BelataceptBelatacept
MedChemExpress (MCE)
HY-108813
706808-37-9
BMS 224818
LEA 29Y
99.30%
Please store the product under the recommended conditions in the Certificate of Analysis.
Belatacept (BMS 224818) is a selective T-cell costimulation blocker and a costimulator of the CD28-CD80/86 pathway. Belatacept binds to the CD 80/86 ligand and inhibits CD-28-mediated T cell costimulation and IFN-γ production. Belatacept can be used in studies of immunosuppression in organ transplantation.
Belatacept (0-5 mg/mL, 1 h) inhibits T-cell proliferation in a dose-dependent manner[2]. Belatacept (500 ng/mL, 7 days) enhances predominance of effector-memory T-cells after allogeneic stimulation[2]. Belatacept (100, 500 ng/mL, 7 days) has no effect on differentiation and allogeneic IFNγ production of isolated effector-memory T cells[2]. Belatacept (10?μg/mL, 1 h) does not inhibit follicular T Cell-dependent B-Cell differentiation[4]. Belatacept (40?μg/mL, 10 days) reduces plasmablast differentiation, Ig production, and the major transcription factor Blimp-1 in a T cell-independent manner[5]. Belatacept (40?μg/mL, 30 min) induces activation of the STAT3 transcription factor in stimulated B cells and reduced the expression of CD86[5].
Belatacept (intraperitoneal injection, 60 mg/kg) inhibits ABMR (Antibody-Mediated Rejection), and inhibits acute rejection when combined with BTLA (B and T lymphocyte attenuator) overexpression therapy[3]. Belatacept (intravenous injection, 20 mg/kg) displays immunosuppressive activities in monkeys immunized with sheep red blood cell[6].
CD80/86[1] In Vitro Belatacept (0-5 mg/mL, 1 h) inhibits T-cell proliferation in a dose-dependent manner[2]. Belatacept (500 ng/mL, 7 days) enhances predominance of effector-memory T-cells after allogeneic stimulation[2]. Belatacept (100, 500 ng/mL, 7 days) has no effect on differentiation and allogeneic IFNγ production of isolated effector-memory T cells[2]. Belatacept (10?μg/mL, 1 h) does not inhibit follicular T Cell-dependent B-Cell differentiation[4]. Belatacept (40?μg/mL, 10 days) reduces plasmablast differentiation, Ig production, and the major transcription factor Blimp-1 in a T cell-independent manner[5]. Belatacept (40?μg/mL, 30 min) induces activation of the STAT3 transcription factor in stimulated B cells and reduced the expression of CD86[5]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Belatacept Related Antibodies Cell Viability Assay[2] Cell Line: PBMCs from healthy volunteers
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[1]. George Melvin, et al. Belatacept: A worthy alternative to cyclosporine?. J Pharmacol Pharmacother. 2012 Jan-Mar
3(1): 90–92. [Content Brief]
[2]. Gretchen N de Graav, et al. Down-Regulation of Surface CD28 under Belatacept Treatment: An Escape Mechanism for Antigen-Reactive T-Cells. PLoS One. 2016 Feb 26
11(2):e0148604. [Content Brief]
[3]. Hengcheng Zhang, et al. Combined Immunotherapy With Belatacept and BTLA Overexpression Attenuates Acute Rejection Following Kidney Transplantation. Front Immunol. 2021 Feb 24
12:618737. [Content Brief]
[4]. Gretchen N de Graav, et al. Belatacept Does Not Inhibit Follicular T Cell-Dependent B-Cell Differentiation in Kidney Transplantation. Front Immunol. 2017 May 31
8:641. [Content Brief]
[5]. laire Leibler, et al. Control of Humoral Response in Renal Transplantation by Belatacept Depends on a Direct Effect on B Cells and Impaired T Follicular Helper-B Cell Crosstalk. J Am Soc Nephrol. 2018 Mar
29(3):1049-1062. [Content Brief]
[6]. Christian P Larsen, et al. Rational development of LEA29Y (belatacept), a high-affinity variant of CTLA4-Ig with potent immunosuppressive properties. Am J Transplant. 2005 Mar
5(3):443-53. [Content Brief]
