体外研究
(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].
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. |
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体内研究
(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 Cmax(rat 4.9 ng/mL) following intra-arterial injection[5].
Cladribine exhibits Cmax(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].
| 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: | Cmax(4.9 ng/mL i.a.; 1.1 ng/mL s.c.), T1/2β (3.5 h i.a.; 4.5 s.c.). |
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