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Eculizumab (Anti-Human C5, Humanized Antibody) is a long-acting humanized monoclonal antibody targeted against complementC5. Eculizumab inhibits the cleavage of C5 into C5a and C5b and inhibits deployment of the terminal complement system including the formation of membrane attack complex (MAC). Eculizumab prevents anti-ganglioside antibody-mediated neuropathy in mice. Eculizumab can be used in hemolysis studies .
Avacincaptad pegol (ARC1905) sodium is a 40KDa PEG-conjugated aptamer. Avacincaptad pegol sodium targets complement factor 5 (C5), inhibits the cleavage of C5 into C5a and C5b, limits inflammatory stimulation and complement membrane attack complex (MAC), and is used to study age-related macular degeneration (AMD). Avacincaptad pegol sodium limits irregular cell apoptosis by targeting downstream factors in the complement cascade while preserving the early steps of the complement system .
Zilucoplan (RA101495), a 15-amino acid macrocyclic peptide, is a potent complement component 5 (C5) inhibitor. Zilucoplan can be used in research of immune-mediated necrotising myopathy (IMNM) .
JR14a is a potent thiophene antagonist of human complement C3a receptor. JR14a shows selectivity for the human C3a receptor over C5a receptor. JR14a can suppress C3aR-mediated inflammation .
Crovalimab (SKY59; RO7112689) is a novel humanized antibody against C5 in a pH-dependent manner with KDs of 15.2 nM and 16.8 μM at pH 7.4 and 5.8, respectively. Crovalimab binds human FcRn with great affinity (KD: 17 μM at pH 6.0). Crovalimab can block cleavage of C5 by the C5 convertase and inhibite the activity of a C5 variant (p.Arg885His). Crovalimab inhibits C5b-9 formation significantly in all three complement pathways, the classical pathway (CP), lectin pathway (LP), and alternative pathway (AP). Crovalimab has the potential for paroxysmal nocturnal hemoglobinuria (PNH) and complement-mediated diseases research .
Cobra Venom Factor (CVF) is a selective activator targeting complement components C3, C5, and factor B in the complement system. After binding to factor B, Cobra Venom Factor is cleaved by factor D, forming a stable C3/C5 convertase resistant to regulatory proteins H and I. This continuously hydrolyzes C3 and C5, depleting serum complement while inducing neutrophil migration, vascular leakage, and increased TNF-α levels. Cobra Venom Factor can be used to deplete complement and mimic complement activation-related pathological states, and is applied in animal models of complement-mediated diseases such as acute respiratory distress syndrome (ARDS), sepsis, and shock. Cobra Venom Factor can be isolated from the venom of cobras (e.g., Naja atra, Naja melanoleuca, Naja kaouthia, etc.) .
PMX-53 (3D53) is a synthetic peptidic and a potent and orally active complementC5a receptor (CD88) antagonist with an IC50 of 20 nM. PMX-53 is also a low-affinity MrgX2 agonist that stimulates MrgX2-mediated mast cell degranulation. PMX-53 specifically binds to C5aR1 and does not bind to the second C5aR (C5L2) and C3aR. PMX-53 has anti-inflammatory, anticancer and antiatherosclerotic effects .
Ravulizumab (ALXN1210) is a humanized monoclonal antibody that specifically binds with high affinity to the human complement protein C5. Ravulizumab can be used for the research of paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, and myasthenia gravis .
Cemdisiran (ALN-CC5) is an N-acetylgalactosamine-conjugated RNAi agent and also a complement component C5 inhibitor. Cemdisiran targets C5 mRNA, cleaves C5 mRNA via the endogenous RNA interference pathway, and inhibits the production of C5 protein in the liver. Cemdisiran exerts a dose-dependent inhibitory effect on total C5 concentrations in cynomolgus monkeys. When used in combination with Pozelimab (HY-P99786) in cynomolgus monkeys, Cemdisiran achieves a more sustained and complete inhibitory effect on complement activity. Cemdisiran can be used in the research of paroxysmal nocturnal hemoglobinuria and other complement-mediated diseases .
