Monoclonal antibodies (mAbs) can be classified based on their source, target, and mechanism of action.
Monoclonal antibodies are named based on their origin:
| Suffix | Type | Description | Example |
|---|---|---|---|
| -omab | Murine | 100% mouse-derived | Tositumomab |
| -ximab | Chimeric | ~65% human, ~35% mouse | Infliximab |
| -zumab | Humanized | >90% human, small mouse portion | Trastuzumab |
| -umab | Fully human | 100% human-derived | Adalimumab |
Note: Murine antibodies (-omab) have a higher risk of immunogenic reactions (e.g., HAMA response: human anti-mouse antibody reaction).
mAbs are categorized based on their primary target molecule.
Monoclonal antibodies (mAb or moAb) are monospecific antibody that are made by identical immune cells that are all clones of a unique parent cell, in contrast to polyclonal antibodies which are made from several different immune cells. Monoclonal antibodies have monovalent affinity, in that they bind to the same epitope.
Given almost any substance, it is possible to produce monoclonal antibodies that specifically bind to that substance; they can then serve to detect or purify that substance. This has become an important tool in biochemistry, molecular biology, and medicine. When used as medications, the non-proprietary drug name ends in -mab (see “Nomenclature of monoclonal antibodies”), and many immunotherapy specialists use the word mab acronymically.
see Monoclonal antibody therapy.
established a library of monoclonal antibodies (mAbs) against a tumor cell line derived from a patient with GBM. We identified mAbs that reacted with tumor cell lines from patients with GBM but not with nonmalignant human brain cells. We then detected the antigens they recognized using expression cloning. CAR-T cells derived from a candidate mAb were generated and tested in vitro and in vivo.
Results: We detected 507 mAbs that bound to tumor cell lines from patients with GBM. Among them, E61 and A13 reacted with tumor cell lines from most patients with GBM, but not with nonmalignant human brain cells. We found that B7-H3 was the antigen recognized but E61. CAR-T cells were established using the antigen-recognition domain of E61-secreted cytokines and exerted cytotoxicity in co-culture with tumor cells from patients with GBM.
Conclusions: Cancer-specific targets for CAR-T cells were identified using a mAb library raised against primary GBM tumor cells from a patient. We identified a GBM-specific mAb and its antigen. More mAbs against various GBM samples and novel target antigens are expected to be identified using this strategy 1).