Cladribine

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

克拉屈滨是一种腺苷脱氨酶抑制剂，用于治疗毛细胞白血病和多发性硬化症。

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. (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 (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 AssayCell 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.

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.).

Biodribin | ?2-Chlorodeoxyadenosine | Jk 6251 | Leustatin | NSC 105014 | RWJ 26251

Endocrinology/Hormones

AChR

Adenosine deaminase (MM1.S cells)| Adenosine deaminase (RPMI8226 cells)| Adenosine deaminase (U266 cells)

Cancer

——

4291-63-8

285.69

C10H12ClN5O3

>98% (HPLC)

DMSO: 57 mg/mL (199.51 mM)

O[C@@H]1[C@@H](CO)O[C@@H](N2C=NC3=C(N)N=C(Cl)N=C23)C1

(2R,3S,5R)-5-(6-amino-2-chloro-9H-purin-9-yl)-2-(hydroxymethyl)tetrahydrofuran-3-ol

(-20℃)

With Ice Pack

≥ 2 years