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Curdione ((+)-Curdione) is an orally active sesquiterpenoid. Curdione inhibits platelet aggregation. Curdione induces ferroptosis in colorectal cancer via m6A methylation mediated by METTL14 and YTHDF2. Curdione inhibits ferroptosis in Isoproterenol (HY-B0468)-induced myocardial infarction by regulating the Keap1/Trx1/GPX4 signaling pathway, suppressing oxidative stress (ROS) and apoptosis. Curdione ameliorates Doxorubicin (HY-15142)-induced cardiotoxicity by inhibiting oxidative stress (ROS) and activating the Nrf2/HO-1 pathway. Curdione ameliorates sepsis-induced lung injury by inhibiting platelet-mediated neutrophil extracellular trap formation. Curdione ameliorates Bleomycin (HY-17565A)-induced pulmonary fibrosis by inhibiting TGF-β-induced fibroblast-to-myofibroblast differentiation. Curdione exhibits neuroprotective effects against focal cerebral ischemia-reperfusion injury in rats. Curdione exerts antiproliferative effects against human uterine leiomyosarcoma by targeting IDO1. Curdione protects vascular endothelial cells and atherosclerosis by regulating DNMT1-mediated ERBB4 promoter methylation. Curdione inhibits inducible prostaglandin E2 production (IC50 = 1.1 μM) and cyclooxygenase 2 expression[1][2][3][4][5][6][7][8][9][10][11][12].
In Vitro
Curdione (12.5-50 μM, 48 h) decreases the cell viability, promotes intracellular ROS production, increases the expression levels of METTL14 and YTHDF2, and decreases the expression levels of SLC7A11, SLC3A2, HOXA13, and GPX4 in CT26 cells[1].
Curdione (12.5-50 μM, 48 h) decreases GSH concentration, increases MDA, m6A, ferrous iron and LPO levels and increases the mRNA levels of SLC7A11 and HOXA13 in CT26 and SW480 cells[1].
Curdione (50 μM, 48 h) reduces cellular ROS concentration, Fe2+ and MDA levels, and increases GSH activity, induces ferroptosis via m6A modification of the XC system and the methylation transferase METTL14 in shRNA-METTL14 CT26 and SW480 cells[1].
Curdione (12.5-50 μM, 48 h) induces cell apoptosis, and its apoptosis inhibitors (Z-VAD-FMK (HY-16658B)) have no effect on ferroptosis in SW480 cells[1].
Curdione (25-100 μM, 24 h) improves the survival rate in Isoproterenol (ISO) (HY-B0468)-induced H9c2 cells, decreases the cell injury in Erastin (HY-15763)-induced H9c2 cells[2].
Curdione (25-100 μM, 24 h) bounds to Keap1, regulates the Keap1/Trx1/GPX4 signaling pathway in H9c2 cells[2].
Curdione (100-200 μM) inhibits neutrophil extracellular trap (NET) formation in neutrophils isolated from mouse bone marrow stimulated with Phorbol 12-myristate 13-acetate (PMA) (HY-18739) or pyogenic platelets[3].
Curdione (160-500 μM, 48 h) does not affect cell viability, inhibits the differentiation of fibroblasts into myofibroblasts, inhibits TGF-β/Smad3 signaling in HPFs[5].
Curdione (0-500 μM, 12-72 h) reduces cell viability, inhibits the proliferation mediated by IDO1 against SK-UT-1 and SK-LMS-1 cells, with IC50s of 327 and 309.9 μM[7].
Curdione (0-100 μM, 24 h) induces G2/M phase arrest, apoptosis and autophagy mediated by IDO1 in SK-UT-1 and SK-LMS-1 cells[7].
Curdione (0-200 μg/mL, 72 h) induces apoptosis, impaires mitochondrial membrane potential occurred in MCF-7 cells (IC50 = 125.632 μg/mL)[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Inducted apoptosis, promoted the development of ferroptosis.
Had no statistically significant difference of ferroptosis when combined with Z-VAD-FMK (HY-16658B) (10 μM).
H9c2 cells/ Flag-Keap1, HA-GPX4, and Myc-Trx1 plasmids and tranfected to 293T cells
Concentration:
25 μM, 50 μM, 100 μM
Incubation Time:
24 h
Result:
Inhibited Keap1 expression and increased ISO-induced Trx1 expression, reduced interaction between Keap1 and Trx1 and increased complex between Trx1 and GPX4.
Up-regulated the cell cycle checkpoint proteins P21 and CyclinB1 and down-regulated Cdc2.
Increased cleavage of caspase 3, 6, and 9 without affecting caspase 8.
Up-regulateed LC3 and Beclin-1, and down-regulated P62, IDO1.
Induced apoptosis, increased the expressions of Bax, cleaved caspase-3 and caspase-9, decreased Bcl-2 expression.
In Vivo
Curdione (50-200 mg/kg, i.v., once a day, 22 days) inhibits tumor growth, induces ferroptosis mediated by m6A methylation via METTL14 and YTHDF2 in CRC xenograft nude mice[1].
