rilotumumab

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Ligands
rilotumumab

GtoPdb Ligand ID: 7986

Synonyms: AMG 102 | AMG102

Comment: Rilotumumab is a monoclonal antibody directed against hepatocyte growth factor (HGF), developed as a treatment for solid tumours.
Annotated peptide sequences for this antibody are available from its IMGT/mAb-DB record. Peptide sequence BLAST search using the heavy and light chain variable regions of rilotumumab provides 100% matches to sequences covered by patent US8609090 [1], and to the antibody with designation 2.12.1.

No information available.

No information available.

Summary of Clinical Use
The manufacturer (Amgen) terminated all company-sponsored clinical studies of rilotumumab in advanced gastric in November 2014, due to safety concerns arising from a Phase 3 trial (RILOMET-2; NCT02137343). Phase 3 study NCT01697072 is also terminated.

Summary of Clinical Use

The manufacturer (Amgen) terminated all company-sponsored clinical studies of rilotumumab in advanced gastric in November 2014, due to safety concerns arising from a Phase 3 trial (RILOMET-2; NCT02137343). Phase 3 study NCT01697072 is also terminated.

Mechanism Of Action and Pharmacodynamic Effects
Rilotumumab binds to and neutralizes HGF, preventing binding to its receptor c-Met and thereby inhibiting c-Met activation. c-Met is a receptor tyrosine kinase that is overexpressed or mutated in a variety of epithelial cancer cell types and plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis. Inhibition of c-Met-mediated signal transduction may result in the induction of apoptosis in c-Met+ve tumour cells.

Mechanism Of Action and Pharmacodynamic Effects

Rilotumumab binds to and neutralizes HGF, preventing binding to its receptor c-Met and thereby inhibiting c-Met activation. c-Met is a receptor tyrosine kinase that is overexpressed or mutated in a variety of epithelial cancer cell types and plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis. Inhibition of c-Met-mediated signal transduction may result in the induction of apoptosis in c-Met+ve tumour cells.