Cladribine - CAS 4291-63-8
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Not Intended for Therapeutic Use. For research use only.
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Adenosine Deaminase
Cladribine is an adenosine deaminase inhibitor for U266, RPMI8226, and MM1.S cells with IC50 of approximately 2.43 μM, 0.75 μM, and 0.18 μM, respectively.
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2-CdA, 2-chlorodeoxyadenosine
1.Successful treatment with cladribine of Erdheim-Chester disease with orbital and central nervous system involvement developing after treatment of Langerhans cell histiocytosis.
Perić P, Antić B, Knezević-Usaj S, Radić-Tasić O, Radovinović-Tasić S, Vasić-Vilić J, Sekulović L, Tarabar O, Tukić L, Jovandić S, Magić Z. Vojnosanit Pregl. 2016 Jan;73(1):83-7.
INTRODUCTION: Erdheim-Chester disease (ECD) is a rare, systemic form of non-Langerhans cell histiocytosis of the juvenile xanthogranuloma family with characteristic bilateral symmetrical long bone osteosclerosis, associated with xanthogranulomatous extra skeletal organ involvement. In ECD, central nervous system (CNS) and orbital lesions are frequent, and more than half of ECD pa tients carry the V600E mutation of the protooncogene BRAF. The synchronous or metachronous development of ECD and Langerhans cell histiocytosis (LCH) in the same patients is rare, and the possible connection between them is still obscure. Cladribine is a purine substrate analogue that is toxic to lymphocytes and monocytes with good hematoencephalic penetration.
2.Cladribine, gemcitabine, busulfan, and SAHA combination as a potential pretransplant conditioning regimen for lymphomas: A preclinical study.
Ji J1, Valdez BC2, Li Y1, Liu Y1, Teo EC1, Nieto Y1, Champlin RE1, Andersson BS1. Exp Hematol. 2016 Mar 11. pii: S0301-472X(16)30024-8. doi: 10.1016/j.exphem.2016.03.001. [Epub ahead of print]
Hematopoietic stem cell transplantation (HSCT) is an effective treatment for patients with refractory lymphomas. Nucleoside analogs (NAs) and DNA alkylating agents are efficacious in treating hematologic malignancies. To design an efficacious and more economical pretransplant regimen for lymphoma patients, we analyzed the cytotoxicity of cladribine (Clad), gemcitabine (Gem), busulfan (Bu), and suberoylanilide hydroxamic acid (SAHA) in lymphoma cell lines. J45.01 and U937 lymphoma cell lines were exposed to drugs, alone or in combination, for 48 hours and analyzed with the MTT and annexin V assays, Western blotting, and flow cytometry. On the basis of the IC5-10 values of the drugs, the Clad+Gem+Bu combination inhibited the proliferation of both cell lines to ∼55%-60%. Addition of SAHA to this combination decreased proliferation further to ∼30%. Exposure to the Clad+Gem+Bu+SAHA combination activated the DNA damage response and ATM-CHK2 pathway; modified histones; decreased mitochondrial membrane potential, which caused leakage of apoptosis-inducing factors; and activated apoptosis.
3.Simultaneous determination of clofarabine and cytarabine in human plasma by LC-MS/MS.
Büttner B1, Oertel R2, Schetelig J3, Middeke JM4, Bornhäuser M4, Seeling A5, Knoth H6. J Pharm Biomed Anal. 2016 Apr 1;125:286-291. doi: 10.1016/j.jpba.2016.03.056. [Epub ahead of print]
Combination of cytostatic agents is a basic principle in the treatment of cancer. For the treatment of acute myeloid leukemia (AML), purine analogs, like clofarabine and cytarabine act synergistically. Little is known, however, on their interaction in vivo. We developed a method for the simultaneous determination of clofarabine and cytarabine in human plasma. The substances were extracted from plasma samples by protein precipitation with acetonitrile. Cladribine was the internal standard (IS). The analytes were separated on Synergi HydroRP column (150mm×2.0mm, 4μm) and a triple-quadrupole mass spectrometry with an electrospray ionisation (ESI) source was applied for detection. The mobile phase consisted of acetonitrile, ammonium acetate 2mM and 0.5% formic acid in a gradient mode at a flow rate of 0.5ml/min. The injection volume was 10μl and the total run time was 6.0min. Retention times were 2.46min for clofarabine, 0.97min for cytarabine and 2.
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