Antibodies to human GITR are provided, as well as uses thereof, e.g., in treatment of proliferative and immune disorders.

Anti-gitr antibodies

CD3-binding molecules capable of binding to human and non-human CD3, and in particular to such molecules that are cross-reactive with CD3 of a non-human mammal (e.g., a cynomolgus monkey) are presented. Uses of such antibodies and antigen-binding fragments in the treatment of cancer, autoimmune and/or inflammatory diseases and other conditions are presented.

Cd3-binding molecules capable of binding to human and non-human cd3

A bispecific binding agent comprising at least two binding domains, wherein a first binding domain binds to the B cell maturation antigen BCMA and wherein a second binding domain binds to CD3, pharmaceutical compositions containing such agent and use for the treatment of plasma cell disorders or B cell disorders which correlate with BCMA expression.

Agents and methods for treating diseases that correlate with bcma expression

Monoclonal antibodies that bind and inhibit activation of fibroblast growth factor receptor 3 (FGFR3) are disclosed. The antibodies can be used to treat cell proliferative diseases and disorders, including certain forms of cancer, associated with activation of FGFR3.

Fibroblast growth factor receptor 3 (fgfr3) binding proteins

The present invention is directed to the production and use of monoclonal antibodies, or antigen binding fragments thereof, that specifically bind the T cell antigen receptor (TCR) and their use for immunomodulation. In preferred embodiments, the antibody or antigen binding fragment of the invention specifically binds the constant region of the alpha chain of the TCR, or otherwise specifically binds the alpha chain regardless of TCR clonal origin (i.e., is pan specific for TCR). The antibodies of the invention may be used, for example, in immunosuppressive therapies for transplant maintenance and the treatment of autoimmune diseases, and/or as targeting molecules for use in the treatment of T-cell malignancies.

T-Cell Receptor Antibodies And Methods of Use Thereof

The invention provides bispecific antibodies with selective cytotoxicity against malignant B-cells. The bispecific antibodies bind to an effector cell antigen and to a 28/32 kDa heterodimeric protein on the surface of malignant B-cells. The invention also includes the monospecific components of the bispecific antibodies, humanized versions thereof, and humanized bispecific antibodies. The invention further provides therapeutic and diagnostic methods employing these antibodies.

Humanized antibodies against cd3

A Polymorphism in the C1qA Component of Complement Correlates with Prolonged Complete Remission Following Rituximab Therapy of Follicular Lymphoma.

Purpose: This phase II trial investigated the safety and efficacy of re-treatment with rituximab, a chimeric anti-CD20 monoclonal antibody, in patients with lowgrade or follicular non-Hodgkin’s lymphoma who relapsed after a response to rituximab therapy. Patients and Methods: Fifty-eight patients were enrolled onto this study, and two were re-treated within the study. Patients received an intravenous infusion of 375 mg/m 2 of rituximab weekly for 4 weeks. All patients had at least two prior therapies and had received at least one prior course of rituximab, with a median interval of 14.5 months between rituximab courses. Results: Most adverse experiences (AEs) were transient grade 1 or 2 events occurring during the treatment period. Clinically significant myelosuppression was not observed; hematologic toxicity was generally mild and reversible. No patient developed human antichimeric antibodies after treatment. The type, frequency, and severity of AEs in this study were not apparently different from those reported in the phase III trial of rituximab. The overall response rate in 57 assessable patients was 40% (11% complete response and 30% partial responses). Median time to progression (TTP) in responders and median duration of response (DR) have not been reached, but Kaplan-Meier estimated medians are 17.8 months (range, 5.41 to 26.6 months) and 16.3 months (range, 3.71 to 25.1 months), respectively. These estimated medians are longer than the medians achieved in the patients’ prior course of rituximab (TTP and DR of 12.4 and 9.8 months, respectively, P > .1) and in a previously reported phase III trial (TTP in responders and DR of 13.2 and 11.6 months, respectively). Responses are ongoing in seven of 23 responders. Conclusion: In this re-treatment population, safety and efficacy were not apparently different from those after initial rituximab exposure. J Clin Oncol 18:3135-3143. © 2000 by American Society of Clinical Oncology.

Rituximab A nti-CD20 M onoclonal A ntibody T herapy i n Non-Hodgkin's L ymphoma: S afety a nd E fficacy o f Re-Treatment

high-affinity CD16 polymorphism Rituximab infusion induces NK activation in lymphoma patients with the

L'invention decrit des anticorps bispecifiques ayant une cytotoxicite selective contre les cellules B malignes. Lesdits anticorps bispecifiques se lient a un antigene de cellule effectrice ainsi qu'a une proteine heterodimere de 28/32 kDa sur la surface de cellules B malignes. L'invention concerne aussi les constituants monospecifiques desdits anticorps bispecifiques, des versions humanisees de ceux-ci et des anticorps bispecifiques humanises. L'invention decrit egalement des methodes therapeutiques et diagnostiques faisant intervenir ces anticorps.

Anticorps bispecifique efficace dans le traitement des lymphomes malins a cellules b et lignee cellulaire

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