TABLE 4.
JAK/STAT signaling modulators, their targets, and mechanism in esophageal carcinoma/cells.
| Compounds/small molecule inhibitors | Targets | Clinical status | Mechanism |
|---|---|---|---|
| WP1066 | JAK2 | Phase I | Inhibits JAK2 phosphorylation thereby attenuating cell migration and invasion by inhibiting MMPs |
| Pacritinib | JAK2 | Pre-clinical | Pre-clinical studies showed that fibrotic areas of the mouse liver were effectively reduced by reducing CK18 biomarker |
| CTS | JAK2 | Pre-clinical | In mouse models, CTS promotes apoptosis of tumor cells and helps to activate tumor-suppressive M1 cells |
| STAT3 | |||
| Ruxolitinib | JAK1/2 | Pre-clinical | Inhibits cell proliferation and colony-forming ability of HCC cells |
| Stattic | STAT3 | Pre-clinical | Stattic inhibits tumor cell function in HCC such as cell proliferation and invasiveness |
| OPB-111077 | STAT3 | Phase I | Inhibits STAT3 in patients who are at an advanced stage of HCC and are not responding to sorafenib therapy |
| OPB-31121 | STAT3 | Phase I/II | Inhibits STAT3 in patients who are at an advanced stage of HCC and are not responding to sorafenib therapy |
| Napanucasin (BBI608) | STAT3 | Phase Ib/II | Promotes antitumor activity in advanced HCC patients with prior systemic Sorafenib therapy |
| AZD9150 | STAT3 | Phase Ib/II | Promotes antitumor activity in advanced HCC patients with prior systemic Sorafenib therapy |