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Article ; Online: Therapeutic bispecific antibody formats: a patent applications review (1994-2017).

Godar, Marie / de Haard, Hans / Blanchetot, Christophe / Rasser, Jacobus

2018 Volume 28, Issue 3, Page(s) 251–276

Abstract: Introduction: Bispecific antibodies have become increasingly of interest by enabling new therapeutic applications such as retargeting cellular immunity towards tumor cells. About 23 bispecific antibody platforms have therefore been developed, generating ...

Abstract	Introduction: Bispecific antibodies have become increasingly of interest by enabling new therapeutic applications such as retargeting cellular immunity towards tumor cells. About 23 bispecific antibody platforms have therefore been developed, generating about 62 molecules which are currently being evaluated for potential treatment of a variety of indications, such as cancer and inflammatory diseases, among which three molecules were approved. This class of drugs will represent a multi-million-dollar market over the coming years. Many companies have consequently invested in the development of bispecific antibody platforms, creating an important patent activity in this field. Areas covered: The present review gives an overview of the patent literature over the period 1994-2017 of different immunoglobulin gamma-based bispecific antibody platforms and the molecules approved or in clinical trials. Expert opinion: Bispecific antibodies are progressively accepted as potentially superior therapeutic molecules in a broad range of diseases. This frantic activity creates a maze of hundreds of patents that pose considerable legal risks for both newcomers and established companies. It can consecutively be anticipated that the number of patent conflicts will increase. Nevertheless, it can be expected that patents related to the use of a bispecific antibody will have tremendous commercial value.
MeSH term(s)	Antibodies, Bispecific/administration & dosage ; Antibodies, Bispecific/immunology ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/immunology ; Drug Design ; Drug Industry ; Humans ; Immunity, Cellular/immunology ; Immunoglobulin G/immunology ; Neoplasms/drug therapy ; Neoplasms/immunology ; Patents as Topic
Chemical Substances	Antibodies, Bispecific ; Antineoplastic Agents ; Immunoglobulin G
Language	English
Publishing date	2018-01-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1186201-4
ISSN	1744-7674 ; 0962-2594 ; 1354-3776
ISSN (online)	1744-7674
ISSN	0962-2594 ; 1354-3776
DOI	10.1080/13543776.2018.1428307
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Article ; Online: A Targetable, Noncanonical Signal Transducer and Activator of Transcription 3 Activation Induced by the Y-Less Region of IL-22 Receptor Orchestrates Imiquimod-Induced Psoriasis-Like Dermatitis in Mice.

Michiels, Camille / Puigdevall, Léna / Cochez, Perrine / Achouri, Younes / Cheou, Paméla / Hendrickx, Emilie / Dauguet, Nicolas / Blanchetot, Christophe / Dumoutier, Laure

The Journal of investigative dermatology

2021 Volume 141, Issue 11, Page(s) 2668–2678.e6

Abstract: Exacerbated IL-22 activity induces tissue inflammation and immune disorders such as psoriasis. However, because IL-22 is also essential for tissue repair and defense at barrier interfaces, targeting IL-22 activity to treat psoriasis bears the risk of ... ...

Abstract	Exacerbated IL-22 activity induces tissue inflammation and immune disorders such as psoriasis. However, because IL-22 is also essential for tissue repair and defense at barrier interfaces, targeting IL-22 activity to treat psoriasis bears the risk of deleterious effects at mucosal sites such as the gut. We previously showed in vitro that IL-22 signaling relies on IL-22 receptor alpha (IL-22Rα) Y-dependent and -independent pathways. The second depends on the C-terminal Y-less region of IL-22Rα and leads to a massive signal transducer and activator of transcription 3 (STAT3) activation. Because STAT3 activation is associated with the development of psoriasis, we hypothesized that the specific inhibition of the noncanonical STAT3 activation by the Y-less region of IL-22Rα could reduce psoriasis-like disease while leaving intact its tissue defense functions in the gut. We show that mice expressing a C-terminally truncated version of IL-22Rα (ΔCter
MeSH term(s)	Animals ; Citrobacter rodentium ; Enterobacteriaceae Infections/immunology ; Imiquimod/toxicity ; Interleukins/pharmacology ; Mice ; Mice, Inbred C57BL ; Psoriasis/chemically induced ; Receptors, Interleukin/physiology ; STAT3 Transcription Factor/physiology ; Interleukin-22
Chemical Substances	Interleukins ; Receptors, Interleukin ; STAT3 Transcription Factor ; Stat3 protein, mouse ; interleukin-22 receptor ; Imiquimod (P1QW714R7M)
Language	English
Publishing date	2021-05-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2021.04.016
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Article ; Online: Development and characterization of agonistic antibodies targeting the Ig-like 1 domain of MuSK.

