Table 2.
Neurotherapeutic Strategies for Lung Cancer
| Therapy type | Drug | Treatment Pathway | Clinical Status | references |
|---|---|---|---|---|
| Beta-blockers | Propranolol | Beta-adrenergic signaling, reduces tumor growth | [204, 205] | |
| α2-Adrenergic receptor agonists | Prazosin | Increases oxidative stress, reduces tumor viability | / | [221, 222] |
| Dopamine receptor antagonist | Quetiapine | Inactivates ERK/AKT pathways, induces apoptosis | / | [136, 138] |
| Partial agonist of acetylcholine receptors | cytisine | Preventing lung cancer through smoking cessation therapy | NCT03654105 | [233] |
| Acetylcholine receptor antagonist | Dafinacin | By blocking the YAP-ChAT-ACh-M3R-WNT signaling axis to reverse EGFR-TKI resistance | / | [190] |
| Glutamate receptor antagonist | Memantine | Inhibit tumor growth | / | [180, 181] |
| SSRI | Fluoxetine | Inhibits ERK/NF-κB signaling, induces apoptosis | NCT00005850 | [122] |
| SNRI | Duloxetine | Enhances caspase activity, induces apoptosis | / | [231] |
| Thymosin | Thymalfasin | Monotherapy + Combination Therapy. Inhibition of the STAT3/MMP2 pathway. | / | [230] |
|
TMEM16A inhibitor |
cryptochlorogenic acid(CCA) | Inhibiting TMEM16A ion channel activity to regulate MAPK and EMT pathways | / | [232] |