Catalog No.S1218

Clofarabine Chemical Structure

Molecular Weight(MW): 303.68

Clofarabine inhibits the enzymatic activities of ribonucleotide reductase (IC50 = 65 nM) and DNA polymerase.

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In DMSO USD 90 In stock
USD 70 In stock
USD 270 In stock
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Cited by 6 Publications

2 Customer Reviews

  • Immunoblot analysis of cell lysates of NCI-H929 cells treated with CLO (5 μM, 3-48 h) GAPDH served as the loading control for each membrane, and data are representative of at least two independent experiments

    Clin Cancer Res, 2017, 23(17):5225-5237. Clofarabine purchased from Selleck.

    Population-based pharmacokinetic modeling of plasma pharmacokinetic study and cerebral microdialysis study. Representative individual plasma and/or tumor ECF concentration-time profile of unbound clofarabine from plasma pharmacokinetic study (a) and cerebral microdialysis study (b) (open circles and triangles represent observed clofarabine unbound plasma and tumor ECF concentrations, respectively; Dotted and solid lines represent model-predicted individual unbound plasma and tumor ECF concentrations, respectively). Box plot comparison of individual volume of peripheral compartment (c) and systemic clearance (d) between plasma pharmacokinetic study (45 mg/kg clofarabine) and cerebral microdialysis study (30 mg/kg clofarabine).

    Cancer Chemoth Pharm, 2015, 75:897-906.. Clofarabine purchased from Selleck.

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Biological Activity

Description Clofarabine inhibits the enzymatic activities of ribonucleotide reductase (IC50 = 65 nM) and DNA polymerase.
Ribonucleotide reductase [1]
(Cell-free assay)
65 nM
In vitro