Lim, Jamie L / Augustinus, Roy / Plomp, Jaap J / Roya-Kouchaki, Kasra / Vergoossen, Dana L E / Fillié-Grijpma, Yvonne / Struijk, Josephine / Thomas, Rachel / Salvatori, Daniela / Steyaert, Christophe / Blanchetot, Christophe / Vanhauwaert, Roeland / Silence, Karen / van der Maarel, Silvère M / Verschuuren, Jan J / Huijbers, Maartje G

Scientific reports

2023 Volume 13, Issue 1, Page(s) 7478

Abstract: Muscle-specific kinase (MuSK) is crucial for acetylcholine receptor (AChR) clustering and thereby neuromuscular junction (NMJ) function. NMJ dysfunction is a hallmark of several neuromuscular diseases, including MuSK myasthenia gravis. Aiming to restore ... ...

Abstract	Muscle-specific kinase (MuSK) is crucial for acetylcholine receptor (AChR) clustering and thereby neuromuscular junction (NMJ) function. NMJ dysfunction is a hallmark of several neuromuscular diseases, including MuSK myasthenia gravis. Aiming to restore NMJ function, we generated several agonist monoclonal antibodies targeting the MuSK Ig-like 1 domain. These activated MuSK and induced AChR clustering in cultured myotubes. The most potent agonists partially rescued myasthenic effects of MuSK myasthenia gravis patient IgG autoantibodies in vitro. In an IgG4 passive transfer MuSK myasthenia model in NOD/SCID mice, MuSK agonists caused accelerated weight loss and no rescue of myasthenic features. The MuSK Ig-like 1 domain agonists unexpectedly caused sudden death in a large proportion of male C57BL/6 mice (but not female or NOD/SCID mice), likely caused by a urologic syndrome. In conclusion, these agonists rescued pathogenic effects in myasthenia models in vitro, but not in vivo. The sudden death in male mice of one of the tested mouse strains revealed an unexpected and unexplained role for MuSK outside skeletal muscle, thereby hampering further (pre-) clinical development of these clones. Future research should investigate whether other Ig-like 1 domain MuSK antibodies, binding different epitopes, do hold a safe therapeutic promise.
MeSH term(s)	Male ; Animals ; Mice ; Mice, SCID ; Receptor Protein-Tyrosine Kinases/metabolism ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Myasthenia Gravis/metabolism ; Receptors, Cholinergic/metabolism ; Autoantibodies ; Muscle Weakness ; Acetylcholine
Chemical Substances	Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptors, Cholinergic ; Autoantibodies ; Acetylcholine (N9YNS0M02X)
Language	English
Publishing date	2023-05-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-32641-1
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Article ; Online: Personalized medicine with biologics for severe type 2 asthma: current status and future prospects.

Godar, Marie / Blanchetot, Christophe / de Haard, Hans / Lambrecht, Bart N / Brusselle, Guy

mAbs

2017 Volume 10, Issue 1, Page(s) 34–45

Abstract: Asthma affects more than 300 million people worldwide and poses a large socioeconomic burden, particularly in the 5% to 10% of severe asthmatics. So far, each entry of new biologics in clinical trials has led to high expectations for treating all severe ... ...

