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 MYTDfZRwfG:6aXPpeJkh[XO|YYm= MVPDc41xd3WwZDD3ZZMhfGW|dHXkJIZweiCleYTveI95cWOrdImgZYdicW6|dDDLOVYzKGOnbHygcIlv\XNuIFnDOVA:OC5yMEOg{txO NXnFU2ZCOTd|MkW1Oi=>
HEp-2 cell MVTDfZRwfG:6aXPpeJkh[XO|YYm= M2jYcWNwdXCxdX7kJJdieyC2ZYP0[YQh\m:{IHP5eI91d3irY3n0fUBi\2GrboP0JGhGeC1{IHPlcIwhdGmwZYOsJGlEPTB;MD6wNVIh|ryP Mke4NVc{OjV3Nh?=
NCI-H23 cells Ml;mR5l1d3SxeHnjbZR6KGG|c3H5 NG\Qb4o2KGSjeYO= M1L3bWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG5EUS2KMkOgZ4VtdHNiYX\0[ZIhPSCmYYnzJIJ6KFOUQjDhd5NigSxiR1m1NF0xNjB2IN88US=> NUTiXYNrOTl7MkmwNFQ>
NCI-H23 cells NEjuTppHfW6ldHnvckBie3OjeR?= NYqzWmpFPSCmYYnz M1PMTmN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2kuUDJ|IHPlcIx{KGGodHXyJFUh\GG7czDifUBUWkJiYYPzZZktKEeLNUC9NE4xPCEQvF2= NGnLVJozOTdzMUC1OC=>
CCRF-CEM cell lines NFKy[nVEgXSxdH;4bYNqfHliYYPzZZk> M4fLbGNwdXCxdX7kJJdieyC2ZYP0[YQh\m:{IHP5eI91d3irY3n0fUBi\2GrboP0JGNEWkZvQ1XNJINmdGxibHnu[ZMtKEmFNUC9NE4xPSEQvF2= NVPRW|dGOTd|MkW1Oi=>
MT4 cells M4LObGZ2dmO2aX;uJIF{e2G7 NX\qdJFpPSCmYYnz Mly5R5l1d3O2YYTpZ{Bi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3UOEBk\WyuczDh[pRmeiB3IHThfZMh[nliU2LCJIF{e2G7LDDHTVUxRTBwMEWxJO69VQ>? M1qz[VIyPzFzMEW0
PC3 cells M4PSZmN6fG:2b4jpZ4l1gSCjc4PhfS=> M4jR[VUh\GG7cx?= NGPaT2VEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBRSzNiY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHNTSiCjc4PhfUwhT0l3ME2wMlA3OyEQvF2= NHiyOVUyQTl{OUCwOC=>
BT549 cells NHfyPWtEgXSxdH;4bYNqfHliYYPzZZk> M1fNNVUh\GG7cx?= M2rXd2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGJVPTR7IHPlcIx{KGGodHXyJFUh\GG7czDifUBUWkJiYYPzZZktKEeLNUC9NE4xPjVizszN M1G5flE6QTJ7MEC0
A549 cells M{nTOmZ2dmO2aX;uJIF{e2G7 NVXQb5pzPSCmYYnz M1[zPWN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzJIFnfGW{IEWg[IF6eyCkeTDTVmIh[XO|YYmsJGdKPTB;MD6wPFYh|ryP NEHyTWozOTdzMUC1OC=>
HL60 cells MlK0SpVv[3Srb36gZZN{[Xl? NF:4[os1QCCq NF20SoREgXSxc4TheIlkKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gTGw3OCClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUCuNUDPxE1? NXPC[pNyOjN6MkC1O|I>
HCT116 cells MnKwSpVv[3Srb36gZZN{[Xl? M4[1RlUh\GG7cx?= MVzDfZRwe3SjdHnjJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSFPUNVE3KGOnbHzzJIFnfGW{IEWg[IF6eyCkeTDTVmIh[XO|YYmsJGdKPTB;MD6xNFYh|ryP NFX6To8zOTdzMUC1OC=>
DU145 cells NV32PVZMTnWwY4Tpc44h[XO|YYm= NUPEZ4RwPSCmYYnz M3rnSWN6fG:|dHH0bYMh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDEWVE1PSClZXzsd{Bi\nSncjC1JIRigXNiYomgV3JDKGG|c3H5MEBIUTVyPUCuNVI2KM7:TR?= M2f1WFIyPzFzMEW0
HCT15 cells MUXGeY5kfGmxbjDhd5NigQ>? MnSyOUBl[Xm| NGTq[JFEgXSxc4TheIlkKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gTGNVOTViY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHNTSiCjc4PhfUwhT0l3ME2wMlE5KM7:TR?= NGLSfJYzOTdzMUC1OC=>
L1210 cell MXTDfZRwfG:6aXPpeJkh[XO|YYm= Mkf3R49ueG:3bnSge4F{KHSnc4Tl[EBnd3JiY4n0c5RwgGmlaYT5JIFo[Wmwc4SgUFEzOTBiY3XscEBtcW6nczygTWM2OD1{LkOg{txO NUjCbJFvOTd|MkW1Oi=>
Hs578 cells MVrGeY5kfGmxbjDhd5NigQ>? MY[1JIRigXN? NE\EPWFEgXSxc4TheIlkKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gTJM2PzhiY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHNTSiCjc4PhfUwhT0l3ME2xMlI1OSEQvF2= NX3aWFhFOjF5MUGwOVQ>

... 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