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231226s2023 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2023.109629
|2 doi
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|a pubmed25n1188.xml
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|a (DE-627)NLM356522784
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|a (NLM)37149117
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|a (PII)S1521-6616(23)00128-6
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Simmons, Ken T
|e verfasserin
|4 aut
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1 |
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|a Anti-C1s humanized monoclonal antibody SAR445088
|b A classical pathway complement inhibitor specific for the active form of C1s
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|c 2023
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 23.05.2023
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|a Date Revised 23.05.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2023 Sanofi, U.S. Published by Elsevier Inc. All rights reserved.
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|a The objective of this study was to characterize the complement-inhibiting activity of SAR445088, a novel monoclonal antibody specific for the active form of C1s. Wieslab® and hemolytic assays were used to demonstrate that SAR445088 is a potent, selective inhibitor of the classical pathway of complement. Specificity for the active form of C1s was confirmed in a ligand binding assay. Finally, TNT010 (a precursor to SAR445088) was assessed in vitro for its ability to inhibit complement activation associated with cold agglutinin disease (CAD). TNT010 inhibited C3b/iC3b deposition on human red blood cells incubated with CAD patient serum and decreased their subsequent phagocytosis by THP-1 cells. In summary, this study identifies SAR445088 as a potential therapeutic for the treatment of classical pathway-driven diseases and supports its continued assessment in clinical trials
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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4 |
|a C1s
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4 |
|a Classical pathway
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|a Cold agglutinin disease
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|a Complement
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|a Therapeutic antibody
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| 650 |
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|a Complement C1s
|2 NLM
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| 650 |
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|a EC 3.4.21.42
|2 NLM
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| 650 |
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|a Antibodies, Monoclonal, Humanized
|2 NLM
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| 650 |
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|a Antibodies, Monoclonal
|2 NLM
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| 650 |
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7 |
|a Complement Inactivating Agents
|2 NLM
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| 700 |
1 |
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|a Chan, Joanne
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hussain, Sami
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Rose, Eileen L
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Markham, Kate
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Byun, Tony S
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Panicker, Sandip
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Parry, Graham C
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Storek, Michael
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 251(2023) vom: 10. Juni, Seite 109629
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnas
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| 773 |
1 |
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|g volume:251
|g year:2023
|g day:10
|g month:06
|g pages:109629
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2023.109629
|3 Volltext
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