Abstract	Asthma affects more than 300 million people worldwide and poses a large socioeconomic burden, particularly in the 5% to 10% of severe asthmatics. So far, each entry of new biologics in clinical trials has led to high expectations for treating all severe asthma forms, but the outcome has only been successful if the biologic, as add-on treatment, targeted specific patient subgroups. Indeed, we now realize that asthma is a heterogeneous disease with multiple phenotypes, based on distinct pathophysiological mechanisms, called endotypes. Thus, asthma therapy is gradually moving to a personalized medicine approach, tailored to individual's asthma endotypes identified through biomarkers. Here, we review the clinical efficacy of antibody-related therapeutics undergoing clinical trials, or those already approved, for the treatment of severe type 2 asthma. Biologics targeting type 2 cytokines have shown consistent efficacy, especially in patients with evidence of type 2 inflammation, suggesting that the future of asthma biologics is promising.
MeSH term(s)	Animals ; Anti-Asthmatic Agents/adverse effects ; Anti-Asthmatic Agents/therapeutic use ; Anti-Inflammatory Agents/adverse effects ; Anti-Inflammatory Agents/therapeutic use ; Asthma/diagnosis ; Asthma/drug therapy ; Asthma/immunology ; Asthma/metabolism ; Biological Products/adverse effects ; Biological Products/therapeutic use ; Clinical Decision-Making ; Cytokines/antagonists & inhibitors ; Cytokines/immunology ; Cytokines/metabolism ; Humans ; Inflammation Mediators/antagonists & inhibitors ; Inflammation Mediators/immunology ; Inflammation Mediators/metabolism ; Lung/drug effects ; Lung/immunology ; Lung/metabolism ; Lung/physiopathology ; Patient Selection ; Precision Medicine/methods ; Signal Transduction/drug effects
Chemical Substances	Anti-Asthmatic Agents ; Anti-Inflammatory Agents ; Biological Products ; Cytokines ; Inflammation Mediators
Language	English
Publishing date	2017-11-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1942-0870
ISSN (online)	1942-0870
DOI	10.1080/19420862.2017.1392425
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Article ; Online: Increased expression of IL-24 in chronic spontaneous urticaria.

de Montjoye, Laurence / Herman, Anne / Hendrickx, Emilie / Chéou, Paméla / Blanchetot, Christophe / Hofman, Erik / Baeck, Marie / Dumoutier, Laure

Allergy

2019 Volume 74, Issue 9, Page(s) 1811–1813

MeSH term(s)	Autoantibodies/immunology ; Chronic Urticaria/diagnosis ; Chronic Urticaria/etiology ; Chronic Urticaria/metabolism ; Gene Expression ; Humans ; Immunoglobulin E/immunology ; Interleukins/genetics ; Interleukins/immunology ; Interleukins/metabolism ; Mast Cells/immunology ; Mast Cells/metabolism ; RNA, Messenger/metabolism
Chemical Substances	Autoantibodies ; Interleukins ; RNA, Messenger ; interleukin-24 ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2019-05-28
Publishing country	Denmark
Document type	Letter
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.13832
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Uh III Zs.150: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: The ROS-NOX connection in cancer and angiogenesis.

Blanchetot, Christophe / Boonstra, Johannes

Critical reviews in eukaryotic gene expression

2008 Volume 18, Issue 1, Page(s) 35–45

Abstract: Initially viewed as dangerous byproducts of aerobic life, reactive oxygen species (ROS) nowadays appear to be essential secondary messengers of many signaling cascades and cellular functions. The establishment of ROS as important signaling molecules has ... ...

Abstract	Initially viewed as dangerous byproducts of aerobic life, reactive oxygen species (ROS) nowadays appear to be essential secondary messengers of many signaling cascades and cellular functions. The establishment of ROS as important signaling molecules has been confirmed by the existence of specialized ROS producing complexes expressed in nonphagocytic cells, the NADPH oxidase complex (NOX). Because of the diversity of their proteic targets (besides lipids and DNA), ROS have multiple and sometimes contradictory functions. In the present review, we focus on several different signaling pathways influenced by ROS and NOX in tumorigenesis, focusing on proliferation and angiogenesis. We review the ROS targets regulating proliferation, including cellular signaling (phosphatases, AP1, and nuclear factor-kappa B [NF-kappaB]) and cell cycle targets (CDC25, cyclin D, and forkhead proteins), and the role of NOX during proliferation. Finally, we review the direct and indirect involvement of ROS and NOX in (tumor) angiogenesis through the regulation of different biologic systems such as vascular endothelial growth factor, angiotensin II, hypoxia-inducible factor, AP1, and inflammation.
MeSH term(s)	Animals ; Cell Cycle ; Cell Proliferation ; Humans ; Inflammation/metabolism ; Models, Biological ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Neoplasms/enzymology ; Neoplasms/metabolism ; Neovascularization, Pathologic/enzymology ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Transcription, Genetic ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Reactive Oxygen Species ; Vascular Endothelial Growth Factor A ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2008-01-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1071345-1
ISSN	1045-4403
ISSN	1045-4403
DOI	10.1615/critreveukargeneexpr.v18.i1.30
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Article ; Online: A bispecific antibody strategy to target multiple type 2 cytokines in asthma.