Avacincaptad pegol (Izervay) is a selective inhibitor targeting complement component C5, and is a pegylated ribonucleic acid aptamer. Avacincaptad pegol inhibits the cleavage of C5 into pro-inflammatory C5a and C5b, which forms the membrane attack complex (C5b-9), thereby reducing inflammatory cell recruitment and retinal cell damage. Avacincaptad pegol can slow the growth of geographic atrophy (GA) lesions and reduce the risk of persistent vision loss. Avacincaptad pegol can be used in research of geographic atrophy associated with age-related macular degeneration (AMD) and has been approved by the FDA .
Compound C5-IN-1 (Compound 7) is a selective allosteric inhibitor of complement component protein C5. Compound C5-IN-1 prevents C5 from being cleaved by C5 convertase, inhibits the cleavage of C5 into C5a and C5b, and thus blocks the formation of membrane attack complex (MAC). Compound C5-IN-1 has an IC50 of 0.77 μM and 5 nM in 50% human whole blood and 2% human serum to block MAC deposition induced by zymosan, respectively. Compound C5-IN-1 can be used to study diseases related to complement overactivation, such as paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS) .
Vilobelimab (CaCP-29, IFX-1) is a monoclonal anti-C5a antibody to the allergen C5a, a pro-inflammatory complement division product that plays a central role in mediating organ dysfunction. Vilobelimab acts as a C5a inhibitor, inhibiting neutrophil activation, chemotaxis, and reducing inflammatory signalling, and may be used in studies related to sepsis, COVID-19, etc .
Gefurulimab (ALXN-1720) is a high-affinity antibody inhibitor targeting complement protein C5, which can specifically bind to C5 and inhibit its cleavage into C5a and C5b. Gefurulimab can block the activation of the terminal complement pathway and reduce inflammatory damage. Gefurulimab can effectively reduce the formation of membrane attack complex (MAC) and has good pharmacokinetic properties. Gefurulimab can be used to study kidney and autoimmune diseases related to abnormal activation of the complement system, such as IgA nephropathy, lupus nephritis, and myasthenia gravis .
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 .
Avdoralimab (IPH 5401) is a fully human IgGκ monoclonal antibody that targets the complementC5a receptor 1 (C5aR1) that prevents its binding to C5a. Avdoralimab can be used for complement-driven inflammatory diseases and solid tumours research .
C5a Receptor agonist, W5Cha (Peptide 1) is a selective complementC5a 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 .
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.
JPE-1375 is a complementC5a receptor 1(C5aR1) antagonist. JPE-1375 effectively inhibits polymorphonuclear leukocyte mobilization (EC50=6.9 μM) and reduces TNF levels (EC50=4.5 μM) in mice. JPE-1375 can be used in studies of autoimmune and inflammatory diseases .
CP-289,503 is an inhibitor of the complementC5a receptor with an IC50 of 1 μM. C5a acts as an activator of leukocytes and phagocytes during complement system activation. The C5a receptor can bind to C5a, which can stimulate the upregulation of cell surface integrins and degranulation of inflammatory cells, leading to endothelial cell damage. C5a receptor inhibitors can block C5a signaling and inhibit a variety of inflammatory diseases .
Vensobafusp alfa (KP-104) is a fusion protein composed of an IgG4 monoclonal antibody directed against terminal complement protein C5 fused to the complement factor H 1-5 domain (FH1-5). Vensobafusp alfa shows anti-inflammatory and immunomodulatory activities. The isotype control for Vensobafusp alfa can refer to Human IgG4 (S228P) kappa, Isotype Control (HY-P99003) . .
Zilucoplan (PEG2) is a Zilucoplan (HY-P3502) derivative, where the linker section replaces PEG24 by PEG2. Zilucoplan is a potent complement component 5 (C5) inhibitor .
