Name	2-pyridylhydrazone dithiocarbamate s-acetic acid
Drug Type	Small molecule

In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target				[1]
Target for Ferroptosis	Suppressor
Responsed Disease	Hepatocellular carcinoma		ICD-11: 2C12	Disease Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	Hep-G2 cells	Hepatoblastoma	Homo sapiens	CVCL_0027
Response regulation	2-pyridylhydrazone dithiocarbamate s-acetic acid (PdtaA) induced both apoptosis and cell cycle arrest. Notably, PdtaA also induced ferroptosis via downregulation of GPx4 and xCT in liver cancer cells. Autophagy inhibitor 3-methyladenin or genetic knockdown of NCOA4 was employed to inhibit ferritinophagy, which significantly neutralized the action of PdtaA in both apoptosis and ferroptosis.

In total 2 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target				[1]
Target for Ferroptosis	Driver
Responsed Disease	Hepatocellular carcinoma		ICD-11: 2C12	Disease Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	Hep-G2 cells	Hepatoblastoma	Homo sapiens	CVCL_0027
Response regulation	2-pyridylhydrazone dithiocarbamate s-acetic acid (PdtaA) induced both apoptosis and cell cycle arrest. Notably, PdtaA also induced ferroptosis via downregulation of GPx4 and xCT in liver cancer cells. Autophagy inhibitor 3-methyladenin or genetic knockdown of NCOA4 was employed to inhibit ferritinophagy, which significantly neutralized the action of PdtaA in both apoptosis and ferroptosis.
Experiment 2 Reporting the Ferroptosis-centered Drug Act on This Target				[2]
Target for Ferroptosis	Driver
Responsed Disease	Hepatocellular carcinoma		ICD-11: 2C12	Disease Info
Pathway Response	Ferroptosis			hsa04216
	Cell adhesion molecules			hsa04514
Cell Process	Cell ferroptosis
In Vitro Model	Hep-G2 cells	Hepatoblastoma	Homo sapiens	CVCL_0027
Response regulation	Knockdown of NCOA4 significantly attenuated the regulatory effect of 2-pyridylhydrazone dithiocarbamate s-acetic acid (PdtaA) on related proteins which highlighted that the strength of ferritinophagic flux (NCOA4/ferritin) was a driving force in determination of the status of EMT and ferroptosis. PdtaA treatment resulted in ferritinophagy that triggered ROS production in liver cancer cells.

Ref 1	Ferritinophagy-Mediated ROS Production Contributed to Proliferation Inhibition, Apoptosis, and Ferroptosis Induction in Action of Mechanism of 2-Pyridylhydrazone Dithiocarbamate Acetate. Oxid Med Cell Longev. 2021 Oct 14;2021:5594059. doi: 10.1155/2021/5594059. eCollection 2021.
Ref 2	Ferritinophagic Flux Was a Driving Force in Determination of Status of EMT, Ferroptosis, and NDRG1 Activation in Action of Mechanism of 2-Pyridylhydrazone Dithiocarbamate S-Acetic Acid. J Oncol. 2021 Dec 7;2021:3015710. doi: 10.1155/2021/3015710. eCollection 2021.