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Catalog No.S1218

11 publications

Clofarabine Chemical Structure

CAS No. 123318-82-1

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

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Selleck's Clofarabine has been cited by 11 publications

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  • 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 (RNR) (IC50 = 65 nM) and DNA polymerase. Clofarabine induces autophagy and apoptosis.
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 NHKyfpZEgXSxdH;4bYNqfHliYYPzZZk> NUD5cHhqS2:vcH;1coQhf2G|IITld5Rm\CCob4KgZ5l1d3SxeHnjbZR6KGGpYXnud5QhUzV4MjDj[YxtKGyrbnXzMEBKSzVyPUCuNFA{KM7:TR?= MonoNVc{OjV3Nh?=
HEp-2 cell NEjMR4tEgXSxdH;4bYNqfHliYYPzZZk> NXvwTnV4S2:vcH;1coQhf2G|IITld5Rm\CCob4KgZ5l1d3SxeHnjbZR6KGGpYXnud5QhUEWyLUKgZ4VtdCCuaX7ld{whUUN3ME2wMlAyOiEQvF2= M4O1U|E4OzJ3NU[=
NCI-H23 cells MoTIR5l1d3SxeHnjbZR6KGG|c3H5 Ml;zOUBl[Xm| MVrDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDOR2kuUDJ|IHPlcIx{KGGodHXyJFUh\GG7czDifUBUWkJiYYPzZZktKEeLNUC9NE4xPCEQvF2= NXi0U3Y5OTl7MkmwNFQ>
NCI-H23 cells MnrxSpVv[3Srb36gZZN{[Xl? NWfBbpJ7PSCmYYnz NITQOY1EgXSxc4TheIlkKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gUmNKNUh{MzDj[YxteyCjZoTldkA2KGSjeYOgZpkhW1KEIHHzd4F6NCCJSUWwQVAvODRizszN MWqyNVcyOTB3NB?=
CCRF-CEM cell lines MYjDfZRwfG:6aXPpeJkh[XO|YYm= NXTvXW9jS2:vcH;1coQhf2G|IITld5Rm\CCob4KgZ5l1d3SxeHnjbZR6KGGpYXnud5QhS0OURj3DSW0h[2WubDDsbY5meyxiSVO1NF0xNjB3IN88US=> NWHzXoc2OTd|MkW1Oi=>
MT4 cells Mk\RSpVv[3Srb36gZZN{[Xl? NVrhN4dMPSCmYYnz M3zIPWN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNWFQh[2WubIOgZYZ1\XJiNTDkZZl{KGK7IGPSRkBie3OjeTygS2k2OD1yLkC1NUDPxE1? MofwNlE4OTFyNUS=
PC3 cells MYPDfZRwfG:6aXPpeJkh[XO|YYm= NFHUU4w2KGSjeYO= M1ntPGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHBEOyClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNFY{KM7:TR?= NUHi[oFkOTl7MkmwNFQ>
BT549 cells NXrlR3pwS3m2b4TvfIlkcXS7IHHzd4F6 MlrmOUBl[Xm| NEPrT45EgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBDXDV2OTDj[YxteyCjZoTldkA2KGSjeYOgZpkhW1KEIHHzd4F6NCCJSUWwQVAvODZ3IN88US=> MV[xPVkzQTByNB?=
A549 cells NFvGcmVHfW6ldHnvckBie3OjeR?= NVPUUVZyPSCmYYnz NV;RSW9jS3m2b4P0ZZRq[yCjY4Tpeol1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHNTSiCjc4PhfUwhT0l3ME2wMlA5PiEQvF2= M{Ls[FIyPzFzMEW0
HL60 cells MXXGeY5kfGmxbjDhd5NigQ>? M3:1TlQ5KGh? MUjDfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSFy2NEBk\WyuczDh[pRmeiB2ODDodpMh[nliTWTUJIF{e2G7LDDJR|UxRTBwMTFOwG0> MoTPNlM5OjB3N{K=
HCT116 cells NUPCVplHTnWwY4Tpc44h[XO|YYm= MlTwOUBl[Xm| Mn\FR5l1d3O2YYTpZ{Bi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjDWFEyPiClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNVA3KM7:TR?= MlrBNlE4OTFyNUS=
DU145 cells MYDGeY5kfGmxbjDhd5NigQ>? M{H0fFUh\GG7cx?= M{fldGN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDEWVE1PSClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNVI2KM7:TR?= NFfvS3AzOTdzMUC1OC=>
HCT15 cells MWfGeY5kfGmxbjDhd5NigQ>? NWDMbZJNPSCmYYnz M{nrWmN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIR3QyPSClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNVgh|ryP M3WwelIyPzFzMEW0
L1210 cell NEXsS5dEgXSxdH;4bYNqfHliYYPzZZk> NILyZplEd22yb4Xu[EB4[XNidHXzeIVlKG[xcjDjfZRwfG:6aXPpeJkh[WejaX7zeEBNOTJzMDDj[YxtKGyrbnXzMEBKSzVyPUKuN{DPxE1? NXvOb4trOTd|MkW1Oi=>
Hs578 cells NIS5NZhHfW6ldHnvckBie3OjeR?= NHnybHo2KGSjeYO= M3z4d2N6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDId|U4QCClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUGuNlQyKM7:TR?= M3z3UlIyPzFzMEW0

... 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
Smiles C1=NC2=C(N=C(N=C2N1C3C(C(C(O3)CO)O)F)Cl)N

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03609814 Active not 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 Active not 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