Cladribine is an adenosine deaminase inhibitor used to treat hairy cell leukemia and multiple sclerosis.(In Vitro):Cladribine (0.25-4 μM; 24-48 hours) inhibits human DLBCL cells proliferation.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.Cladribine (1-4 μM; 24 hours) induces apoptosis and activates extrinsic and intrinsic signaling pathways in human DLBCL cells.Cladribine (1-4 μM; 24 hours) activates endoplasmic reticulum stress.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.\n(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.Cladribine (0.5 mg/kg; i.p.; daily; for 60 days) increases amyloid beta peptide generation and plaque burden in APdE9 mice.Cladribine exhibits Cmax (rat 4.9 ng/mL) following intra-arterial injection.Cladribine exhibits Cmax (rat 1.1 ng/mL) following subcutaneous injection.Cladribine exhibits elimination half-lives (rat 3.5 h) and plasma clearance (rat 2.8 L/h/kg) following intra-arterial injection.Cladribine exhibits elimination half-lives (rat 4.5 h) and plasma clearance (rat 2.3 L/h/kg) following subcutaneous injection.Cladribine administration with s.c. injection may produce more favourable pharmacokinetic profiles than i.a. injection following a single dose.
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. Cladribine (0.5 mg/kg; i.p.; daily; for 60 days) increases amyloid beta peptide generation and plaque burden in APdE9 mice. Cladribine exhibits Cmax (rat 4.9 ng/mL) following intra-arterial injection. Cladribine exhibits Cmax (rat 1.1 ng/mL) following subcutaneous injection. Cladribine exhibits elimination half-lives (rat 3.5 h) and plasma clearance (rat 2.8 L/h/kg) following intra-arterial injection. Cladribine exhibits elimination half-lives (rat 4.5 h) and plasma clearance (rat 2.3 L/h/kg) following subcutaneous injection. Cladribine administration with s. c. injection may produce more favourable pharmacokinetic profiles than i. a. injection following a single dose. Animal model: Male Sprague-Dawley rats, ischemic injury model. 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). Dosage: 2 mg/kg for s. c. , 1 mg/kg for i. a. (Pharmacokinetic Analysis). Administration: Subcutaneous injection, intra-arterial. Result: Cmax (4.9 ng/mL i. a. ; 1.1 ng/mL s. c.), T1/2 β (3.5 h i. a. ; 4.5 s. c.).
In Vitro
Cladribine (0.25-4 μM; 24-48 hours) inhibits human DLBCL cells proliferation. 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. Cladribine (1-4 μM; 24 hours) induces apoptosis and activates extrinsic and intrinsic signaling pathways in human DLBCL cells. Cladribine (1-4 μM; 24 hours) activates endoplasmic reticulum stress. 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. Cell Proliferation Assay. 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. 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. 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 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. Cell line: U2932 cells, WSU-DLCL2 cells. Concentration: 0 μM, 1 μM, 2 μM, 4 μM. Incubation time: 24 hours. Result: Activated ER stress.
5 mg, 10 mg, 50 mg, 100 mg, 200 mg, 1 ml x 10 mM (in DMSO)
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