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 NV62RpluS3m2b4TvfIlkcXS7IHHzd4F6 M171OGNwdXCxdX7kJJdieyC2ZYP0[YQh\m:{IHP5eI91d3irY3n0fUBi\2GrboP0JGs2PjJiY3XscEBtcW6nczygTWM2OD1yLkCwN{DPxE1? NUTzRYlUOTd|MkW1Oi=>
HEp-2 cell MoHER5l1d3SxeHnjbZR6KGG|c3H5 MVLDc41xd3WwZDD3ZZMhfGW|dHXkJIZweiCleYTveI95cWOrdImgZYdicW6|dDDISZAuOiClZXzsJIxqdmW|LDDJR|UxRTBwMEGyJO69VQ>? M{fKbFE4OzJ3NU[=
NCI-H23 cells NYTwUG8zTnWwY4Tpc44h[XO|YYm= M4PGOFUh\GG7cx?= NIr4XWZEgXSxc4TheIlkKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gUmNKNUh{MzDj[YxteyCjZoTldkA2KGSjeYOgZpkhW1KEIHHzd4F6NCCJSUWwQVAvODRizszN M2r5UFIyPzFzMEW0
CCRF-CEM cell lines NYTrO3Q4S3m2b4TvfIlkcXS7IHHzd4F6 NV;wVWgzS2:vcH;1coQhf2G|IITld5Rm\CCob4KgZ5l1d3SxeHnjbZR6KGGpYXnud5QhS0OURj3DSW0h[2WubDDsbY5meyxiSVO1NF0xNjB3IN88US=> M3jLU|E4OzJ3NU[=
MT4 cells NVzDVmhQTnWwY4Tpc44h[XO|YYm= MknpOUBl[Xm| M4nSWGN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNWFQh[2WubIOgZYZ1\XJiNTDkZZl{KGK7IGPSRkBie3OjeTygS2k2OD1yLkC1NUDPxE1? M2PkclIyPzFzMEW0
PC3 cells NV;BVlN2S3m2b4TvfIlkcXS7IHHzd4F6 NWP0SmR{PSCmYYnz MX7DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDQR|Mh[2WubIOgZYZ1\XJiNTDkZZl{KGK7IGPSRkBie3OjeTygS2k2OD1yLkC2N{DPxE1? M3TpWlE6QTJ7MEC0
BT549 cells M{nXRmN6fG:2b4jpZ4l1gSCjc4PhfS=> MWG1JIRigXN? MV7DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDCWFU1QSClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNFY2KM7:TR?= M1v6W|E6QTJ7MEC0
A549 cells NYnIVVdDTnWwY4Tpc44h[XO|YYm= MV61JIRigXN? M4r4UWN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzJIFnfGW{IEWg[IF6eyCkeTDTVmIh[XO|YYmsJGdKPTB;MD6wPFYh|ryP NXK2Znl5OjF5MUGwOVQ>
HL60 cells Ml3sSpVv[3Srb36gZZN{[Xl? NIHUOpM1QCCq M{DwXGN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIUFYxKGOnbHzzJIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;MD6xJO69VQ>? NH\xclkzOzh{MEW3Ni=>
HCT116 cells NGTae2ZHfW6ldHnvckBie3OjeR?= MVG1JIRigXN? MmnhR5l1d3O2YYTpZ{Bi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjDWFEyPiClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNVA3KM7:TR?= NYr0VFRTOjF5MUGwOVQ>
DU145 cells NXzuUYFQTnWwY4Tpc44h[XO|YYm= M2npe|Uh\GG7cx?= M{n2XmN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDEWVE1PSClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNVI2KM7:TR?= NXHibVZYOjF5MUGwOVQ>
HCT15 cells M1P2WGZ2dmO2aX;uJIF{e2G7 Mn;VOUBl[Xm| M4[zOGN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIR3QyPSClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNVgh|ryP MUGyNVcyOTB3NB?=
L1210 cell NG\jXotEgXSxdH;4bYNqfHliYYPzZZk> MmTFR49ueG:3bnSge4F{KHSnc4Tl[EBnd3JiY4n0c5RwgGmlaYT5JIFo[Wmwc4SgUFEzOTBiY3XscEBtcW6nczygTWM2OD1{LkOg{txO M1\PVFE4OzJ3NU[=
Hs578 cells MXrGeY5kfGmxbjDhd5NigQ>? MmjoOUBl[Xm| M4i2SWN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDId|U4QCClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUGuNlQyKM7:TR?= NYfEWmRmOjF5MUGwOVQ>

... 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 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