Zilucoplan TFA (RA101495), a 15-amino acid macrocyclic peptide, is a potent complement component 5 (C5) inhibitor. Zilucoplan TFA can be used in research of immune-mediated necrotising myopathy (IMNM) .
4-Octylphenol is a hormone disruptor that has gender-specific effects on male reproductive cells, significantly reducing the mitotic index and the number of spermatogonia. 4-Octylphenol can cause inflammatory damage to fish gills by activating the complement system through the C3a/C3aR axis and the C5a/C5aR1 axis, this leads to complement activation and causes immune suppression due to the imbalance between Th1/Th2 cells and regulatory T cells (Treg)/Th17 cells, as well as inflammatory damage via the Toll-like receptor 7 (Toll-like Receptor (TLR))/IκBα/NF-κB pathway .
ARC186 (sodium) is an unconjugated 40KDa PEG aptamer with a sequence identical to HY-147080 Avacincaptad pegol (ARC1905) sodium. ARC1905 is highly potent complement inhibitors that function by blocking the convertase-catalyzed activation of C5.
Pexelizumab (h5G1. 1-SC) is a humanized scFv monoclonal antibody directed against the C5complement component. Pexelizumab inhibits apoptosis and leukocyte infiltration. Pexelizumab can be used for the research of cerebral IR injury and myocardial infarction .
Omoprubart is an anti-C5complement recombinant humanized monoclonal antibody. Omolubat can prevent C5 from cleaving into C5a and C5b, thereby inhibiting the formation and activation of the C5b-dependent membrane attack complex (MAC) on the surface of susceptible cells, leading to cell lysis (destruction). Omoprubart can be used for the study of paroxysmal nocturnal hemoglobinuria (PNH).
Olendalizumab (ALXN1007) is a mouse-derived and humanized IgG2-G4-κ antibody, targeting to Complement protein C5a (Ki=60 pM). Olendalizumab targets the complement inflammatory pathway. Moreover, Olendalizumab can be used for research of complement mediated disorder caused by corona virus .
Avacopan (Standard) is the analytical standard of Avacopan. This product is intended for research and analytical applications. Avacopan (CCX168) is a potent, selective and orally available complement 5a receptor(C5aR) inhibitor with an IC50 of 0.1 nM.
ARC186 (sodium) is an unconjugated 40KDa PEG aptamer with a sequence identical to HY-147080 Avacincaptad pegol (ARC1905) sodium. ARC1905 is highly potent complement inhibitors that function by blocking the convertase-catalyzed activation of C5.
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 .
Ruxoprubart (NM8074) is an inhibitor of complement factor B (Bbsubunit). Ruxoprubart selectively binds to active Bb to inhibit the alternative complement pathway without affecting the classical complement pathway. By blocking the activities of AP C3 and C5 convertases, Ruxoprubart effectively inhibits red blood cell hemolysis and reduces C3b deposition, thereby preventing intravascular and extravascular hemolysis. Ruxoprubart can be used in research related to paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, C3 glomerulopathy, and IgA nephropathy .
Elfritatug (UCB4594) is a humanized monoclonal antibody targeting human leukocyte antigen-G (HLA-G). By binding to HLA-G on the surface of tumor cells, Elfritatug blocks its immunosuppressive effect, thereby enhancing the body's immune response against tumors .
Cobra Venom Factor (CVF) is a selective activator targeting complement components C3, C5, and factor B in the complement system. After binding to factor B, Cobra Venom Factor is cleaved by factor D, forming a stable C3/C5 convertase resistant to regulatory proteins H and I. This continuously hydrolyzes C3 and C5, depleting serum complement while inducing neutrophil migration, vascular leakage, and increased TNF-α levels. Cobra Venom Factor can be used to deplete complement and mimic complement activation-related pathological states, and is applied in animal models of complement-mediated diseases such as acute respiratory distress syndrome (ARDS), sepsis, and shock. Cobra Venom Factor can be isolated from the venom of cobras (e.g., Naja atra, Naja melanoleuca, Naja kaouthia, etc.) .
