Avdoralimab (IPH 5401) is a fully human IgGκ monoclonal antibody that targets the complement C5a receptor 1 (C5aR1) that prevents its binding to C5a. Avdoralimab can be used for complement-driven inflammatory diseases and solid tumours research[1].
ADH-503 ((Z)-Leukadherin-1 choline) is an orally active and allosteric CD11b agonist. ADH-503 leads to the repolarization of tumorassociated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and enhances dendritic cell responses[1].
NRP1 antagonist 2 (Compound 1) is an NRP1 antagonist[1].
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[1][2].
Citrostadienol is a steroid compound with anti-inflammatory and anticomplementary activities. Citrostadienol demonstrates inhibition activities on classical complement pathway (IC50 of 46 nM)[1].
PMX53 (Ac-Phe-cyclo(Orn-Pro-D-Cha-Trp-Arg)) is a potent C5a receptor (CD88) antagonist with IC50 of 20 nM, also is an agonist for Mas-related gene 2 (MrgX2) in human mast cells; PMX-53 (10 nM) inhibited C5a-induced Ca(2+) mobilization in HMC-1 cells, but at higher concentrations (>30 nM) it caused degranulation in LAD2 mast cells, CD34(+) cell-derived mast cells, and RBL-2H3 cells stably expressing MrgX2; inhibits zymosan-, carrageenan-, LPS- and antigen-induced hypernociception in rats.
NDT 9513727 is a potent, selective, orally active and competitive inverse agonist of the human C5aR (C5a receptor), with an IC50 of 11.6 nM. NDT 9513727 can be used for the research of human inflammatory diseases[1].
Avacopan (CCX168) is a potent, selective and orally available complement 5a receptor inhibitor with an IC50 of 0.1 nM.
Avacincaptad pegol is a C5 complement inhibitor that may reduce inflammation-related retinal pigment epithelium (RPE) damage. Avacincaptad pegol caqn be used for the research of stargardt macular dystrophy (STGD1) and geographic atrophy (GA)[1][2].
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[1][2].
LNP023 hydrochloride is an orally bioavailable, highly potent and highly selective factor B inhibitor. LNP023 shows direct, reversible, and high-affinity binding to human factor B with a KD of 7.9 nM. LNP023 inhibits factor B with an IC50 value of 10 nM[1][2].
Sutimlimab, a first-in-class complement protein component 1, s subcomponent (C1s) inhibitor, can be used for the research of cold agglutinin disease. C1s is a serine protease which cleaves C4 and C2 to form the C3 convertase[1].
Mirococept (APT070) is an antibody targeting to complement system C3b/C4b, as well as a membrane-localizing C3 convertase inhibitor. Mirococept reduces the release of C-peptide and pro-inflammatory cytokines, and reduces the infiltration of inflammatory cells. Mirococept reduces intraislet inflammation, which is beneficial to islet transplantation. Mirococept also inhibits increased intestinal and pulmonary vascular permeability to reduce neutrophil influx[1][2].
CP-447697 is a lipophilic C5a receptor antagonist with an IC50 value of 31 nM. CP-447697 can be used for the research of inflammation[1].
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[1][2].
L-156602 is a C5a receptor antagonist. L-156602 inhibits inflammation, and the migration of monocytes and neutrophils to the infiltrating site in mouse inflammatory models. L-156602 suppresses the efferent phase of delayed-type hypersensitivity (DTH)[1][2].
Vemircopan is a complement factor D inhibitor[1].
BCX 1470 inhibits the esterolytic activity of factor D (IC50=96 nM) and C1s (IC50=1.6 nM), 3.4- and 200-fold better, respectively, than that of trypsin.IC50 Value: 96 nM (Factor D); 1.6 nM (C1s); 326 nM (Trypsin) [1]Target: Factor D; C1sBCX 1470(Thrombin inhibitor) is serine protease inhibitor.BCX 1470(Thrombin inhibitor) blocks the esterolytic and hemolytic activities of the complement enzymes Cls and factor D in vitro, also blocked development of RPA-induced edema in the rat.
C5aR-IN-3 is a potent inhibitor of C5aR. Increased level of C5a has been associated with disorders such as autoimmune disorders and inflammatory disorders. C5aR-IN-3 has the potential for the research of inflammation diseases (extracted from patent WO2022028586A1, compound 89)[1].
PMX 205 is a potent complement C5a receptor (C5aR; CD88) antagonist.
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[1].
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[1].
BR103 is a potent, metabolically stable and highly selective small molecule agonist of complement C3a receptor (C3aR) with EC50 of 22 ± 8 nM; displays high selectivity for C3aR over C5aR; induces paw oedema and mast cell activation in vivo in rats.
Vesencumab (MNRP-1685A) is IG1 antibody against neuropilin-1 (NRP-1). Vesencumab binds to NRP-1 and prevents the subsequent coupling of NRP-1 to VEGFR-2. Vesencumab has anti-angiogenic and anti-neoplastic activities. Vesencumab can be used in the research of metastatic solid tumors, including ovarian cancer[1][2].
BCX 1470 inhibits the esterolytic activity of factor D (IC50=96 nM) and C1s (IC50=1.6 nM), 3.4- and 200-fold better, respectively, than that of trypsin.IC50 Value: 96 nM (Factor D); 1.6 nM (C1s); 326 nM (Trypsin) [1]Target: Factor D; C1sBCX 1470(Thrombin inhibitor) is serine protease inhibitor.BCX 1470(Thrombin inhibitor) blocks the esterolytic and hemolytic activities of the complement enzymes Cls and factor D in vitro, also blocked development of RPA-induced edema in the rat.
3-Phenoxybenzaldehyde has weak complement classical pathway inhibition and hemolytic activity[1].
Cemdisiran is an N-acetylgalactosamine (GalNAc) conjugated siRNA for the treatment of complement-mediated diseases by suppressing liver production of complement 5 (C5) protein.
Lipoteichoic acid, a cell wall component of Staphylococcus aureus, activates the complement system via C3 induction and CD55 inhibition[1].
Compstatin control peptide is a complement inhibitor.
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.