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1. Full Text Receptor residence time trumps drug-likeness and oral bioavailability in determining efficacy of complement C5a antagonists
by Seow, Vernon and Lim, Junxian and Cotterell, Adam J and Yau, Mei-Kwan and Xu, Weijun and Lohman, Rink-Jan and Kok, W. Mei and Stoermer, Martin J and Sweet, Matthew J and Reid, Robert C and Suen, Jacky Y and Fairlie, David P
Scientific Reports, ISSN 2045-2322, 04/2016, Volume 6, Issue 1, p. 24575
Drug discovery and translation are normally based on optimizing efficacy by increasing receptor affinity, functional potency, drug-likeness (rule-of-five... 
RESPONSES | ESTIMATE SOLUBILITY | POTENT | ACTIVATION | PERMEABILITY | SMALL-MOLECULE | MULTIDISCIPLINARY SCIENCES | GPCR | CYCLIC ANTAGONISTS | IDENTIFICATION | DISCOVERY | Receptor, Anaphylatoxin C5a - chemistry | Monocytes - cytology | Humans | Immunosuppressive Agents - pharmacokinetics | Molecular Conformation | Complement C5a - metabolism | Biological Availability | Male | Monocytes - metabolism | Monocytes - immunology | Molecular Structure | Chemotaxis - immunology | Immunosuppressive Agents - administration & dosage | Macrophages - immunology | Disease Models, Animal | Edema - immunology | Rats | Edema - drug therapy | Chemotaxis - drug effects | Macrophages - cytology | Molecular Dynamics Simulation | Complement C5a - antagonists & inhibitors | Monocytes - drug effects | Edema - metabolism | Macrophages - metabolism | Animals | Macrophages - drug effects | Molecular Docking Simulation | Complement C5a - immunology | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Immunosuppressive Agents - chemistry | Receptor, Anaphylatoxin C5a - metabolism | Edema | Complement component C5a | Rodents | Affinity | Antagonists | Inflammation | Bioavailability | Macrophages
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2. Full Text Orthosteric and allosteric action of the C5a receptor antagonists
by Liu, Heng and Kim, Hee Ryung and Deepak, R.N.V. Krishna and Wang, Lei and Chung, Ka Young and Fan, Hao and Wei, Zhiyi and Zhang, Cheng and Argonne National Lab. (ANL), Argonne, IL (United States). Advanced Photon Source (APS)
Nature Structural and Molecular Biology, ISSN 1545-9993, 06/2018, Volume 25, Issue 6, pp. 472 - 481
The C5a receptor (C5aR) is a G-protein-coupled receptor (GPCR) that can induce strong inflammatory response to the anaphylatoxin C5a. Targeting C5aR has... 
ACTIVATION | SMALL-MOLECULE | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROTEIN-COUPLED RECEPTORS | IDENTIFICATION | CELL BIOLOGY | AMINO-ACID | BIOPHYSICS | STRUCTURAL BASIS | CYCLIC ANTAGONISTS | CONFORMATIONAL-ANALYSIS | BINDING | Receptor, Anaphylatoxin C5a - chemistry | Aniline Compounds - pharmacology | Signal Transduction | Allosteric Regulation | Humans | Crystallization | Crystallography, X-Ray | Peptides, Cyclic - pharmacology | Imidazoles - pharmacology | Allosteric Site | Protein Conformation | Molecular Docking Simulation | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Nipecotic Acids - pharmacology | Benzodioxoles - pharmacology | Receptor, Anaphylatoxin C5a - metabolism | Antagonists (Biochemistry) | Proteins | Complement receptors | Cellular signal transduction | Structure | Health aspects | Protein binding | Drugs | G protein-coupled receptors | Peptides | Inflammatory response | Drug delivery | Inflammation | Organic chemistry | Allosteric properties | Computer applications | Anaphylatoxin C5a | Docking | Crystal structure
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3. Full Text Complement C5A Antagonist Treatment Improves the Acute Circulatory and Inflammatory Consequences of Experimental Cardiac Tamponade
by Érces, DĂ¡niel and NĂ³grĂ¡dy, MiklĂ³s and Nagy, EnikÅ‘ and Varga, Gabriella and Vass, Andrea and SĂ¼veges, GĂ¡bor and Imai, Masaki and Okada, Noriko and Okada, Hidechika and Boros, MihĂ¡ly and Kaszaki, JĂ³zsef
Critical Care Medicine, ISSN 0090-3493, 11/2013, Volume 41, Issue 11, pp. e344 - e351
OBJECTIVE:Cardiogenic shock often leads to splanchnic macro- and microcirculatory complications, and these events are linked to local and systemic inflammatory... 
