Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0242)

Name	Tetraarsenic tetrasulfide
Synonyms	Tetraarsenic tetrasulfide; 12279-90-2; ZIK02R2PSD; As4S4 cpd; XIONGHUANG; ARSENIC DISULPHIDE; REALGAR [CHP]; UNII-ZIK02R2PSD; REALGAR [WHO-DD]; ARSENIC MONOSULPHIDE; ARSENIC SULPHIDE RED; ARSENIC SULFIDE [MI]; TETRAARSENIC TETRASULPHIDE; DTXSID50153717; TETRA-ARSENIC TETRA-SULFIDE; ARSENICUM SULPHURATUM RUBRUM; TETRA-ARSENIC TETRA-SULPHIDE; 2,4,6,8-Tetrathia-1,3,5,7-tetraarsatricyclo[3.3.0.03,7]octane; TETRAARSENIC TETRASULFIDE [WHO-DD]; ARSENICUM SULPHURATUM RUBRUM [HPUS]; Q27295581; 2,4,6,8-tetrathia-1,3,5,7-tetrarsatricyclo[3.3.0.03,7]octane Click to Show/Hide
Structure
Structure	3D MOL 2D MOL
Formula	As4S4
IUPAC Name	2,4,6,8-tetrathia-1,3,5,7-tetrarsatricyclo[3.3.0.03,7]octane
Canonical SMILES	S1[As]2S[As]3[As]1S[As]2S3
InChI	InChI=1S/As4S4/c5-1-2-7-3(5)4(6-1)8-2
InChIKey	XPDICGYEJXYUDW-UHFFFAOYSA-N
PubChem CID	139298

Full List of Ferroptosis Target Related to This Drug

Phospholipid hydroperoxide glutathione peroxidase (GPX4)

Target Info

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	Lung cancer		ICD-11: 2C25	Disease Info
Responsed Regulator	RAF proto-oncogene serine/threonine-protein kinase (RAF1)		Suppressor	Regulator Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	MAPK signaling pathway			hsa04010
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell apoptosis
	Cell proliferation
In Vitro Model	NCI-H23 cells	Lung adenocarcinoma	Homo sapiens	CVCL_1547
	A-549 cells	Lung adenocarcinoma	Homo sapiens	CVCL_0023
	NCI-H460 cells	Lung large cell carcinoma	Homo sapiens	CVCL_0459
	H1650-ER1 cells	Minimally invasive lung adenocarcinoma	Homo sapiens	CVCL_4V01
Response regulation	On H23 cells treated with realgar, the expression of GPX4, SCL7A11 decreased while ACSL4 expression increased; this effect could also be amplified by Sorafenib. In conclusion, the present study indicated that realgar may induce ferroptosis by regulating the Raf, and hence plays a role in antiKRAS mutant lung cancer.

Long-chain-fatty-acid--CoA ligase 4 (ACSL4)

Target Info

In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target				[1]
Target for Ferroptosis	Driver
Responsed Disease	Lung cancer		ICD-11: 2C25	Disease Info
Responsed Regulator	RAF proto-oncogene serine/threonine-protein kinase (RAF1)		Suppressor	Regulator Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	MAPK signaling pathway			hsa04010
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell apoptosis
	Cell proliferation
In Vitro Model	NCI-H23 cells	Lung adenocarcinoma	Homo sapiens	CVCL_1547
	A-549 cells	Lung adenocarcinoma	Homo sapiens	CVCL_0023
	NCI-H460 cells	Lung large cell carcinoma	Homo sapiens	CVCL_0459
	H1650-ER1 cells	Minimally invasive lung adenocarcinoma	Homo sapiens	CVCL_4V01
Response regulation	On H23 cells treated with realgar, the expression of GPX4, SCL7A11 decreased while ACSL4 expression increased; this effect could also be amplified by Sorafenib. In conclusion, the present study indicated that realgar may induce ferroptosis by regulating the Raf, and hence plays a role in antiKRAS mutant lung cancer.

Cystine/glutamate transporter (SLC7A11)

Target Info

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	Lung cancer		ICD-11: 2C25	Disease Info
Responsed Regulator	RAF proto-oncogene serine/threonine-protein kinase (RAF1)		Suppressor	Regulator Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	MAPK signaling pathway			hsa04010
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell apoptosis
	Cell proliferation
In Vitro Model	NCI-H23 cells	Lung adenocarcinoma	Homo sapiens	CVCL_1547
	A-549 cells	Lung adenocarcinoma	Homo sapiens	CVCL_0023
	NCI-H460 cells	Lung large cell carcinoma	Homo sapiens	CVCL_0459
	H1650-ER1 cells	Minimally invasive lung adenocarcinoma	Homo sapiens	CVCL_4V01
Response regulation	On H23 cells treated with realgar, the expression of GPX4, SCL7A11 decreased while ACSL4 expression increased; this effect could also be amplified by Sorafenib. In conclusion, the present study indicated that realgar may induce ferroptosis by regulating the Raf, and hence plays a role in antiKRAS mutant lung cancer.

Unspecific Target

In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target				[1]
Responsed Disease	Lung cancer		ICD-11: 2C25	Disease Info
Responsed Regulator	GTPase KRas (KRAS)		Driver	Regulator Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	MAPK signaling pathway			hsa04010
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell apoptosis
	Cell proliferation
In Vitro Model	NCI-H23 cells	Lung adenocarcinoma	Homo sapiens	CVCL_1547
	A-549 cells	Lung adenocarcinoma	Homo sapiens	CVCL_0023
	NCI-H460 cells	Lung large cell carcinoma	Homo sapiens	CVCL_0459
	H1650-ER1 cells	Minimally invasive lung adenocarcinoma	Homo sapiens	CVCL_4V01
Response regulation	Realgar-induced ferroptosis may be mediated via KRAS/Raf/MAPK. Realgar may be targeted to regulate Raf kinase, thereby further regulating the downstream JNK/ERK signaling cascade to suppress KRAS cells and exert an anticancer activity. In conclusion, realgar may induce ferroptosis by regulating the Raf, and hence plays a role in antiKRAS mutant lung cancer.

References

Ref 1	Realgarinduced KRAS mutation lung cancer cell death via KRAS/Raf/MAPK mediates ferroptosis. Int J Oncol. 2022 Dec;61(6):157. doi: 10.3892/ijo.2022.5447. Epub 2022 Nov 2.