1. Metabolic Enzyme/Protease
    Apoptosis
  2. Adenosine Deaminase
    Apoptosis
  3. Cladribine

Cladribine (Synonyms: 2-Chloro-2′-deoxyadenosine; CldAdo; 2CdA)

Cat. No.: HY-13599 Purity: 99.97%
Handling Instructions

Cladribine (2CdA), a purine nucleoside analog, is an orally active adenosine deaminase inhibitor. Cladribine functions as an inhibitor of DNA synthesis to block the repair of the damaged DNA. Cladribine can inhibit DNA methylation. Cladribine has anti-lymphoma activity and can be used for the research of several hematologic malignancies and multiple sclerosis.

For research use only. We do not sell to patients.

Cladribine Chemical Structure

Cladribine Chemical Structure

CAS No. : 4291-63-8

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Customer Review

Based on 3 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Cladribine purchased from MCE. Usage Cited in: Chem Pharm Bull (Tokyo). 2017 Aug 1;65(8):768-775.

    Changes in Bcl-2 protein expression in MCF-7 cells after treatment with Cladribine, Dasatinib or Gefitinib alone or in combination for 12 h. Expression of Bcl-2 protein is analyzed by western blotting analysis.
    • Biological Activity

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    Description

    Cladribine (2CdA), a purine nucleoside analog, is an orally active adenosine deaminase inhibitor. Cladribine functions as an inhibitor of DNA synthesis to block the repair of the damaged DNA. Cladribine can inhibit DNA methylation. Cladribine has anti-lymphoma activity and can be used for the research of several hematologic malignancies and multiple sclerosis[1][2].

    IC50 & Target

    Adenosine deaminase[2]

    In Vitro

    Cladribine (0.25-4 μM; 24-48 hours) inhibits human DLBCL cells proliferation[1].
    Cladribine (1-4 μM; 24 hours) induces G1 phase arrest via decreasing the expressions of Cyclin D1 and Cyclin E, and increasing the expressions of p21 and p27 in DLBCL cells[1].
    Cladribine (1-4 μM; 24 hours) induces apoptosis and activates extrinsic and intrinsic signaling pathways in human DLBCL cells[1].
    Cladribine (1-4 μM; 24 hours) activates endoplasmic reticulum stress[1].
    Cladribine inhibits cell proliferation of multiple myeloma (MM) cells in a dose-dependent manner; with IC50s of approximately 2.43 μM, 0.75 μM and 0.18 μM for U266, RPMI8226 and MM1.S cells, respectively[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Proliferation Assay[1]

    Cell Line: The human DLBCL cell lines (U2932, OCI-LY10, SUDHL2, WSU-DLCL2, DB)
    Concentration: 0 μM, 0.25 μM, 0.5 μM, 1 μM, 2 μM, 4 μM
    Incubation Time: 24 hours, 48 hours
    Result: Exhibited notable suppression of cell proliferation in five DLBCL cells.

    Western Blot Analysis[1]

    Cell Line: U2932 cells, WSU-DLCL2 cells
    Concentration: 0 μM, 1 μM, 2 μM, 4 μM
    Incubation Time: 24 hours
    Result: Decreased the expressions of Cyclin D1 and Cyclin E, and increased the expressions of p21 and p27.

    Apoptosis Analysis[1]

    Cell Line: U2932 cells, WSU-DLCL2 cells
    Concentration: 0 μM, 1 μM, 2 μM, 4 μM
    Incubation Time: 24 hours
    Result: Induced apoptosis and activates exogenous and endogenous apoptotic signaling pathways.

    Cell Cycle Analysis[1]

    Cell Line: U2932 cells, WSU-DLCL2 cells
    Concentration: 0 μM, 1 μM, 2 μM, 4 μM
    Incubation Time: 24 hours
    Result: Caused G1 phase arrest.

    RT-PCR[1]

    Cell Line: U2932 cells, WSU-DLCL2 cells
    Concentration: 0 μM, 1 μM, 2 μM, 4 μM
    Incubation Time: 24 hours
    Result: Activated ER stress.
    In Vivo

    Cladribine (10 μg/kg; i.p.; 3 times/week, for 2 weeks) may have benefits in the treatment of ischemia/reperfusion injury to the biochemical and histopathologic parameters[3].
    Chronic Cladribine administration (0.5 mg/kg; i.p.; daily, for 60 days) increases amyloid beta peptide generation and plaque burden in APdE9 mice[4].
    Cladribine administration with s.c. injection may produce more favourable pharmacokinetic profiles than i.a. injection following a single dose[5].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: Male Sprague-Dawley rats, ischemic injury model[3]
    Dosage: 10 μg/kg
    Administration: Intraperitoneal injection, 3 times/week, for 2 weeks
    Result: Might increase expression of Sphk1 and consecutively SphK1 suppressed HIF-1α.
    Animal Model: Male Sprague Dawley rats (350-450 g)[5]
    Dosage: 2 mg/kg for s.c., 1 mg/kg for i.a. (Pharmacokinetic Analysis)
    Administration: Subcutaneous injection, intra-arterial
    Result: The AUC and t1/2 β after a single 1 mg/kg i.a. and 2 mg/kg s.c. injection were 0.66 vs 1.2 microg x h/ml and 3.5 vs 4.5 hours, respectively.
    Clinical Trial
    Molecular Weight

    285.69

    Formula

    C₁₀H₁₂ClN₅O₃

    CAS No.

    4291-63-8

    SMILES

    OC[[email protected]@H]1[[email protected]](C[[email protected]](N2C=NC3=C2N=C(Cl)N=C3N)O1)O

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    4°C, protect from light

    *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 30 mg/mL (105.01 mM)

    H2O : 10 mg/mL (35.00 mM; Need ultrasonic)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 3.5003 mL 17.5015 mL 35.0030 mL
    5 mM 0.7001 mL 3.5003 mL 7.0006 mL
    10 mM 0.3500 mL 1.7501 mL 3.5003 mL
    *Please refer to the solubility information to select the appropriate solvent.
    References

    Purity: 99.97%

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    Keywords:

    Cladribine2-Chloro-2′-deoxyadenosine CldAdo 2CdAAdenosine DeaminaseApoptosishairycellleukemiaHCLchroniclymphocyticCLLmantlelymphomaMCLfollicularFLmucosa-associatedlymphoidtissueMALTDLBCLmultiplesclerosisInhibitorinhibitorinhibit

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    Product Name:
    Cladribine
    Cat. No.:
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