Ferroptosis-centered Drug Response Information
General Information of the Drug (ID: ferrodrug0356)
Name |
2-Imino-6-methoxy-2H-chromene-3-carbothioamide
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Synonyms |
2-Imino-6-methoxy-2H-chromene-3-carbothioamide; 2-imino-6-methoxychromene-3-carbothioamide; NSC684971; 71796-75-3; CHEMBL2004669; DTXSID20356657; STL171476; AKOS003794097; NSC-684971; NCI60_030552; 2-imino-6-methoxy-chromene-3-carbothioamide; 2-imino-6-methoxychromene-3-carboximidothioic acid; AH-034/06206012
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Structure |
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Formula |
C11H10N2O2S
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IUPAC Name |
2-imino-6-methoxychromene-3-carbothioamide
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Canonical SMILES |
COC1=CC2=C(C=C1)OC(=N)C(=C2)C(=S)N
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InChI |
InChI=1S/C11H10N2O2S/c1-14-7-2-3-9-6(4-7)5-8(11(13)16)10(12)15-9/h2-5,12H,1H3,(H2,13,16)
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InChIKey |
LUCOUNTXDLWPQS-UHFFFAOYSA-N
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PubChem CID |
Full List of Ferroptosis Target Related to This Drug
Cystine/glutamate transporter (SLC7A11)
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 | Colorectal cancer | ICD-11: 2B91 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
mTOR signaling pathway | hsa04150 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | DLD-1 cells | Colon adenocarcinoma | Homo sapiens | CVCL_0248 | |
HCT 116 cells | Colon carcinoma | Homo sapiens | CVCL_0291 | ||
In Vivo Model |
Five-week-old female BALB/c nude mice were purchased from Beijing Weitong Lihua Experimental Animal Technical Co., Ltd. (Beijing, China). The mice were randomly assigned to the treatment and control groups until the tumor size reached approximately 100 mm3. The mice in the treatment group were injected with 0.174 mg/mL IMCA (100 uL), and those in the control group were injected with an equal volume of normal saline. The nude mice were euthanized, and samples were obtained from their tumor, heart, hepar, kidney, and blood after 33 days of IMCA treatment.
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Response regulation | 2-imino-6-methoxy-2H-chromene-3-carbothioamide (IMCA) significantly induced the ferroptosis of colorectal cancer cells. Mechanistically, IMCA downregulated the expression of SLC7A11 and decreased the contents of cysteine and glutathione, which resulted in reactive oxygen species accumulation and ferroptosis. | ||||