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Deferiprone is a potent, orally active, brain-penetrant, cell-penetrant, skin-permeable, free iron chelating agent. Deferiprone inhibits the proliferation and migration, and stimulates apoptosis in tumor cell. Deferiprone can inhibit KDM. Deferiprone has antianemic, neuroprotective, anti-inflammatory, antioxidant, and antidotal activity. Deferiprone can be used in cancer, cardiovascular disease, infection, inflammation, and neurological disease study.
For research use only. We do not sell to patients.
Immunofluorescence staining for MyHC, MyoD and MyoG in C2C12 cells treated with 0, 10, 50 and 100 µM Deferiprone (DFP) in differentiation medium for 3 days.
A549 cells were treated with b-ELE for 24 h, CA-AM was added to cells at the final
concentration of 0.5 μM, followed by adding iron chelator Deferiprone (DFP, 100 μM) for 1 h.
Deferiprone (DFP) (1 mM, 24 h) treatment resulted in a moderate reduction of the levels of TIMM23 and HSPD1/HSP60, and no change of ATP5F1A by immunoblotted.
Deferiprone is a potent, orally active, brain-penetrant, cell-penetrant, skin-permeable, free iron chelating agent. Deferiprone inhibits the proliferation and migration, and stimulates apoptosis in tumor cell. Deferiprone can inhibit KDM. Deferiprone has antianemic, neuroprotective, anti-inflammatory, antioxidant, and antidotal activity. Deferiprone can be used in cancer, cardiovascular disease, infection, inflammation, and neurological disease study[1][2][3][4][5][6][7][8].
Cellular Effect
Cell Line
Type
Value
Description
References
A-375
IC50
27.24 μM
Compound: DFP
Cytotoxicity against human A-375 cells assessed as reduction in cell viability preincubated for 4 hrs under dark condition in presence of 5-aminolevulinic acid followed by irradiation with blue light at 2.5 J.cm^-2 energy level for 5 mins and measured after 18 hrs by MTT assay
Cytotoxicity against human A-375 cells assessed as reduction in cell viability preincubated for 4 hrs under dark condition in presence of 5-aminolevulinic acid followed by irradiation with blue light at 2.5 J.cm^-2 energy level for 5 mins and measured after 18 hrs by MTT assay
Cytotoxicity against human HeLa cells assessed as reduction in cell viability preincubated for 4 hrs under dark condition in presence of 5-aminolevulinic acid followed by irradiation with blue light at 2.5 J.cm^-2 energy level for 5 mins and measured after 18 hrs by MTT assay
Cytotoxicity against human HeLa cells assessed as reduction in cell viability preincubated for 4 hrs under dark condition in presence of 5-aminolevulinic acid followed by irradiation with blue light at 2.5 J.cm^-2 energy level for 5 mins and measured after 18 hrs by MTT assay
Cytotoxicity against human MCF7 cells assessed as reduction in cell viability preincubated for 4 hrs under dark condition in presence of 5-aminolevulinic acid followed by irradiation with blue light at 2.5 J.cm^-2 energy level for 5 mins and measured after 18 hrs by MTT assay
Cytotoxicity against human MCF7 cells assessed as reduction in cell viability preincubated for 4 hrs under dark condition in presence of 5-aminolevulinic acid followed by irradiation with blue light at 2.5 J.cm^-2 energy level for 5 mins and measured after 18 hrs by MTT assay
Deferiprone (66-660 μM, 48-96 h) has a significant inhibitory effect on proliferation in TRAMP-C2, Myc-CaP, and 22rv1 cells[1].
Deferiprone (100 μM, up to 192 h) inhibits cell migration in TRAMP-C2, Myc-CaP, and 22rv1 cells[1].
Deferiprone (100 μM, 24 h) reduces the expression and activity of m-Acon in TRAMP-C2, Myc-CaP, and 22rv1 cells[1].
Deferiprone (up to 1μM, 0.5-24 h) decreases the free iron in thalassemic red blood cells[2].
Deferiprone (10 mins) inhibits human platelet aggregation stimulated by AA and ADP and epinephrine and collagen, with the IC50 values of 0.24, 0.25, 3.36 and 3.73 mM, respectively[3].
Deferiprone (0.1-3.2 μM, 5 mins) inhibits COX-1 activity with the IC50 value of 0.33 μM[3].
Deferiprone (4 mM, 5 mins) preventes ADP-induced formation of cAMP[3].
Deferiprone (156.25 μg/mL, 24 h) enhances survival rate and reduces LDH Levels and displays normal cell morphology in aged Fibroblasts[4].
Deferiprone (25μM, 6 h) amplifies the antibacterial activity of conventional antibiotics against S. epidermidis[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
0 to 30 h for TRAMP-C2, and Myc-CaP; 0 to 192 h for 22rv1
Result:
Inhibited cell migration starting at different time points for each cell line, ranging from 12 h in TRAMP-C2 cell to 48 h in 22rv1 cells, and 30 h in Myc-CaP cells.
