Cudarolimab
Term · Oncology and biomedicine · MLC-T-ONC-012827
An agonistic fully human anti-OX40 (tumor necrosis factor receptor superfamily member 4; TNFRSF4; CD134; OX40L receptor) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cudarolimab selectively binds to and activates OX40. Receptor activation induces proliferation of memory and effector T lymphocytes and results in a T-cell-mediated immune response against tumor cells, which leads to tumor cell lysis. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and provides a co-stimulatory signal that promotes both the proliferation and survival of activated T-cells.
| Identifier | MLC-T-ONC-012827 |
|---|---|
| Field | Oncology and biomedicine |
| Synonyms | anti-OX40 monoclonal antibody IBI101 |
| References | National Cancer Institute Thesaurus (CC BY 4.0) |
Record as JSON
{
"id": "MLC-T-ONC-012827",
"term": "Cudarolimab",
"field": "Oncology and biomedicine",
"definition": "An agonistic fully human anti-OX40 (tumor necrosis factor receptor superfamily member 4; TNFRSF4; CD134; OX40L receptor) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cudarolimab selectively binds to and activates OX40. Receptor activation induces proliferation of memory and effector T lymphocytes and results in a T-cell-mediated immune response against tumor cells, which leads to tumor cell lysis. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and provides a co-stimulatory signal that promotes both the proliferation and survival of activated T-cells.",
"synonyms": [
"anti-OX40 monoclonal antibody IBI101"
],
"references": [
"National Cancer Institute Thesaurus"
],
"url": "https://mlchart.com/terminology/oncology/cudarolimab/"
}
Record 5,493 of 17,717 in Oncology and biomedicine terminology (MLC-0111). Request the full dataset.