Curdione (25-100 mg/kg, i.g., once a day, 7 days) attenuates myocardial injury, alleviates ferroptosis via regulating Keap1/Trx1/GPX4 signaling pathway in ISO-induced myocardial infarction male (MI) mice model[2].
Curdione (50-100 mg/kg, i.p., once) improves lung injury, reduce inflammation and oxidative stress levels, inhibit the activation of MAPK kinase and NF-κB P65, lung neutrophil infiltration and NET formation, regulate platelet activation, and reduce the interaction between neutrophils and platelets in the lungin cecal ligation and puncture (CLP) sepsis mice model[3].
Curdione (100 mg/kg, i.p., every 2 days, 21 days) reduces pulmonary fibrosis, expression of fibrosis-specific markers, and inhibits differentiation of fibroblasts into myofibroblasts Bleomycin (BLM) (HY-17565A)-induced Idiopathic pulmonary fibrosis (IPF) mouse model[5].
Curdione (100 mg/kg, i.g., once a day, 7 days) exerts neuroprotective effects against cerebral ischemia/reperfusion-induced brain injury through antioxidant and anti-apoptotic effects middle cerebral artery occlusion (MCAO) SD rats model[6].
Curdione (100-200 mg/kg, i.p., once a day, 21 days) suppresses the growth of uLMS by targeting IDO1 and activating apoptosis and autophagy in SK-UT-1 xenograft model[7].
Curdione (50-150 mg/kg, every two days, 16 days) inhibits tumor growth in MCE-7 xenograft BALB/c nude mice model[9]
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Suppressed tumor volume and mass, exhibited pronounced ruffling and nuclear chromatin boundary setting, accompanied by necrosis and fibrosis, and decreased cell density.
Increased iron, MDA, and LPO levels, and decreased GSH levels.
Increased protein expression of METTL14, YTHDF2, SLC7A11, and decreased protein expression levels of SLC3A2, HOXA13, and GPX4.
Increased mRNA expression of YTHDF2, SLC7A11, SLC3A2, HOXA13, and PTGS2 and decreased mRNA expression of GPX4.
Animal Model:
ISO (100 mg/kg)-induced MI C57BL/6 mice (21-25 g, 6-8 weeks) model[2]
Dosage:
25 mg/kg, 50 mg/kg, 100 mg/kg
Administration:
i.g., once a day, 7 days
Result:
Improved ejection fraction (EF), reduced ISO-increased CK-MB levels, restored normal muscle fiber structure, and reduced the degree of inflammatory cell infiltration in cardiac tissue.
Lowered MDA and iron levels and increaseed GSH, GPX4, FTH1 levels.
Inhibited Keap1 expression and increased ISO-induced Trx1 expression.
Reduced lung congestion, alveolar wall thickening, and inflammatory cell infiltration in lung sections, reduced lung injury scores, pulmonary edema, and reduced exudate protein levels in BALF and lung W/D ratio, as well as LDH activity in BALF.
Reduced CLP-induced increases in DHE and MDA, increased superoxide dismutase (SOD) levels, and decreased IL-1β, IL-6, and TNF-α levels in BALF.
Inhibited the phosphorylation of MAPK kinase and NF-κB P65, and reduced the activation of NF-κB P65.
Reduced CXCL4 and CXCL7 in BALF and reduced platelet activation in lung tissue.
Decreased MPO-positive neutrophils, total cell counts in BALF, and the number of infiltrating neutrophils in BALF.
Reduced fluorescence intensity of platelet activation markers CD42d/GP5, neutrophil marker Ly6G and the formation of NETs in the lungs.
Reduced infarct size and neurological deficits and promoted motor function and cognitive function recovery.
Reversed the obvious pathological abnormalities of the MCAO group, including loose arrangement of neurons, nuclear consolidation, loss of color staining or dark color.
Increased the activities of SOD, CAT and GSH-PX, suppressed the increase in the MDA content caused by the injury with cerebral ischemia/reperfusion.
Down-regulated Bax expression and up-regulated Bcl-2 expression, thereby increasing the Bcl-2/Bax ratio, reduced Cyt-C, c-caspase-3, and c-caspase-9 protein levels.
Exhibited anti-uLMS growth efficacy with minimal systemic toxicity, down-regulated IDO1, ki67, and p62, and up-regulated the cleaved caspase-3, Beclin1 and LC3 in tumor tissues.
Room temperature in continental US; may vary elsewhere.
Storage
Powder
-20°C
3 years
4°C
2 years
In solvent
-80°C
2 years
-20°C
1 year
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (423.10 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
4.2310 mL
21.1551 mL
42.3101 mL
5 mM
0.8462 mL
4.2310 mL
8.4620 mL
10 mM
0.4231 mL
2.1155 mL
4.2310 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.75 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (27.5 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
This protocol yields a clear solution of ≥ 2.75 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (27.5 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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