Zilucoplan (RA101495), a 15-amino acid macrocyclic peptide, is a potent complement component 5 (C5) inhibitor. Zilucoplan can be used in research of immune-mediated necrotising myopathy (IMNM) .
PMX-53 (3D53) is a synthetic peptidic and a potent and orally active complementC5a receptor (CD88) antagonist with an IC50 of 20 nM. PMX-53 is also a low-affinity MrgX2 agonist that stimulates MrgX2-mediated mast cell degranulation. PMX-53 specifically binds to C5aR1 and does not bind to the second C5aR (C5L2) and C3aR. PMX-53 has anti-inflammatory, anticancer and antiatherosclerotic effects .
C5a Receptor agonist, W5Cha (Peptide 1) is a selective complementC5a 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 .
Zilucoplan TFA (RA101495), a 15-amino acid macrocyclic peptide, is a potent complement component 5 (C5) inhibitor. Zilucoplan TFA can be used in research of immune-mediated necrotising myopathy (IMNM) .
C5aR1 antagonist peptide is a biological active peptide. (This linear peptide is derived from the C-terminus of the chemokine, complement fragment 5 anaphylatoxin (C5a). This peptide functions to inhibit C5a binding and function at human and rat C5a receptors. C5a is crucial to triggering cellular immune responses and its overexpression is involved in arthritis, Alzheimer’s disease, cystic fibrosis, systemic lupus erythematosus, and other immunoinflammatory diseases.)
Eculizumab (Anti-Human C5, Humanized Antibody) is a long-acting humanized monoclonal antibody targeted against complementC5. Eculizumab inhibits the cleavage of C5 into C5a and C5b and inhibits deployment of the terminal complement system including the formation of membrane attack complex (MAC). Eculizumab prevents anti-ganglioside antibody-mediated neuropathy in mice. Eculizumab can be used in hemolysis studies .
Crovalimab (SKY59; RO7112689) is a novel humanized antibody against C5 in a pH-dependent manner with KDs of 15.2 nM and 16.8 μM at pH 7.4 and 5.8, respectively. Crovalimab binds human FcRn with great affinity (KD: 17 μM at pH 6.0). Crovalimab can block cleavage of C5 by the C5 convertase and inhibite the activity of a C5 variant (p.Arg885His). Crovalimab inhibits C5b-9 formation significantly in all three complement pathways, the classical pathway (CP), lectin pathway (LP), and alternative pathway (AP). Crovalimab has the potential for paroxysmal nocturnal hemoglobinuria (PNH) and complement-mediated diseases research .
Ravulizumab (ALXN1210) is a humanized monoclonal antibody that specifically binds with high affinity to the human complement protein C5. Ravulizumab can be used for the research of paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, and myasthenia gravis .
Vilobelimab (CaCP-29, IFX-1) is a monoclonal anti-C5a antibody to the allergen C5a, a pro-inflammatory complement division product that plays a central role in mediating organ dysfunction. Vilobelimab acts as a C5a inhibitor, inhibiting neutrophil activation, chemotaxis, and reducing inflammatory signalling, and may be used in studies related to sepsis, COVID-19, etc .
Gefurulimab (ALXN-1720) is a high-affinity antibody inhibitor targeting complement protein C5, which can specifically bind to C5 and inhibit its cleavage into C5a and C5b. Gefurulimab can block the activation of the terminal complement pathway and reduce inflammatory damage. Gefurulimab can effectively reduce the formation of membrane attack complex (MAC) and has good pharmacokinetic properties. Gefurulimab can be used to study kidney and autoimmune diseases related to abnormal activation of the complement system, such as IgA nephropathy, lupus nephritis, and myasthenia gravis .
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 .