Reduced the expression of m-Acon, by 2-fold in Myc-CaP and 22 rv1 cells and decreased by 79% in TRAMP-C2 cells.
In Vivo
Deferiprone (100 mg/kg/daily for i.g., 4 weeks) has a neuroprotective effect in the rTg(tauP301L)4510 mouse model of tauopathy[6].
Deferiprone (50-200 mg/kg/daily for p.o., 5-10 day) reduces the nephrotoxicity in Cisplatin (HY-17394)-induced rat acute renal failure[7].
Deferiprone (13.82, 27.64 mg/kg/d for i.g., 4 weeks) exhibits anti- apoptosis and neuroprotective activity in rat Alzheimer’s disease model[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
The rTg(tauP301L)4510 mouse model of tauopathy[6].
Dosage:
100 mg/kg/daily, 4 weeks
Administration:
Intragastric administration (i.g.)
Result:
Improved Y-maze and open field performance, and decreased 28% iron levels in brain, and reduced AT8-labeled p-tau within the hippocampus in transgenic tau mice.
Animal Model:
Cisplatin(HY-17394)-induced rat acute renal failure model [7]
Dosage:
50, 100, 200 mg/kg, 5-10 day
Administration:
Oral administration
Result:
Reduced the creatinine, BUN, malondialdehyde, iron concentrations, and the amounts of TfR, and indreased the levels of HIF-1a and related anti-apoptotic genes expression in Cisplatin (HY-17394)-injected animals.
Animal Model:
Aluminium-linked apoptosis in rat hippocampus model (Alzheimer’s disease model) [8]
Dosage:
13.82, 27.64 mg/kg/d, 4 week
Administration:
Intragastric administration lasting 6 days with 1 day interval per week
Result:
Decreased the apoptosis and the expression of Caspase-3 and Bax, and increased the expression of Bcl-2 in Aluminium-linked apoptosis in rat hippocampus.
Room temperature in continental US; may vary elsewhere.
Storage
Powder
-20°C
3 years
4°C
2 years
In solvent
-80°C
6 months
-20°C
1 month
Solvent & Solubility
In Vitro:
DMSO : 7.14 mg/mL (51.31 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : 3.33 mg/mL (23.93 mM; Need ultrasonic)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
7.1865 mL
35.9324 mL
71.8649 mL
5 mM
1.4373 mL
7.1865 mL
14.3730 mL
10 mM
0.7186 mL
3.5932 mL
7.1865 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, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
*
Note: If you choose water as the stock solution, please dilute it to the working solution,
then filter and sterilize it with a 0.22 μm filter before use.
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 ≥ 0.71 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (7.1 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 ≥ 0.71 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 (7.1 mg/mL) to 900 μLCorn oil, and mix evenly.
For the following dissolution methods, please prepare the working solution directly.
It is recommended to prepare fresh solutions and use them promptly within a short period of time. 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.
Protocol 1
Add each solvent one by one: PBS
Solubility: 10 mg/mL (71.86 mM); Clear solution; Need ultrasonic
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, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Optional Solvent
ConcentrationSolventMass
1 mg
5 mg
10 mg
25 mg
H2O / DMSO
1 mM
7.1865 mL
35.9324 mL
71.8649 mL
179.6622 mL
5 mM
1.4373 mL
7.1865 mL
14.3730 mL
35.9324 mL
10 mM
0.7186 mL
3.5932 mL
7.1865 mL
17.9662 mL
15 mM
0.4791 mL
2.3955 mL
4.7910 mL
11.9775 mL
20 mM
0.3593 mL
1.7966 mL
3.5932 mL
8.9831 mL
DMSO
25 mM
0.2875 mL
1.4373 mL
2.8746 mL
7.1865 mL
30 mM
0.2395 mL
1.1977 mL
2.3955 mL
5.9887 mL
40 mM
0.1797 mL
0.8983 mL
1.7966 mL
4.4916 mL
50 mM
0.1437 mL
0.7186 mL
1.4373 mL
3.5932 mL
*
Note: If you choose water as the stock solution, please dilute it to the working solution,
then filter and sterilize it with a 0.22 μm filter before use.
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.
Customer Validation
mRNA levels of MyHC, MyoD and MyoG in C2C12 cells treated with 0, 10, 25, 50, 75 and
100 µM Deferiprone (DFP) in differentiation medium for 3 days.
Customer Validation
Immunofluorescence staining for MyHC, MyoD and MyoG in C2C12 cells treated with 0, 10, 50 and 100 µM Deferiprone (DFP) in differentiation medium for 3 days.
Customer Validation
A549 cells were treated with b-ELE for 24 h, CA-AM was added to cells at the final
concentration of 0.5 μM, followed by adding iron chelator Deferiprone (DFP, 100 μM) for 1 h.
Customer Validation
Deferiprone (DFP) (1 mM, 24 h) treatment resulted in a moderate reduction of the levels of TIMM23 and HSPD1/HSP60, and no change of ATP5F1A by immunoblotted.
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