Cladribine

Cladribine (2-Chloro-2′-deoxyadenosine), 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. Cladribine 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].
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].
Cladribine (0.5 mg/kg; i.p.; daily; for 60 days) increases amyloid beta peptide generation and plaque burden in APdE9 mice^[4].
Cladribine exhibits C_max (rat 4.9 ng/mL) following intra-arterial injection^[5].
Cladribine exhibits C_max (rat 1.1 ng/mL) following subcutaneous injection^[5].
Cladribine exhibits elimination half-lives (rat 3.5 h) and plasma clearance (rat 2.8 L/h/kg) following intra-arterial injection^[5].
Cladribine exhibits elimination half-lives (rat 4.5 h) and plasma clearance (rat 2.3 L/h/kg) following subcutaneous injection^[5].
Cladribine administration with s.c. injection may produce more favourable pharmacokinetic profiles than i.a. injection following a single dose^[5].