Avdoralimab (IPH 5401) is a fully human IgGκ monoclonal antibody that targets the complementC5a receptor 1 (C5aR1) that prevents its binding to C5a. Avdoralimab can be used for complement-driven inflammatory diseases and solid tumours research .
Vensobafusp alfa (KP-104) is a fusion protein composed of an IgG4 monoclonal antibody directed against terminal complement protein C5 fused to the complement factor H 1-5 domain (FH1-5). Vensobafusp alfa shows anti-inflammatory and immunomodulatory activities. The isotype control for Vensobafusp alfa can refer to Human IgG4 (S228P) kappa, Isotype Control (HY-P99003) . .
Pexelizumab (h5G1. 1-SC) is a humanized scFv monoclonal antibody directed against the C5complement component. Pexelizumab inhibits apoptosis and leukocyte infiltration. Pexelizumab can be used for the research of cerebral IR injury and myocardial infarction .
Omoprubart is an anti-C5complement recombinant humanized monoclonal antibody. Omolubat can prevent C5 from cleaving into C5a and C5b, thereby inhibiting the formation and activation of the C5b-dependent membrane attack complex (MAC) on the surface of susceptible cells, leading to cell lysis (destruction). Omoprubart can be used for the study of paroxysmal nocturnal hemoglobinuria (PNH).
Olendalizumab (ALXN1007) is a mouse-derived and humanized IgG2-G4-κ antibody, targeting to Complement protein C5a (Ki=60 pM). Olendalizumab targets the complement inflammatory pathway. Moreover, Olendalizumab can be used for research of complement mediated disorder caused by corona virus .
Ruxoprubart (NM8074) is an inhibitor of complement factor B (Bbsubunit). Ruxoprubart selectively binds to active Bb to inhibit the alternative complement pathway without affecting the classical complement pathway. By blocking the activities of AP C3 and C5 convertases, Ruxoprubart effectively inhibits red blood cell hemolysis and reduces C3b deposition, thereby preventing intravascular and extravascular hemolysis. Ruxoprubart can be used in research related to paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, C3 glomerulopathy, and IgA nephropathy .
Anti-ComplementC5aR1 Antibody is a human recombinant antibody expressed in CHO cells, targeting C5AR/C5AR1/C5R1. Anti-ComplementC5aR1 Antibody has a huIgG4SP type heavy chain and a huκ type light chain, with a predicted molecular weight (MW) of 146.4 kDa. The isotype control for Anti-ComplementC5aR1 Antibody can be referenced as Human IgG1 kappa, Isotype Control (HY-P99001).
Elfritatug (UCB4594) is a humanized monoclonal antibody targeting human leukocyte antigen-G (HLA-G). By binding to HLA-G on the surface of tumor cells, Elfritatug blocks its immunosuppressive effect, thereby enhancing the body's immune response against tumors .
Complement C5 is activated by C5 convertase, inducing C5-C9 assembly to form the membrane attack complex. The transient C6 binding site on C5b is critical for the formation of the cleavage complex. Complement C5 Protein, Human (HEK293, His) is the recombinant human-derived Complement C5 protein, expressed by HEK293 , with C-His labeled tag.
Complement C5 is activated by C5 convertase, inducing C5-C9 assembly to form the membrane attack complex. The transient C6 binding site on C5b is critical for the formation of the cleavage complex. Complement C5 Protein, Human (HEK293, Fc) is the recombinant human-derived Complement C5 protein, expressed by HEK293, with C-hFc labeled tag.
Complement C5 is activated by C5 convertase, inducing C5-C9 assembly to form the membrane attack complex. The transient C6 binding site on C5b is critical for the formation of the cleavage complex. Complement C5a Protein, Human (His) is the recombinant human-derived Complement C5/C5a protein, expressed by E. coli , with N-His labeled tag.
