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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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. 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 M2\VfmN6fG:2b4jpZ4l1gSCjc4PhfS=> MmrOR49ueG:3bnSge4F{KHSnc4Tl[EBnd3JiY4n0c5RwgGmlaYT5JIFo[Wmwc4SgT|U3OiClZXzsJIxqdmW|LDDJR|UxRTBwMECzJO69VQ>? NE\FO3UyPzN{NUW2
HEp-2 cell MYrDfZRwfG:6aXPpeJkh[XO|YYm= NWPtUoNnS2:vcH;1coQhf2G|IITld5Rm\CCob4KgZ5l1d3SxeHnjbZR6KGGpYXnud5QhUEWyLUKgZ4VtdCCuaX7ld{whUUN3ME2wMlAyOiEQvF2= M{GwNlE4OzJ3NU[=
NCI-H23 cells Mo\ER5l1d3SxeHnjbZR6KGG|c3H5 MXi1JIRigXN? M{HzWWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG5EUS2KMkOgZ4VtdHNiYX\0[ZIhPSCmYYnzJIJ6KFOUQjDhd5NigSxiR1m1NF0xNjB2IN88US=> NETrOmcyQTl{OUCwOC=>
NCI-H23 cells MmjkSpVv[3Srb36gZZN{[Xl? MkXmOUBl[Xm| MVrDfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWgzOyClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNFQh|ryP Mlr6NlE4OTFyNUS=
CCRF-CEM cell lines MYXDfZRwfG:6aXPpeJkh[XO|YYm= MXTDc41xd3WwZDD3ZZMhfGW|dHXkJIZweiCleYTveI95cWOrdImgZYdicW6|dDDDR3JHNUOHTTDj[YxtKGyrbnXzMEBKSzVyPUCuNFUh|ryP NY\nRmlQOTd|MkW1Oi=>
PC3 cells MVzDfZRwfG:6aXPpeJkh[XO|YYm= MoiyOUBl[Xm| NUCyNVRuS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hWEN|IHPlcIx{KGGodHXyJFUh\GG7czDifUBUWkJiYYPzZZktKEeLNUC9NE4xPjNizszN NVfGbYhlOTl7MkmwNFQ>
BT549 cells M17ycmN6fG:2b4jpZ4l1gSCjc4PhfS=> NIfSVWw2KGSjeYO= MXTDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDCWFU1QSClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNFY2KM7:TR?= NHzHZpoyQTl{OUCwOC=>
A549 cells M2fQT2Z2dmO2aX;uJIF{e2G7 NIm2ems2KGSjeYO= MYTDfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iQUW0PUBk\WyuczDh[pRmeiB3IHThfZMh[nliU2LCJIF{e2G7LDDHTVUxRTBwMEi2JO69VQ>? MnewNlE4OTFyNUS=
HL60 cells M4H4PGZ2dmO2aX;uJIF{e2G7 NG\xWXY1QCCq NVnhSW1pS3m2b4P0ZZRq[yCjY4Tpeol1gSCjZ3HpcpN1KGi3bXHuJGhNPjBiY3XscJMh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlEh|ryP NX3lNYlSOjN6MkC1O|I>
HCT116 cells NXfOOVZSTnWwY4Tpc44h[XO|YYm= NYWxTZVxPSCmYYnz M2HOTmN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIR3QyOTZiY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHNTSiCjc4PhfUwhT0l3ME2wMlExPiEQvF2= M3zHd|IyPzFzMEW0
DU145 cells NFnrXFdHfW6ldHnvckBie3OjeR?= MoO0OUBl[Xm| MYrDfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iRGWxOFUh[2WubIOgZYZ1\XJiNTDkZZl{KGK7IGPSRkBie3OjeTygS2k2OD1yLkGyOUDPxE1? NXewdHNmOjF5MUGwOVQ>
HCT15 cells NIHBT2dHfW6ldHnvckBie3OjeR?= NGXHNGw2KGSjeYO= MmjrR5l1d3O2YYTpZ{Bi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjDWFE2KGOnbHzzJIFnfGW{IEWg[IF6eyCkeTDTVmIh[XO|YYmsJGdKPTB;MD6xPEDPxE1? NHnNToczOTdzMUC1OC=>
L1210 cell NH3iSHhEgXSxdH;4bYNqfHliYYPzZZk> NX:2RppVS2:vcH;1coQhf2G|IITld5Rm\CCob4KgZ5l1d3SxeHnjbZR6KGGpYXnud5QhVDF{MUCgZ4VtdCCuaX7ld{whUUN3ME2yMlMh|ryP M1vFcFE4OzJ3NU[=
Hs578 cells NGS4[oxHfW6ldHnvckBie3OjeR?= NHnObIg2KGSjeYO= MkDGR5l1d3O2YYTpZ{Bi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjzOVc5KGOnbHzzJIFnfGW{IEWg[IF6eyCkeTDTVmIh[XO|YYmsJGdKPTB;MT6yOFEh|ryP M4LEVlIyPzFzMEW0

... 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:
2% DMSO+30% PEG 300 +1% Tween 80+ddH2O

* 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
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01629082 Completed Myeldysplastic Syndrome (MDS)|Chronic Myelomonocytic Leukemia|Bone Marrow Diseases|Neutropenia|Acute Myeloid Leukemia (AML) National Heart, Lung, and Blood Institute (NHLBI)|Celgene Corporation|National Institutes of Health Clinical Center (CC) June 5, 2012 Phase 1
NCT02211755 Recruiting Neoplasms|Myelodysplastic Syndromes National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) July 30, 2014 Phase 1
NCT01701986 Recruiting Lymphoma M.D. Anderson Cancer Center October 25, 2012 Phase 1|Phase 2
NCT02727803 Recruiting Leukemia|Lymphoma|Myeloma|Myeloproliferative Diseases M.D. Anderson Cancer Center May 2016 Phase 2
NCT02686593 Recruiting Acute Myeloid Leukemia The University of Hong Kong February 2016 Phase 2
NCT02925351 Recruiting Autoimmune Disease|Crohn Disease|Inflammatory Disorder|Rheumatoid Arthritis|Systemic Lupus Erythematosus|Takayasu Arteritis Jonsson Comprehensive Cancer Center|National Cancer Institute (NCI) January 2016 --

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID