Agents | Known for | Mechanism | Outcome/effects | Study model | Ref |
---|---|---|---|---|---|
Bafilomycin A1 | Inhibitor of vacuolar H+-ATPase | Inhibition of autophagy accumulates the damaged mitochondria | Effective cytotoxicity in hypoxic condition | HL-60, MOLM-13, AML patients samples | [194] |
Hydroxy-chloroquine | Anti-malarial drug | Inhibition of autophagy activates caspase 9 in Ara-C-resistant AML cells | Inducing intrinsic mitochondria apoptosis | U937, OCI-AMLM-2, AML patients samples | [192] |
 |  | Inhibition of autophagy converted CD34( +)/ROSlow AML cells to CD34( +)/ROShigh AML cells | Increasing ROS production and inducing apoptosis | HL-60, K562, THP1, OCIM3, MOLM13, NB4, AML patients samples | [119] |
SAR405 | VPS34 inhibitor | SAR405 inhibits the autophagy process in FLT3-ITD AML cells | Inhibition of proliferation and Inducing apoptosis | MV4-11, MOLM-14, OCI-AML3, AML patients samples | [199] |
 |  |  | Impairment of proliferation | MV4-11, MOLM-14, OCI-AML3, AML patients samples | [93] |
THZ-P1-2 | PI5P4K inhibitor | Lysosomal–autophagosomal defect and increased TFEB activation (mechanism studied in HeLa cells) | Anti-proliferative | THP1, OCI/AML-2, SKM1 | [209] |
VPS34-IN1 | VPS34 inhibitor | Reduction of intracellular vesicle trafficking, inhibition of basal and L-asparaginase-induced autophagy, modulation of mTORC1 and FLT3-ITD signaling | Mitochondrial apoptotic cell death/Anti-leukemic | HL-60, MOLM-14, several AML cell lines | [211] |
XRK3F2 | Inhibitor of ZZ domain of p62 | Inhibition the binding of p62 with defective mitochondria to block mitophagy | Inhibition of leukemia-initiating potential of leukemia cells | K562, HL-60, patient-derived tumor xenograft model | [212] |
Chidamide | HDAC inhibitor | Inhibition of SIRT1 expression to inhibit the Ara-C or sorafenib-induced autophagy | Enhancement of cytotoxicity of chemotherapy drugs | THP-1, MV4-11 | [214] |
TAK-165 | HER2 inhibitor | HER2-independet inhibition of autophagy, but induction of chaperone-mediated autophagy (CMA) during TAK-165/AC220 combinatorial treatment | Enhanced efficacy of AC220 to induce cancer cell death | HEL, ES-2, OCI-AML3 | [215] |