Complement C5 is activated by C5 convertase, inducing C5-C9 assembly to form the membrane attack complex. The transient C6 binding site on C5b is critical for the formation of the cleavage complex. Complement C5 Protein, Human (R885H, HEK293, His) is the recombinant human-derived Complement C5 protein, expressed by HEK293, with C-His labeled tag.
Complement C5 is activated by C5 convertase, inducing C5-C9 assembly to form the membrane attack complex. The transient C6 binding site on C5b is critical for the formation of the cleavage complex. Complement C5 Protein, Human (W917S, HEK293, His) is the recombinant human-derived Complement C5 protein, expressed by HEK293, with C-His labeled tag.
Complement C5/C5a Protein activates late complement components to form the membrane attack complex, C5-C9. C5b binds C6, initiating lytic complex assembly. C5a, produced by C5 degradation, acts as an anaphylatoxin, inducing local inflammation. C5a stimulates intracellular calcium release, smooth muscle contraction, vascular permeability, histamine release, and acts as a chemokine, guiding leukocyte migration. Complement C5a Protein, Mouse (Biotinylated) is the recombinant mouse-derived Complement C5/C5a protein, expressed by E. coli , with tag free.
Complement C5a Protein, Mouse is a recombinant mouse complement component 5a (C5a). C5a is a potent pro-inflammatory mediator and acts as an essential part of the innate immune response.
Complement C5a Protein, Mouse (His) is a recombinant mouse complement component 5a (C5a). C5a is a potent pro-inflammatory mediator and acts as an essential part of the innate immune response.
Complement C5/C5a Protein, a component of the complement system, is involved in the immune response and inflammation. It is cleaved to generate C5a, a potent pro-inflammatory mediator. Complement C5/C5a Protein's role in immune regulation and its potential as a therapeutic target make it a promising candidate for the treatment of inflammatory disorders and autoimmune diseases. Complement C5a anaphylatoxin Protein, Pig (P.pastoris, His) is the recombinant pig-derived Complement C5a anaphylatoxin protein, expressed by P. pastoris , with N-His labeled tag.
Complement C5/C5a Protein, Human is a recombinant human complement C5a. C5a is a 74-amino acid glycoprotein generated on activation of the C system. Complement C5 is cleaved by proteolysis in the terminal phase of complement activation generating the pro-inflammatory C5a and membrane attack complex nucleator C5b. C5a is an inflammatory mediator generated by complement activation that positively regulates various arms of immune defense, including Toll-like receptor 4 (TLR4) signaling. Complement C5a Protein, Human is a human-derived recombinant protein that expressed by E. coli.
Complement C5 is activated by C5 convertase, inducing C5-C9 assembly to form the membrane attack complex. The transient C6 binding site on C5b is critical for the formation of the cleavage complex. Complement C5a Protein, Cynomolgus is the recombinant cynomolgus-derived Complement C5/C5a protein, expressed by E. coli , with tag free.
C5AR1 Protein-VLP, Human (HEK293, His) is recommended for animal immunization, ELISA. It is not recommended for receptor-ligand interaction detection and SPR/BLI assay since there are other irrelevant membrane proteins of the host on the VLP envelope, and the receptor-ligand interaction will have strong background interference. High requirements for chips and experimental protocols are needed for SPR/BLI assays. If VLP control is required, it is recommended HY-P701236. Tags can only be detected under denaturing conditions.
Complement C2 is a component of the classical pathway of the complement system and is cleaved by activated factor C1, resulting in the formation of two distinct fragments: C2b and C2a. The subsequent serine protease activity of C2a is critical for its subsequent interaction with the complement factor C4b, leading to the formation of C3 or C5 convertase. C2/Complement C2 Protein, Mouse (HEK293, His) is the recombinant mouse-derived C2/Complement C2 protein, expressed by HEK293 , with C-His labeled tag.