Histamine | High-mobility group box protein-1 | Complement C5a antagonist | Cardiac tamponade | Intestinal microcirculation | Big-endothelin | ACTIVATION | histamine | RAT SMALL-INTESTINE | RECEPTOR | MICROCIRCULATION | cardiac tamponade | high-mobility group box protein-1 | CARDIOGENIC-SHOCK | HEMORRHAGIC-SHOCK | intestinal microcirculation | WHOLE-BLOOD | MYELOPEROXIDASE | big-endothelin | complement C5a antagonist | ENDOTHELIN-1 | ANAPHYLATOXIN | CRITICAL CARE MEDICINE | Cardiac Tamponade - therapy | Endothelin-1 - metabolism | Intestinal Mucosa - blood supply | Male | Random Allocation | Peptides - pharmacology | Complement C5a - antagonists & inhibitors | Cardiac Tamponade - physiopathology | Microcirculation | Animals | Swine | HMGB1 Protein - metabolism | Superoxides - metabolism | Female | Histamine - blood | Hemodynamics | Disease Models, Animal
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4. Full Text C3a and C5a receptor antagonists ameliorate endothelial-myofibroblast transition via the Wnt/β-catenin signaling pathway in diabetic kidney disease
by Li, Ling and Chen, Lijia and Zang, Jing and Tang, Xi and Liu, Yan and Zhang, Jie and Bai, Lin and Yin, Qinghua and Lu, Yanrong and Cheng, Jingqiu and Fu, Ping and Liu, Fang
Metabolism, ISSN 0026-0495, 2015, Volume 64, Issue 5, pp. 597 - 610
Abstract Background Endothelial-myofibroblast transition (EndMT) has been implicated in the pathogenesis of diabetic renal fibrosis. In this study, the effect... 
Endocrinology & Metabolism | C3a receptor antagonists | C5a receptor antagonists | Wnt/β-catenin signaling pathway | Diabetic kidney disease | Endothelial-myofibroblast transition | STRESSED MESANGIAL CELLS | COMPLEMENT C3A | INJURY | BETA-CATENIN | NEPHROPATHY | Wnt/beta-catenin signaling pathway | RENAL FIBROSIS | TO-MESENCHYMAL TRANSITION | LUPUS NEPHRITIS | ENDOCRINOLOGY & METABOLISM | TUBULAR EPITHELIAL-CELLS | EXPRESSION | Cell Line | Myofibroblasts - physiology | Receptors, Complement - antagonists & inhibitors | Diabetic Nephropathies - metabolism | Humans | Middle Aged | Complement C5a - metabolism | Rats | Male | Wnt1 Protein - metabolism | Rats, Sprague-Dawley | Blotting, Western | Receptors, Complement - metabolism | Animals | Adult | Female | Signal Transduction - physiology | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Diabetes Mellitus, Experimental - metabolism | Complement C3a - metabolism | Endothelial Cells - physiology | Receptor, Anaphylatoxin C5a - metabolism
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5. Full Text Inhibiting the C5–C5a receptor axis
by Woodruff, Trent M and Nandakumar, Kutty S and Tedesco, Francesco
Molecular Immunology, ISSN 0161-5890, 2011, Volume 48, Issue 14, pp. 1631 - 1642
â–º We review the therapeutic options to inhibit the C5–C5a receptor axis. â–º We examine methods to inhibit C5 cleavage via targeting C5a convertases or C5... 