Godar, Marie / Deswarte, Kim / Vergote, Karl / Saunders, Michael / de Haard, Hans / Hammad, Hamida / Blanchetot, Christophe / Lambrecht, Bart N

The Journal of allergy and clinical immunology

2018 Volume 142, Issue 4, Page(s) 1185–1193.e4

Abstract: Background: Asthma is a chronic inflammatory airway disease in which innate and adaptive immune cells act together to cause eosinophilic inflammation, goblet cell metaplasia (GCM), and bronchial hyperreactivity (BHR). In clinical trials using ... ...

Abstract	Background: Asthma is a chronic inflammatory airway disease in which innate and adaptive immune cells act together to cause eosinophilic inflammation, goblet cell metaplasia (GCM), and bronchial hyperreactivity (BHR). In clinical trials using biologicals against IL-4 receptor (IL-4R) α or IL-5, only a subset of patients with moderate-to-severe asthma responded favorably, suggesting that distinct pathophysiologic mechanisms are at play in subgroups of patients called endotypes. However, the effect of multiple cytokine blockade using bispecific antibodies has not been tested. Objective: We sought to target simultaneously the IL-4, IL-13, and IL-5 signaling pathways with a novel IL-4Rα/IL-5-bispecific antibody in a murine house dust mite (HDM) model of asthma. Methods: Two mAbs neutralizing IL-4Rα and IL-5 were generated by using a llama-based antibody platform. Their heavy and light chains were then cotransfected in mammalian cells, resulting in a heterogeneous antibody mixture from which the bispecific antibody was isolated by using a dual anti-idiotypic purification process. C57BL/6J mice were finally sensitized and challenged to HDM extracts and treated during challenge with the antibodies. Results: We successfully generated and characterized the monospecific and bispecific antibodies targeting IL-4Rα and IL-5. The monospecific antibodies could suppress eosinophilia, IgE synthesis, or both, whereas only the IL-4Rα/IL-5-bispecific antibody and the combination of monospecific antibodies additionally inhibited GCM and BHR. Conclusion: Type 2 cytokines act synergistically to cause GCM and BHR in HDM-exposed mice. These preclinical results show the feasibility of generating bispecific antibodies that target multiple cytokine signaling pathways as superior inhibitors of asthma features, including the difficult-to-treat GCM.
MeSH term(s)	Animals ; Antibodies, Bispecific/therapeutic use ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Neutralizing/therapeutic use ; Asthma/drug therapy ; Asthma/immunology ; Asthma/pathology ; Asthma/physiopathology ; Camelids, New World ; Cell Line ; Cytokines/antagonists & inhibitors ; Cytokines/immunology ; Eosinophilia/drug therapy ; Eosinophilia/immunology ; Eosinophilia/pathology ; Eosinophilia/physiopathology ; Escherichia coli ; Female ; Goblet Cells/drug effects ; Goblet Cells/pathology ; Humans ; Mice, Inbred C57BL ; Pyroglyphidae/immunology
Chemical Substances	Antibodies, Bispecific ; Antibodies, Monoclonal ; Antibodies, Neutralizing ; Cytokines
Language	English
Publishing date	2018-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2018.06.002
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Article: Editorial.

Blanchetot, Christophe / Tremblay, Michel L

Methods (San Diego, Calif.)

2005 Volume 35, Issue 1, Page(s) 1

MeSH term(s)	Ligands ; Multigene Family ; Protein Tyrosine Phosphatases/genetics ; Protein Tyrosine Phosphatases/physiology ; Substrate Specificity
Chemical Substances	Ligands ; Protein Tyrosine Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2005-01
Publishing country	United States
Document type	Editorial
ZDB-ID	1066584-5
ISSN	1095-9130 ; 1046-2023
ISSN (online)	1095-9130
ISSN	1046-2023
DOI	10.1016/j.ymeth.2004.07.001
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Zs.A 3239: Show issues

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Article ; Online: Anti-C2 Antibody ARGX-117 Inhibits Complement in a Disease Model for Multifocal Motor Neuropathy.

