Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0422)
Name
11-hydroxy-ent-16-kaurene-15-one
Drug Type
Small molecule
Full List of Ferroptosis Target Related to This Drug
Unspecific Target
In total 2 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 Peroxiredoxin-1 (PRDX1) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model A-549 cells Lung adenocarcinoma Homo sapiens CVCL_0023
Hep-G2 cells Hepatoblastoma Homo sapiens CVCL_0027
786-O cells Renal cell carcinoma Homo sapiens CVCL_1051
HBE1 cells Normal Homo sapiens CVCL_0287
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
HUVECs (Human umbilical vein endothelial cells)
In Vivo Model
Thirty male athymic (Balb/c-nu) mice (4-week-old) were purchased from the SPF (Beijing) biotechnology (Beijing, China) and allowed to acclimatize for 1 week. A549/CDDP cells (5 x 106 cells) were injected subcutaneously into the right anterior flanks of the mice. Two weeks after the injection of cells, when the tumors became palpable (around 100 mm3), mice were randomly divided into four groups (n = 6 per group). Tumor-bearing mice were received equal amount of solvent, CDDP (4 mg/kg) or compound 23 (10 mg/kg) or combination CDDP and 23 were injected via intraperitoneal injection. Administration was performed every 3 days for 30 days.

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Response regulation 11-hydroxy-ent-16-kaurene-15-one possessed strong inhibitory activity against several cancer cell lines. Moreover, compound 23 induced both apoptosis and ferroptosis through increasing cellular ROS levels in HepG2 cells. ROS accumulation induced by compound 23 was caused by inhibition of antioxidant systems through targeting peroxiredoxin I (Prdx I) and depletion of GSH in lung adenocarcinoma cells.
Experiment 2 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Responsed Disease Lung cancer ICD-11: 2C25
 Disease Info 
Responsed Regulator Peroxiredoxin-2 (PRDX2) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model A-549 cells Lung adenocarcinoma Homo sapiens CVCL_0023
Hep-G2 cells Hepatoblastoma Homo sapiens CVCL_0027
786-O cells Renal cell carcinoma Homo sapiens CVCL_1051
HBE1 cells Normal Homo sapiens CVCL_0287
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
HUVECs (Human umbilical vein endothelial cells)
In Vivo Model
Thirty male athymic (Balb/c-nu) mice (4-week-old) were purchased from the SPF (Beijing) biotechnology (Beijing, China) and allowed to acclimatize for 1 week. A549/CDDP cells (5 x 106 cells) were injected subcutaneously into the right anterior flanks of the mice. Two weeks after the injection of cells, when the tumors became palpable (around 100 mm3), mice were randomly divided into four groups (n = 6 per group). Tumor-bearing mice were received equal amount of solvent, CDDP (4 mg/kg) or compound 23 (10 mg/kg) or combination CDDP and 23 were injected via intraperitoneal injection. Administration was performed every 3 days for 30 days.

    Click to Show/Hide
Response regulation 11-hydroxy-ent-16-kaurene-15-one possessed strong inhibitory activity against several cancer cell lines. Moreover, compound 23 induced both apoptosis and ferroptosis through increasing cellular ROS levels in HepG2 cells. ROS accumulation induced by compound 23 was caused by inhibition of antioxidant systems through targeting peroxiredoxin II (Prdx II) and depletion of GSH in lung adenocarcinoma cells.
References
Ref 1 ent-Kaurane diterpenoids induce apoptosis and ferroptosis through targeting redox resetting to overcome cisplatin resistance. Redox Biol. 2021 Jul;43:101977. doi: 10.1016/j.redox.2021.101977. Epub 2021 Apr 16.