C2/Complement C2 protein is essential in the classical pathway of the complement system. Activated by factor C1, C2 is cleaved into C2b and C2a. As a serine protease, C2a interacts with C4b, generating the C3 or C5 convertase. This crucial process activates and amplifies the complement cascade. C2/Complement C2 Protein, Human (HEK293, His) is the recombinant human-derived C2/Complement C2 protein, expressed by HEK293 , with C-His labeled tag.
C2/Complement C2 protein is essential in the classical pathway of the complement system. Activated by factor C1, C2 is cleaved into C2b and C2a. As a serine protease, C2a interacts with C4b, generating the C3 or C5 convertase. This crucial process activates and amplifies the complement cascade. C2/Complement C2 Protein, Human (HEK293, Fc) is the recombinant human-derived C2/Complement C2 protein, expressed by HEK293 , with C-hFc labeled tag.
Complement C2 is a component of the classical pathway of the complement system and is cleaved by activated factor C1, resulting in the formation of two distinct fragments: C2b and C2a. The subsequent serine protease activity of C2a is critical for its subsequent interaction with the complement factor C4b, leading to the formation of C3 or C5 convertase. C2/Complement C2 Protein, Cynomolgus (HEK293, His) is the recombinant cynomolgus-derived C2/Complement C2 protein, expressed by HEK293 , with C-His labeled tag.
CFB is an important component of the alternative pathway of the complement system and is cleaved by factor D, producing two fragments: Ba and Bb. The Bb fragment is characterized as a serine protease and subsequently forms a complex with complement factor 3b, ultimately producing a C3 or C5 convertase. Complement Factor B/CFB Protein, Mouse (His) is the recombinant mouse-derived CFB protein, expressed by E. coli , with N-6*His labeled tag.
Complement Factor B/CFB Protein, Human (HEK293, His) is the recombinant human-derived Complement Factor B/CFB protein, expressed by HEK293, with C-6*His labeled tag.
Avacincaptad pegol (ARC1905) sodium is a 40KDa PEG-conjugated aptamer. Avacincaptad pegol sodium targets complement factor 5 (C5), inhibits the cleavage of C5 into C5a and C5b, limits inflammatory stimulation and complement membrane attack complex (MAC), and is used to study age-related macular degeneration (AMD). Avacincaptad pegol sodium limits irregular cell apoptosis by targeting downstream factors in the complement cascade while preserving the early steps of the complement system .
Cemdisiran (ALN-CC5) is an N-acetylgalactosamine-conjugated RNAi agent and also a complement component C5 inhibitor. Cemdisiran targets C5 mRNA, cleaves C5 mRNA via the endogenous RNA interference pathway, and inhibits the production of C5 protein in the liver. Cemdisiran exerts a dose-dependent inhibitory effect on total C5 concentrations in cynomolgus monkeys. When used in combination with Pozelimab (HY-P99786) in cynomolgus monkeys, Cemdisiran achieves a more sustained and complete inhibitory effect on complement activity. Cemdisiran can be used in the research of paroxysmal nocturnal hemoglobinuria and other complement-mediated diseases .
Avacincaptad pegol (Izervay) is a selective inhibitor targeting complement component C5, and is a pegylated ribonucleic acid aptamer. Avacincaptad pegol inhibits the cleavage of C5 into pro-inflammatory C5a and C5b, which forms the membrane attack complex (C5b-9), thereby reducing inflammatory cell recruitment and retinal cell damage. Avacincaptad pegol can slow the growth of geographic atrophy (GA) lesions and reduce the risk of persistent vision loss. Avacincaptad pegol can be used in research of geographic atrophy associated with age-related macular degeneration (AMD) and has been approved by the FDA .
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.
ARC186 (sodium) is an unconjugated 40KDa PEG aptamer with a sequence identical to HY-147080 Avacincaptad pegol (ARC1905) sodium. ARC1905 is highly potent complement inhibitors that function by blocking the convertase-catalyzed activation of C5.
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 .
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Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
MedchemExpress Validation 03
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
MedchemExpress Validation 04
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
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