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Table 2 Novel treatment options that are associated with HGF/MET signaling pathway in glioblastoma

From: MET in glioma: signaling pathways and targeted therapies

Agent

Oral, Intravenous

Molecular type

Mechanisms of Action

Animal model (Subcutaneous, Intracranial)

Clinical trail

Ref.

YYB-101

Intravenous

A humanized monoclonal anti-HGF antibody

Neutralize HGF

Intracranial

NCT02499224 (Phase I)

[79, 80]

Rilotumumab (AMG102)

Intravenous

A neutralizing antibody against HGF

Neutralize HGF

–

NCT01113398 (phase II)

[82, 83]

Onartuzumab

Intravenous

A humanized monovalent monoclonal antibody

Block c-Met receptor

Intracranial (infused intratumorally using osmotic minipumps)

NCT01632228 (phase II)

[84, 85]

Crizotinib

Oral

A tyrosine kinase inhibitor

Target ALK, ROS1, and MET

–

NCT02270034 (phase I) NCT01644773 (phase I)

[86, 87]

Volitinib

Oral

A kinase inhibitor

Inhibit the phosphorylation of c-Met.

Subcutaneous

–

[88]

SGX523

Oral

Small molecule kinase inhibitor

Inhibite c-Met activation

Intracranial

NCT00607399 (phase I), NCT00606879 (phase I)

[89]

INCB28060

Oral

A novel inhibitor of c-MET kinase

Inhibit c-MET enzyme activity

Subcutaneous

–

[75]

Cabozantinib (XL184)

Oral

A molecular kinase inhibitor

Inhibit VEGF receptor 2 (VEGFR2) and MET.

Intracranial

NCT00704288 (phase II)

[92,93,94]

Altiratinib

Oral

A kinase inhibitor

Inhibit the activation of MET, TIE2, VEGFR2, and tropomyosin receptor kinase family kinases.

Intracranial

–

[95]

CM-118

Oral

A novel lead compound

Selectivity inhibit the phosphorylation of c-Met and ALK.

Intracranial

–

[96]

Brefelamide

–

An aromatic amide that was originally isolated from Dictyostelium cellular slime molds.

Inhibit the secretion of HGF and expression and activation of c-Met.

–

–

[97]

PLB-1001

Oral

A MET kinase inhibitor

High selectively inhibit the activation of Met

Subcutaneous and intracranial

NCT02978261 (Phase I)

[20]