monalizumab   Click here for help

GtoPdb Ligand ID: 8323

Synonyms: humZ270 [8] | IPH-2201 | NN8765-3658
Immunopharmacology Ligand
Compound class: Antibody
Comment: Monalizumab (IPH2201) is a humanized IgG4κ anti-NKG2A (KLRC1, CD159a) monoclonal antibody being investigated as an anti-cancer treatment [4,7]. Administered intravenously or subcutaneously. Use of monalizumab is claimed in patent WO2016041947 (called IPH2201 in the patent) [1].
Annotated peptide sequences for this antibody are available from its IMGT/mAb-DB record.
Click here for help

Ligand Activity Visualisation Charts

These are box plot that provide a unique visualisation, summarising all the activity data for a ligand taken from ChEMBL and GtoPdb across multiple targets and species. Click on a plot to see the median, interquartile range, low and high data points. A value of zero indicates that no data are available. A separate chart is created for each target, and where possible the algorithm tries to merge ChEMBL and GtoPdb targets by matching them on name and UniProt accession, for each available species. However, please note that inconsistency in naming of targets may lead to data for the same target being reported across multiple charts.

✖

View interactive charts of activity data across species
No information available.
Summary of Clinical Use Click here for help
Phase 2 clinical trials for head and neck cancer and chronic lymphocytic leukemia (CLL) are underway (click here to link to ClinicalTrials.gov's complete list of monalizumab/IPH2201 trials).
Mechanism Of Action and Pharmacodynamic Effects Click here for help
KLRC1 forms functional heterodimers with CD94 (KLRD1) to form a human leukocyte antigen E (HLA-E) recognition complex on a subset of natural killer (NK) cells and cytotoxic T lymphocytes. KLRC1/CD94/HLA-E binding suppresses immune vigilance, and overexpression of HLA-E is used by cancer cells to evade immune recognition and destruction [2,5-6,9]. Anti-KLRC1 monoclonals such as IPH2201 block KLRC1/CD94 activation, re-establishing NK and T cell-driven destruction of cancer cells, even in the presence of HLA-E [3].