Complement C5 | C5 antibodies | C5a antagonists | C5a receptor | C5a | Therapeutics | COLLAGEN-INDUCED ARTHRITIS | HEMOLYTIC-UREMIC SYNDROME | BIOCHEMISTRY & MOLECULAR BIOLOGY | PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA | IMMUNOLOGY | ISCHEMIA-REPERFUSION INJURY | PERCUTANEOUS CORONARY INTERVENTION | INFLAMMATORY-BOWEL-DISEASE | EXPERIMENTAL ALLERGIC-ASTHMA | TERMINAL COMPLEMENT COMPLEX | TUBULAR EPITHELIAL-CELLS | ANTIGEN-INDUCED ARTHRITIS | Receptors, Complement - antagonists & inhibitors | Humans | Serine Endopeptidases - pharmacology | Inflammation - immunology | Complement Membrane Attack Complex - immunology | Complement C3-C5 Convertases - antagonists & inhibitors | Immunity, Innate | Drug Discovery | Complement C5a - antagonists & inhibitors | Animals | Receptor, Anaphylatoxin C5a | Inflammation - drug therapy | Receptors, Chemokine - antagonists & inhibitors | Complement C5 - antagonists & inhibitors
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6. Full Text T helper 1 immunity requires complement-driven NLRP3 inflammasome activity in CD4+ T cells
by Arbore, Giuseppina and West, Erin E and Spolski, Rosanne and Robertson, Avril A.B and Klos, Andreas and Rheinheimer, Claudia and Dutow, Pavel and Woodruff, Trent M and Yu, Zu Xi and O'Neill, Luke A and Coll, Rebecca C and Sher, Alan and Leonard, Warren J and Köhl, Jörg and Monk, Pete and Cooper, Matthew A and Arno, Matthew and Afzali, Behdad and Lachmann, Helen J and Cope, Andrew P and Mayer-Barber, Katrin D and Kemper, Claudia
Science, ISSN 0036-8075, 06/2016, Volume 352, Issue 6292, pp. aad1210 - aad1210
The NLRP3 inflammasome controls interleukin-1β maturation in antigen-presenting cells, but a direct role for NLRP3 in human adaptive immune cells has not been... 
INTESTINAL INFLAMMATION | ACTIVATION | IFN-GAMMA | MULTIDISCIPLINARY SCIENCES | C5L2 | DISEASE | CYTOKINE | INNATE LYMPHOID-CELLS | DIFFERENTIATION | C5A RECEPTOR CD88 | ANTAGONISTS | Receptor, Anaphylatoxin C5a - agonists | Reactive Oxygen Species - metabolism | Complement Activation | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Th1 Cells - immunology | CD4-Positive T-Lymphocytes - immunology | Mice, Mutant Strains | HEK293 Cells | Receptors, Antigen, T-Cell - agonists | Receptors, Chemokine - antagonists & inhibitors | Disease Models, Animal | Adaptive Immunity | Cryopyrin-Associated Periodic Syndromes - immunology | Autocrine Communication | Receptors, Antigen, T-Cell - metabolism | Receptors, Chemokine - metabolism | Receptors, Chemokine - agonists | Inflammation - immunology | Immunity, Innate | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Inflammasomes - immunology | Mice | Complement C5a - immunology | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Interferon-gamma - biosynthesis | Membrane Cofactor Protein - immunology | Receptor, Anaphylatoxin C5a - metabolism | Antigen presentation | Cellular biology | Lymphocytes | Immune system | Immune systems | Microorganisms | Interleukin | Bacteria | Activation | Complement | Immunity | Assembly
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7. Full Text Randomized trial of C5a receptor inhibitor avacopan in ANCA-associated vasculitis
by Jayne, David R. W and Bruchfeld, Annette N and Harper, Lorraine and Schaier, Matthias and Venning, Michael C and Hamilton, Patrick and Burst, Volker and Grundmann, Franziska and Jadoul, Michel and Szombati, IstvĂ¡n and Tesar, VladimĂ­r and Segelmark, Marten and Potarca, Antonia and Schall, Thomas J and Bekker, Pirow and CLEAR Study Grp and CLEAR Study Group and Medicinska fakulteten and Region Ă–stergötland and Linköpings universitet and Institutionen för medicin och hälsa and Hjärt- och Medicincentrum and Avdelningen för läkemedelsforskning and Njurmedicinska kliniken US
Journal of the American Society of Nephrology, ISSN 1046-6673, 09/2017, Volume 28, Issue 9, pp. 2756 - 2767
Alternative C activation is involved in the pathogenesis of ANCA-associated vasculitis. However, glucocorticoids used as treatment contribute to the morbidity... 
