c-Met inhibitor ANS014004
Term · Oncology and biomedicine · MLC-T-ONC-012666
An orally bioavailable, next-generation, type II inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, c-Met inhibitor ANS014004 selectively targets and specifically binds to the inactive state of c-Met (DFG-out) in the ATP pocket and inhibits the activity of the c-Met protein, including various c-Met oncogenic alterations such as MET exon 14 skipping mutation (METdeltaex14) and acquired mutations in codons D1228 and Y1230. This prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in and inhibit proliferation of tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis. Type II c-Met inhibitors may overcome resistance to type I c-Met inhibitors. Post-treatment resistance to type I c-Met inhibitors often occurs through acquired mutations in codons D1228 and Y1230.
| Identifier | MLC-T-ONC-012666 |
|---|---|
| Field | Oncology and biomedicine |
| References | National Cancer Institute Thesaurus (CC BY 4.0) |
Record as JSON
{
"id": "MLC-T-ONC-012666",
"term": "c-Met inhibitor ANS014004",
"field": "Oncology and biomedicine",
"definition": "An orally bioavailable, next-generation, type II inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, c-Met inhibitor ANS014004 selectively targets and specifically binds to the inactive state of c-Met (DFG-out) in the ATP pocket and inhibits the activity of the c-Met protein, including various c-Met oncogenic alterations such as MET exon 14 skipping mutation (METdeltaex14) and acquired mutations in codons D1228 and Y1230. This prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in and inhibit proliferation of tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis. Type II c-Met inhibitors may overcome resistance to type I c-Met inhibitors. Post-treatment resistance to type I c-Met inhibitors often occurs through acquired mutations in codons D1228 and Y1230.",
"references": [
"National Cancer Institute Thesaurus"
],
"url": "https://mlchart.com/terminology/oncology/c-met-inhibitor-ans014004/"
}
Record 5,007 of 17,717 in Oncology and biomedicine terminology (MLC-0111). Request the full dataset.