Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0369)
Name
Bromelain
Synonyms
MUXF; carbohydrate moiety of bromelain; M0XF(3); Bromelain, Technical Grade; CHEBI:53469; Fuc-alpha-(1->3)-[Man-alpha-(1->6)-[Xyl-beta-(1->2)]-Man-beta-(1->4)-GlcNAc-beta-(1->4)]-GlcNAc; alpha-L-Fuc-(1->3)-[alpha-D-Man-(1->6)-[beta-D-Xyl-(1->2)]-beta-D-Man-(1->4)-beta-D-GlcNAc-(1->4)]-D-GlcNAc; alpha-L-fucopyranosyl-(1->3)-[alpha-D-mannopyranosyl-(1->6)-[beta-D-xylopyranosyl-(1->2)]-beta-D-mannopyranosyl-(1->4)-2-acetamido-2-deoxy-beta-D-glucopyranosyl-(1->4)]-2-acetamido-2-deoxy-D-glucopyranose; alpha-L-fucosyl-(1->3)-[alpha-D-mannosyl-(1->6)-[beta-D-xylosyl-(1->2)]-beta-D-mannosyl-(1->4)-N-acetyl-beta-D-glucosaminyl-(1->4)]-N-acetyl-D-glucosamine; alpha-L-Fucp-(1->3)-[alpha-D-Manp-(1->6)-[beta-D-Xylp-(1->2)]-beta-D-Manp-(1->4)-beta-D-GlcpNAc-(1->4)]-D-GlcpNAc; bromelaine; Epitope ID:115005; GLXC-19140; Q27124066; N_FULL_22100100000000_GS_1023_c1; Man(a1-6)[Xyl(b1-2)]Man(b1-4)GlcNAc(b1-4)[Fuc(a1-3)]GlcNAc

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Structure
3D MOL
2D MOL
Formula
C39H66N2O29
IUPAC Name
N-[(2S,3R,4R,5S,6R)-2-[(2R,3S,4R,5R)-5-acetamido-6-hydroxy-2-(hydroxymethyl)-4-[(2S,3S,4R,5S,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxyoxan-3-yl]oxy-5-[(2S,3S,4S,5S,6R)-4,5-dihydroxy-6-[[(2S,3S,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxymethyl]-3-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxyoxan-2-yl]oxy-4-hydroxy-6-(hydroxymethyl)oxan-3-yl]acetamide
Canonical SMILES
CC1C(C(C(C(O1)OC2C(C(OC(C2OC3C(C(C(C(O3)CO)OC4C(C(C(C(O4)COC5C(C(C(C(O5)CO)O)O)O)O)O)OC6C(C(C(CO6)O)O)O)O)NC(=O)C)CO)O)NC(=O)C)O)O)O
InChI
InChI=1S/C39H66N2O29/c1-9-19(48)24(53)29(58)38(62-9)69-32-18(41-11(3)46)34(59)63-15(6-44)31(32)68-35-17(40-10(2)45)23(52)30(14(5-43)65-35)67-39-33(70-37-27(56)20(49)12(47)7-60-37)26(55)22(51)16(66-39)8-61-36-28(57)25(54)21(50)13(4-42)64-36/h9,12-39,42-44,47-59H,4-8H2,1-3H3,(H,40,45)(H,41,46)/t9-,12+,13+,14+,15+,16+,17+,18+,19+,20-,21+,22+,23+,24+,25-,26-,27+,28-,29-,30+,31+,32+,33-,34?,35-,36-,37-,38-,39-/m0/s1
InChIKey
UNMLVGNWZDHBRA-UFAVQCRNSA-N
PubChem CID
44263865
Full List of Ferroptosis Target Related to This Drug
Long-chain-fatty-acid--CoA ligase 4 (ACSL4)
 Target Info 
In total 8 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator hsa-miR-19b-3p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

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Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
Experiment 2 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator hsa-miR-130a-3p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

    Click to Show/Hide
Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
Experiment 3 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator hsa-miR-150-5p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

    Click to Show/Hide
Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
Experiment 4 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator hsa-miR-144-3p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

    Click to Show/Hide
Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
Experiment 5 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator hsa-miR-16-5p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

    Click to Show/Hide
Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
Experiment 6 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator mmu-miR-7a-5p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

    Click to Show/Hide
Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
Experiment 7 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator hsa-miR-17-5p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

    Click to Show/Hide
Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
Experiment 8 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Responsed Regulator hsa-miR-130a-3p (miRNA) Suppressor
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model NCI-H508 cells Cecum adenocarcinoma Homo sapiens CVCL_1564
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
G13D (Human colorectal cancer cells)
DLD-1 cells Colon adenocarcinoma Homo sapiens CVCL_0248
G12D (Human colorectal cancer cells)
CCD-18Co cells Normal Homo sapiens CVCL_2379
In Vivo Model
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.

    Click to Show/Hide
Response regulation Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4.
References
Ref 1 Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis. Anim Cells Syst (Seoul). 2018 Aug 30;22(5):334-340. doi: 10.1080/19768354.2018.1512521. eCollection 2018.