WEGENERS-GRANULOMATOSIS | SURVIVAL | SYSTEMIC VASCULITIS | ANTIBODY-ASSOCIATED VASCULITIS | RENAL VASCULITIS | CYCLOPHOSPHAMIDE | INFLAMMATION | ENDOTHELIAL-CELLS | DISEASE | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | UROLOGY & NEPHROLOGY | Severity of Illness Index | Glucocorticoids - administration & dosage | Glucocorticoids - therapeutic use | Prednisone - administration & dosage | Prednisone - adverse effects | Double-Blind Method | Humans | Immunosuppressive Agents - therapeutic use | Middle Aged | Nipecotic Acids - therapeutic use | Male | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - drug therapy | Cyclophosphamide - therapeutic use | Rituximab - therapeutic use | Drug Therapy, Combination - adverse effects | Adult | Female | Nipecotic Acids - adverse effects | Aged | Aniline Compounds - therapeutic use | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Aniline Compounds - adverse effects | Glucocorticoids - adverse effects | Prednisone - therapeutic use | Clinical Research | complement 5a receptor | ANCA | avacopan | complement 5a | complement | ANCA-associated vasculitis | Clinical Medicine | Urologi och njurmedicin | Medical and Health Sciences | Klinisk medicin | Medicin och hälsovetenskap | Urology and Nephrology
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8. Full Text C5a receptor (CD88) blockade protects against MPO-ANCA GN
by Xiao, Hong and Dairaghi, Daniel J and Powers, Jay P and Ertl, Linda S and Baumgart, Trageen and Wang, Yu and Seitz, Lisa C and Penfold, Mark E. T and Gan, Lin and Hu, Peiqi and Lu, Bao and Gerard, Norma P and Gerard, Craig and Schall, Thomas J and Jaen, Juan C and Falk, Ronald J and Jennette, J. Charles
Journal of the American Society of Nephrology, ISSN 1046-6673, 02/2014, Volume 25, Issue 2, pp. 225 - 231
Necrotizing and crescentic GN (NCGN) with a paucity of glomerular immunoglobulin deposits is associated with ANCA. The most common ANCA target antigens are... 
GLOMERULONEPHRITIS | PATHOGENESIS | ANTIBODIES | ANTAGONIST | COMPLEMENT ACTIVATION | DISEASE | C5L2 | ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES | UROLOGY & NEPHROLOGY | MICE | VASCULITIS | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - prevention & control | Receptor, Anaphylatoxin C5a - genetics | Glomerulonephritis - prevention & control | Urine - cytology | Humans | Leukocytes | Recombinant Fusion Proteins | Proteinuria - prevention & control | Dose-Response Relationship, Drug | Complement C6 - immunology | Receptors, Chemokine - genetics | Hematuria - prevention & control | Proteinuria - etiology | Peroxidase - immunology | Administration, Oral | Mice, Inbred C57BL | Glomerulonephritis - immunology | Glomerulonephritis - complications | Mice, Inbred C3H | Gene Knock-In Techniques | Mice, Knockout | Receptors, Chemokine - deficiency | Metabolism, Inborn Errors - immunology | Animals | Receptors, Chemokine - physiology | Peroxidase - deficiency | Autoantigens - immunology | Receptor, Anaphylatoxin C5a - deficiency | Immunization, Passive | Mice | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Complement Pathway, Alternative | Metabolism, Inborn Errors - complications | Hematuria - etiology | Brief Communications
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9. Full Text Role of C5a in inflammatory responses
by Guo, Ren-Feng and Ward, Peter A
Annual Review of Immunology, ISSN 0732-0582, 2005, Volume 23, Issue 1, pp. 821 - 852
The complement system not only represents an effective innate immune mechanism of host defense to eradicate microbial pathogens, but it is also widely involved... 
