC50s of 0.006 and 0.05 μM in FD Thioesterolytic Fluorescent Assay and a MAC Deposition Assay, respectively.
    Complement factor D-IN-1
  • HY-145720A
    Cemdisiran sodium
    Cemdisiran sodium is an N-acetylgalactosamine (GalNAc) conjugated siRNA for the research of complement-mediated diseases by suppressing liver production of complement 5 (C5) protein.
    Cemdisiran sodium
  • HY-P2526
    LyP-1
    		98.46%
    LyP-1 is a cyclic 9-amino-acids tumor homing peptide and selectively bind to p32 receptors overexpressed in various tumor-associated cells.
    LyP-1
  • HY-14648S3
    Dexamethasone-4,6α,21,21-d4
    		Inhibitor ≥99.0%
    Dexamethasone-4,6α,21,21-d4 is the deuterium labeled Dexamethasone-4,6α,21,21. Dexamethasone (Hexadecadrol) is a glucocorticoid receptor agonist. Dexamethasone also significantly decreases CD11b, CD18, and CD62L expression on neutrophils, and CD11b and CD18 expression on monocytes. Dexamethasone is highly effective in the control of COVID-19 infection. Dexamethasone inhibits production of exosomes containing inflammatory microRNA-155 in lipopolysaccharide-induced macrophage inflammatory responses.
    Dexamethasone-4,6α,21,21-d<sub>4</sub>
  • HY-Y0641
    3-Phenoxybenzaldehyde
    		Inhibitor 99.74%
    3-Phenoxybenzaldehyde has weak complement classical pathway inhibition and hemolytic activity.
    3-Phenoxybenzaldehyde
  • HY-14648AR
    Dexamethasone acetate (Standard)
    		Inhibitor
    Dexamethasone acetate (Standard) is the analytical standard of Dexamethasone acetate. This product is intended for research and analytical applications. Dexamethasone acetate (Dexamethasone 21-acetate) is a glucocorticoid receptor agonist. Dexamethasone also significantly decreases CD11b, CD18, and CD62L expression on neutrophils, and CD11b and CD18 expression on monocytes. Dexamethasone is highly effective in the control of COVID-19 infection. Dexamethasone inhibits production of exosomes containing inflammatory microRNA-155 in lipopolysaccharide-induced macrophage inflammatory responses.
    Dexamethasone acetate (Standard)
  • HY-153785
    NH2-C6-ARC186 sodium
    		Inhibitor
    NH2-C6-ARC186 sodium is a modified ARC186 (HY-153098) with NH2-C6 that can be coupled to other peptides or molecules. ARC186 is a aptamer and a highly potent complement inhibitor that function by blocking the convertase-catalyzed activation of C5.
    NH2-C6-ARC186 sodium
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Cat. No. Product Name / Synonyms Application Reactivity