Cladribine (2-Chloro-2′-deoxyadenosine) 是一种嘌呤核苷类似物，是具有口服活性的腺苷脱氨酶 (adenosine deaminase) 抑制剂。Cladribine 能作为 DNA 合成 (DNA synthesis) 的抑制剂，可阻断受损 DNA 的修复。Cladribine 可以抑制 DNA 甲基化。Cladribine 具有抗淋巴瘤活性，可用于一些血液恶性肿瘤和多发性硬化的研究。
Cladribine Chemical Structure
CAS No. : 4291-63-8
规格
价格
是否有货
数量
Free Sample (0.1-0.5 mg)
Apply now
10 mM * 1 mL in DMSO
￥500
In-stock
10 mg
￥350
In-stock
50 mg
￥1252
In-stock
100 mg
￥2270
In-stock
200 mg
询价
500 mg
询价
* Please select Quantity before adding items.
Cladribine 相关产品
•相关化合物库:
Covalent Screening Library Plus
Natural Product Like Compound Library
Drug Repurposing Compound Library Plus
FDA-Approved Drug Library Plus
FDA-Approved Drug Library Mini
Bioactive Compound Library Plus
Apoptosis Compound Library
Metabolism/Protease Compound Library
FDA-Approved Drug Library
Anti-Cancer Compound Library
CNS-Penetrant Compound Library
Drug Repurposing Compound Library
Covalent Screening Library
Nucleotide Compound Library
Anti-Cardiovascular Disease Compound Library
Anti-COVID-19 Compound Library
NMPA-Approved Drug Library
Endoplasmic Reticulum Stress Compound Library
Orally Active Compound Library
FDA Approved & Pharmacopeial Drug Library
Drug-Induced Liver Injury (DILI) Compound Library
Anti-Blood Cancer Compound Library
Rare Diseases Drug Library
生物活性
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]
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].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
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.
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].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
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)
[1]. Linyan Xu, et al. Cladribine Induces ATF4 Mediated Apoptosis and Synergizes with SAHA in Diffuse Large B-Cell Lymphoma Cells. Int J Med Sci. 2020; 17(10): 1375–1384.
[2]. Jian Ma, et al. Therapeutic potential of cladribine in combination with STAT3 inhibitor against multiple myeloma. BMC Cancer. 2011 Jun 16;11:255.
[3]. Young Seop Chang, et al. MP28-10 COMBINED EFFECTS OF MELATONIN AND CLADRIBINE ON APOPTOSIS IN ISCHEMIA/REPERFUSION INJURY IN RAT BLADDER. THE JOURNAL OF UROLOGY. April 2016. 195 (4S): e375.
[4]. Crystal D Hayes, et al. Chronic cladribine administration increases amyloid beta peptide generation and plaque burden in mice. PLoS One. 2012;7(10):e45841.
[5]. Yeung, P. K. F., et al. Pharmacokinetics of Cladribine in a Rat Model Following Subcutaneous and Intra-arterial Injections. Drug Metabol Drug Interact. 2008;23(3-4):291-8.