Complement | Inflammation | C5a receptor | C5L2 | BRONCHOALVEOLAR LAVAGE FLUID | TISSUE FACTOR ACTIVITY | RESPIRATORY-DISTRESS SYNDROME | IMMUNOLOGY | HUMAN POLYMORPHONUCLEAR LEUKOCYTES | COMPLEMENT INHIBITORY PROTEIN | ISCHEMIA-REPERFUSION INJURY | PROGRAMMED CELL-DEATH | MULTIPLE ORGAN DYSFUNCTION | HUMAN PERIPHERAL-BLOOD | inflammation | complement | ANTI-C5A MONOCLONAL-ANTIBODIES | Sepsis - immunology | Complement Activation | Signal Transduction | Humans | Neutrophils - immunology | Hypersensitivity - immunology | Inflammation - immunology | Immunity, Innate | Complement C5a - antagonists & inhibitors | Models, Immunological | Animals | Blood Coagulation - immunology | Reperfusion Injury - immunology | Asthma - immunology | Receptor, Anaphylatoxin C5a - immunology | Lung Injury | Complement C5a - immunology | Lung - immunology
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10. Full Text Modulation of the antitumor immune response by complement
by Markiewski, Maciej M and DeAngelis, Robert A and Benencia, Fabian and Ricklin-Lichtsteiner, Salome K and Koutoulaki, Anna and Gerard, Craig and Coukos, George and Lambris, John D
Nature Immunology, ISSN 1529-2908, 2008, Volume 9, Issue 11, pp. 1225 - 1235
The involvement of complement-activation products in promoting tumor growth has not yet been recognized. Here we show that the generation of complement C5a in... 
C5A RECEPTOR | ACTIVATION | ACQUIRED-IMMUNITY | TUMOR-DEVELOPMENT | INFLAMMATION | IMMATURE MYELOID CELLS | CANCER-IMMUNOTHERAPY | IMMUNOLOGY | CD8(+) T-CELLS | REGULATORY PROTEINS | Reactive Oxygen Species - metabolism | Complement Activation | Male | Neoplasms - therapy | Mice, Mutant Strains | Myeloid Cells - immunology | Receptor, Anaphylatoxin C5a - immunology | Female | T-Lymphocytes, Cytotoxic - immunology | Signal Transduction | Reactive Nitrogen Species - metabolism | Down-Regulation | Mice, Inbred C57BL | Mice, Knockout | Complement C5a - antagonists & inhibitors | Xenograft Model Antitumor Assays | Immunosuppression | Animals | Complement C5a - pharmacology | Complement C3-C5 Convertases - genetics | Neoplasms - immunology | Myeloid Cells - metabolism | Mice | Complement C5a - immunology | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Receptor, Anaphylatoxin C5a - metabolism
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11. Full Text Structure of the complement C5a receptor bound to the extra-helical antagonist NDT9513727
by Robertson, Nathan and Rappas, Mathieu and Doré, Andrew S and Brown, Jason and Bottegoni, Giovanni and Koglin, Markus and Cansfield, Julie and Jazayeri, Ali and Cooke, Robert M and Marshall, Fiona H
Nature, ISSN 0028-0836, 01/2018, Volume 553, Issue 7686, pp. 111 - 114
The complement system is a crucial component of the host response to infection and tissue damage. Activation of the complement cascade generates anaphylatoxins... 
ACID | SMALL-MOLECULE | OPIOID RECEPTOR | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | GPCR | OLIGOMERIZATION | IDENTIFICATION | Receptor, Anaphylatoxin C5a - chemistry | Receptor, Anaphylatoxin C5a - genetics | Protein Structure, Secondary | Receptors, G-Protein-Coupled - metabolism | Humans | Imidazoles - chemistry | Benzodioxoles - metabolism | Models, Molecular | Crystallography, X-Ray | Imidazoles - pharmacology | Receptors, Adrenergic, beta-2 - metabolism | Receptors, Adrenergic, beta-2 - chemistry | Animals | Drug Inverse Agonism | HEK293 Cells | Benzodioxoles - chemistry | Mutation | Protein Stability | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Binding Sites | Benzodioxoles - pharmacology | Receptors, G-Protein-Coupled - chemistry | Imidazoles - metabolism | Receptor, Anaphylatoxin C5a - metabolism | Drugs | Inflammatory bowel diseases | G protein-coupled receptors | Peptides | Complement component C5a | Manufacturing engineering | Complement | Antagonists | Helices | Arthritis | Production costs | Receptors | Reperfusion | Ischemia | Anaphylatoxins | Alzheimer's disease | Neurodegenerative diseases | Psoriasis | Medical treatment | Crystallization | Inflammation | Crohn's disease | Bioavailability | Mode of action | Complement activation | Immunogenicity | Rheumatoid arthritis | Sepsis | Ligands
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