GD2 x CD64

Last update 08 May 2025

Basic Info

Related Targets

GD2CD64

Drugs associated with GD2 x CD64

MDX-260

Target

CD64 x GD2

Mechanism

CD64 antagonists [+1]

Active Org.-

Originator Org.

Medarex, Inc.

Active Indication-

Inactive Indication

Glioma [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GD2 x CD64

100 Translational Medicine associated with GD2 x CD64

0 Patents (Medical) associated with GD2 x CD64

Literatures (Medical) associated with GD2 x CD64

01 Apr 2025·Cancer Science

Antibody‐Dependent Cellular Cytotoxicity of iPS Cell‐Derived Natural Killer T Cells by Anti‐GD2 mAb for Neuroblastoma

Article

Author: Hongxuan, Wang ; Takami, Mariko ; Motohashi, Shinichiro ; Aoki, Takahiro ; Ozaki, Ko ; Nishimura, Katsuhiro ; Koseki, Haruhiko ; Komatsu, Shugo ; Yoshizawa, Hiroko ; Ogawa, Keita ; Kobayashi, Midori ; Hishiki, Tomoro ; Takatani, Tomozumi ; Katsumi, Daisuke ; Hirahara, Kiyoshi ; Shimizu, Daiki

ABSTRACTWhile antibody‐dependent cellular cytotoxicity (ADCC) by anti‐disialoganglioside GD2 monoclonal antibody (mAb) has succeeded in increasing the survival rate of high‐risk patients with neuroblastoma, approximately 40%–50% of patients die from the disease. Recently, we developed induced pluripotent stem cell‐derived natural killer T (iPS‐NKT) cells, which exhibit NK‐like cytotoxicity. However, whether iPS‐NKT cells can induce ADCC function is unclear. Here, we investigated the ADCC of iPS‐NKT cells and the efficacy of the combination treatment of anti‐GD2 mAb and iPS‐NKT cells against neuroblastoma. Anti‐GD2 mAb enhanced the cytotoxicity and secretion of cytokines and cytotoxic granules of iPS‐NKT cells, which expressed CD16 to GD2‐expressing neuroblastoma cell lines. We also examined which Fcγ receptors contribute to ADCC of iPS‐NKT cells. CD16 stimulation against iPS‐NKT cells caused cytotoxicity and secretion of interferon‐gamma, tumor necrosis factor, and granzyme B. In contrast, CD32 and CD64 stimulation did not. In vivo, the intratumor administration of anti‐GD2 mAb and iPS‐NKT cells significantly inhibited tumor growth compared with the other treatment groups: no treatment, anti‐GD2 mAb alone, and iPS‐NKT cells alone. In conclusion, iPS‐NKT cells exhibit CD16‐mediated ADCC, and the addition of iPS‐NKT cells to anti‐GD2 mAb therapy may be a potential approach for immunotherapy against neuroblastoma.

01 Aug 1995·BloodQ1 · MEDICINE

In vitro killing of neuroblastoma cells by neutrophils derived from granulocyte colony-stimulating factor-treated cancer patients using an anti-disialoganglioside/anti-Fc gamma RI bispecific antibody

Q1 · MEDICINE

Article

Author: Moutel, S ; Barbet, J ; Fridman, WH ; Deo, YM ; Teillaud, JL ; Romet-Lemonne, JL ; Michon, J

AbstractNeutrophils isolated from cancer patients treated with granulocyte colony-stimulating factor (G-CSF) express high levels of Fc gamma RI. They exhibited an efficient killing of GD2+ neuroblastoma cells in the presence of an antidisialoganglioside (GD2) mouse monoclonal antibody (MoAb; 7A4, IgG3 kappa). However, this cytotoxicity was totally blocked by human monomeric IgG. In contrast, a bispecific antibody (7A4 bis 22/MDX-260), prepared by chemically linking an F(ab') fragment of 7A4 with an F(ab') fragment of an anti-Fc gamma RI MoAb, 22, which binds outside the Fc binding domain, triggered antibody-dependent cell cytotoxicity, even when neutrophils were preincubated with human monomeric IgG. F(ab')2 22 MoAb abrogated the MDX-260 killing without affecting that of 7A4. The 3G8 MoAb, directed against the Fc gamma RIII binding site, did not inhibit the cytotoxicity induced by either antibody. Thus, these results indicate that G-CSF-activated neutrophils exert their cytotoxic effect against neuroblastoma cells through Fc gamma RI and not Fc gamma RIII, and that the saturation of the high affinity Fc gamma RI by monomeric IgG can be overcome by the use of bispecific antibodies binding epitopes outside the IgG Fc gamma RI binding site. A combined administration of such bispecific antibodies and G-CSF may be, therefore, an efficient therapeutic approach to trigger tumor lysis by cytotoxic neutrophils in vivo.

01 Jan 1995·European Journal of CancerQ1 · MEDICINE

In vivo targeting of human neuroblastoma xenograft by anti-GD2/anti-FcγRI (CD64) bispecific antibody

Q1 · MEDICINE

Article

Author: Brixy, F. ; Perdereau, B. ; Michon, J. ; Fridman, W. -H. ; Teillaud, J. -L. ; Moutel, S.

Antidisialoganglioside (GD2) monoclonal antibodies can target in vitro and in vivo neuroblastoma cells. However, their in vivo use is limited by the presence of high levels of circulating IgG which hamper the recruitment of effector cells through the high affinity Fc gamma RI (CD64). A bispecific Fab' x Fab' antiGD2/antiFc gamma RI antibody (7A4 bis 22), which binds outside the IgG binding site of Fc gamma RI, was therefore developed. This antibody binds both human GD2+ neuroblastoma and Fc gamma RI+ activated macrophages in vitro. It can localise a GD2 positive neuroblastoma xenografted on Nu/Nu mice. Scintigraphy tumour/muscle ratios showed that targeting with this antibody has an excellent selectivity for the tumour over normal tissues. Furthermore, although its whole body clearance is more rapid than that of the 7A4 parental antibody over the first 48 h, its selective tumour uptake is similar, as shown by immunoscintigraphy imaging. Thus, such a bispecific antibody may represent an efficient tool for in vivo therapy of neuroblastoma through its ability to recruit Fc gamma RI+ effector cells even in presence of circulating IgG and to bind concomitantly GD2+ tumour cells.

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