Budding, Kevin / Johansen, Lill Eva / Van de Walle, Inge / Dijkxhoorn, Kim / de Zeeuw, Elisabeth / Bloemenkamp, Lauri M / Bos, Jeroen W / Jansen, Marc D / Curial, Chantall A D / Silence, Karen / de Haard, Hans / Blanchetot, Christophe / Van de Ven, Liesbeth / Leusen, Jeanette H W / Pasterkamp, R Jeroen / van den Berg, Leonard H / Hack, C Erik / Boross, Peter / van der Pol, W Ludo

Neurology(R) neuroimmunology & neuroinflammation

2021 Volume 9, Issue 1

Abstract: Background and objectives: To determine the role of complement in the disease pathology of multifocal motor neuropathy (MMN), we investigated complement activation, and inhibition, on binding of MMN patient-derived immunoglobulin M (IgM) antibodies in ... ...

Abstract	Background and objectives: To determine the role of complement in the disease pathology of multifocal motor neuropathy (MMN), we investigated complement activation, and inhibition, on binding of MMN patient-derived immunoglobulin M (IgM) antibodies in an induced pluripotent stem cell (iPSC)-derived motor neuron (MN) model for MMN. Methods: iPSC-derived MNs were characterized for the expression of complement receptors and membrane-bound regulators, for the binding of circulating IgM anti-GM1 from patients with MMN, and for subsequent fixation of C4 and C3 on incubation with fresh serum. The potency of ARGX-117, a novel inhibitory monoclonal antibody targeting C2, to inhibit fixation of complement was assessed. Results: iPSC-derived MNs moderately express the complement regulatory proteins CD46 and CD55 and strongly expressed CD59. Furthermore, MNs express C3aR, C5aR, and complement receptor 1. IgM anti-GM1 antibodies in serum from patients with MMN bind to MNs and induce C3 and C4 fixation on incubation with fresh serum. ARGX-117 inhibits complement activation downstream of C4 induced by patient-derived anti-GM1 antibodies bound to MNs. Discussion: Binding of IgM antibodies from patients with MMN to iPSC-derived MNs induces complement activation. By expressing complement regulatory proteins, particularly CD59, MNs are protected against complement-mediated lysis. Yet, because of expressing C3aR, the function of these cells may be affected by complement activation upstream of membrane attack complex formation. ARGX-117 inhibits complement activation upstream of C3 in this disease model for MMN and therefore represents an intervention strategy to prevent harmful effects of complement in MMN.
MeSH term(s)	Antibodies, Monoclonal, Humanized/pharmacology ; Cells, Cultured ; Complement Activation/immunology ; Complement C2/drug effects ; Humans ; Immunoglobulin M ; Induced Pluripotent Stem Cells ; Motor Neurons ; Polyneuropathies/drug therapy ; Polyneuropathies/immunology
Chemical Substances	Antibodies, Monoclonal, Humanized ; Complement C2 ; Immunoglobulin M
Language	English
Publishing date	2021-11-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000001107
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Article: VEGFR-1/Flt-1 inhibition increases angiogenesis and improves muscle function in a mouse model of Duchenne muscular dystrophy.

Molecular therapy. Methods & clinical development

2021 Volume 21, Page(s) 369–381

Abstract: Duchenne muscular dystrophy is characterized by structural degeneration of muscle, which is exacerbated by localized functional ischemia due to loss of nitric oxide synthase-induced vasodilation. Treatment strategies aimed at increasing vascular ... ...

Abstract	Duchenne muscular dystrophy is characterized by structural degeneration of muscle, which is exacerbated by localized functional ischemia due to loss of nitric oxide synthase-induced vasodilation. Treatment strategies aimed at increasing vascular perfusion have been proposed. Toward this end, we have developed monoclonal antibodies (mAbs) that bind to the vascular endothelial growth factor (VEGF) receptor VEGFR-1 (Flt-1) and its soluble splice variant isoform (sFlt-1) leading to increased levels of free VEGF and proangiogenic signaling. The lead chimeric mAb, 21B3, had high affinity and specificity for both human and mouse sFlt-1 and inhibited VEGF binding to sFlt-1 in a competitive manner. Proof-of-concept studies in the
Language	English
Publishing date	2021-03-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2872938-9
ISSN	2329-0501 ; 2329-0501
ISSN (online)	2329-0501
ISSN	2329-0501
DOI	10.1016/j.omtm.2021.03.013
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