Clofarabine is efficiently transported into cells via two facilitative or equilibrative nucleoside transporters, hENT1 and hENT2, and a concentrative nucleoside transporter, hCNT253. Clofarabine is phosphorylated in a stepwise manner by cytosolic kinases to the nucleotide analogues clofarabine 5′-mono-, di- and triphosphate following entry into cells, with Clofarabine triphosphate being the active form. Clofarabine 5′-mono-, di- and triphosphate are not substrates for nucleoside transporters and must be enzymatically converted by 5′-nucleotidase back to their dephosphorylated nucleoside form for transport out of the cell. Clofarabine triphosphate is a potent inhibitor of ribonucleotide reductase (IC50 = 65 nM), presumably by binding to the allosteric site on the regulatory subunit. Clofarabine has also been shown to act directly on mitochondria by altering the transmembrane potential with release of cytochrome c, apoptotic-inducing factor (AIF), apoptosis protease-activating factor 1 (APAF1) and caspase 9 into the cytosol. Clofarabine demonstrates strong in vitro growth inhibition and cytotoxic activity (IC50 values = 0.028–0.29 μM) in a wide variety of leukaemia and solid tumour cell lines. Clofarabine has been shown to increase the activity of dCK in HL60 cells, and increases the formation of the mono-, di-, and triphosphates of ara-C in K562 cells36. [1] Clofarabine (10 μM) inhibits the repair initiated by 4-hydroperoxycyclophosphamide (4-HC), with inhibition peaking at the intracellular concentrations of 5 μM in chronic lymphocytic leukemia (CLL) lymphocytes. Clofarabine (10 μM) combined with 4-hydroperoxycyclophosphamide (4-HC) produces more than additive apoptotic cell death than the sum of each alone. [2] Clofarabine (1 μM) combined with ara-C (10 μM) results in a biochemical modulation of ara-CTP and synergistic cell kill in K562 cells. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
K562 cell MY\DfZRwfG:6aXPpeJkh[XO|YYm= M4\0bGNwdXCxdX7kJJdieyC2ZYP0[YQh\m:{IHP5eI91d3irY3n0fUBi\2GrboP0JGs2PjJiY3XscEBtcW6nczygTWM2OD1yLkCwN{DPxE1? NF21WJUyPzN{NUW2
HEp-2 cell NF3FSZpEgXSxdH;4bYNqfHliYYPzZZk> NGPSVWJEd22yb4Xu[EB4[XNidHXzeIVlKG[xcjDjfZRwfG:6aXPpeJkh[WejaX7zeEBJTXBvMjDj[YxtKGyrbnXzMEBKSzVyPUCuNFEzKM7:TR?= M33IdlE4OzJ3NU[=
NCI-H23 cells NWTrdGg6S3m2b4TvfIlkcXS7IHHzd4F6 MlSyOUBl[Xm| M2LIVGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG5EUS2KMkOgZ4VtdHNiYX\0[ZIhPSCmYYnzJIJ6KFOUQjDhd5NigSxiR1m1NF0xNjB2IN88US=> NGPsSHQyQTl{OUCwOC=>
NCI-H23 cells NYPacpNzTnWwY4Tpc44h[XO|YYm= NEPDZpM2KGSjeYO= M3jQOmN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2kuUDJ|IHPlcIx{KGGodHXyJFUh\GG7czDifUBUWkJiYYPzZZktKEeLNUC9NE4xPCEQvF2= MY[yNVcyOTB3NB?=
CCRF-CEM cell lines NHfUcldEgXSxdH;4bYNqfHliYYPzZZk> Ml7sR49ueG:3bnSge4F{KHSnc4Tl[EBnd3JiY4n0c5RwgGmlaYT5JIFo[Wmwc4SgR2NTTi2FRV2gZ4VtdCCuaX7ld{whUUN3ME2wMlA2KM7:TR?= M{m5Z|E4OzJ3NU[=
PC3 cells MXrDfZRwfG:6aXPpeJkh[XO|YYm= MlH1OUBl[Xm| M4H1bGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHBEOyClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNFY{KM7:TR?= MY[xPVkzQTByNB?=
BT549 cells M13SN2N6fG:2b4jpZ4l1gSCjc4PhfS=> M{fuSVUh\GG7cx?= NULiUWRrS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSlR3NEmgZ4VtdHNiYX\0[ZIhPSCmYYnzJIJ6KFOUQjDhd5NigSxiR1m1NF0xNjB4NTFOwG0> MWmxPVkzQTByNB?=
A549 cells MXfGeY5kfGmxbjDhd5NigQ>? Mo\JOUBl[Xm| NUHtNJc1S3m2b4P0ZZRq[yCjY4Tpeol1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHNTSiCjc4PhfUwhT0l3ME2wMlA5PiEQvF2= MXGyNVcyOTB3NB?=
HL60 cells NHjEWI9HfW6ldHnvckBie3OjeR?= M4TRfFQ5KGh? NYnzSXN3S3m2b4P0ZZRq[yCjY4Tpeol1gSCjZ3HpcpN1KGi3bXHuJGhNPjBiY3XscJMh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlEh|ryP NYrGepVGOjN6MkC1O|I>
HCT116 cells MVrGeY5kfGmxbjDhd5NigQ>? Mmq5OUBl[Xm| MVnDfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSFPUNVE3KGOnbHzzJIFnfGW{IEWg[IF6eyCkeTDTVmIh[XO|YYmsJGdKPTB;MD6xNFYh|ryP MY[yNVcyOTB3NB?=
DU145 cells NIXCZWhHfW6ldHnvckBie3OjeR?= MoX5OUBl[Xm| MUfDfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iRGWxOFUh[2WubIOgZYZ1\XJiNTDkZZl{KGK7IGPSRkBie3OjeTygS2k2OD1yLkGyOUDPxE1? M1jJXVIyPzFzMEW0
HCT15 cells MVnGeY5kfGmxbjDhd5NigQ>? M4P3OlUh\GG7cx?= MU\DfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSFPUNVUh[2WubIOgZYZ1\XJiNTDkZZl{KGK7IGPSRkBie3OjeTygS2k2OD1yLkG4JO69VQ>? MXWyNVcyOTB3NB?=
L1210 cell NXe4TIxvS3m2b4TvfIlkcXS7IHHzd4F6 M2nrfmNwdXCxdX7kJJdieyC2ZYP0[YQh\m:{IHP5eI91d3irY3n0fUBi\2GrboP0JGwyOjFyIHPlcIwhdGmwZYOsJGlEPTB;Mj6zJO69VQ>? MYOxO|MzPTV4
Hs578 cells M3y5fWZ2dmO2aX;uJIF{e2G7 MXK1JIRigXN? NG\rfohEgXSxc4TheIlkKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gTJM2PzhiY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHNTSiCjc4PhfUwhT0l3ME2xMlI1OSEQvF2= NXzIPZViOjF5MUGwOVQ>

... Click to View More Cell Line Experimental Data

In vivo Clofarabine administered intraperitoneally has significant activity against a wide variety of human tumour xenografts implanted subcutaneously in athymic nude or severe combined immune deficiency mice. [1]


Solubility (25°C)

In vitro DMSO 60 mg/mL (197.57 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300 +1% Tween 80+ddH2O
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 303.68


CAS No. 123318-82-1
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03609814 Recruiting -- Hematologic Malignancies|Nonmalignant Diseases|Immunodeficiencies|Hemoglobinopathies|Genetic Inborn Errors of Metabolism|Fanconi''s Anemia|Thalassemia|Sickle Cell Disease University of California San Francisco February 2016 --
NCT02425904 Recruiting Drug: Clofarabine Langerhans Cell Histiocytosis Dana-Farber Cancer Institute|Sanofi|St. Baldrick''s Foundation|Cookies for Kids'' Cancer|North American Consortium for Histiocytosis May 2015 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID