Cladribine

別名: 2-CdA,2-Chloro-2′-deoxyadenosine,CldAdo,Jk 6251,NSC 105014,RWJ 26251 中文名稱：克拉利賓

目錄號：S1199 Purity: 99.99%

Cladribine是一種腺苷脫氨酶抑制劑，作用于U266， RPMI8226，和MM1.S細胞，IC50分別約為2.43 μM， 0.75 μM，和0.18 μM。

Cladribine Chemical Structure

CAS: 4291-63-8

規(guī)格	價格	庫存
10mM (1mL in DMSO)	979.91	現(xiàn)貨
25mg	792.01	現(xiàn)貨
50mg	1382.86	現(xiàn)貨
1g	7944.3	現(xiàn)貨
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產(chǎn)品質(zhì)控

批次：純度： 99.99%

99.99

Cladribine相關(guān)產(chǎn)品

相關(guān)化合物庫	FDA藥物庫天然產(chǎn)物庫神經(jīng)信號化合物庫血腦屏障通透化合物庫抗阿爾茨海默病化合物庫	點擊展開

細胞實驗數(shù)據(jù)示例

細胞系	實驗類型	孵育時間	活性描述	文獻信息
CT26	Cytotoxicity assay	3 days	Cytotoxicity against mouse CT26 cells after 3 days by MTT assay, IC50=0.131μM	21711054
BT549	Cytotoxicity assay	3 days	Cytotoxicity against human BT549 cells after 3 days by MTT assay, IC50=0.123μM	21711054
BV173	Cytotoxicity assay	3 days	Cytotoxicity against human BV173 cells after 3 days by MTT assay, IC50=0.0008μM	21711054
human SK-UT-1B cells	Proliferation assay	48 h	Antiproliferative activity against human SK-UT-1B cells assessed as cell growth inhibition after 48 hrs by MTT assay, IC50=1 μM	25960323
human MCF7 cells	Proliferation assay	48 h	Antiproliferative activity against human MCF7 cells assessed as cell growth inhibition after 48 hrs by MTT assay, IC50=45 μM	25960323
human RPMI8226 cells	Proliferation assay	48 h	Antiproliferative activity against human RPMI8226 cells assessed as cell growth inhibition after 48 hrs by MTT assay, IC50=6 μM	25960323
human KG1 cells	Proliferation assay	48 h	Antiproliferative activity against human KG1 cells assessed as cell growth inhibition after 48 hrs by MTT assay, IC50=0.2 μM	25960323
human MOLT3 cells	Proliferation assay	48 h	Antiproliferative activity against human MOLT3 cells assessed as cell growth inhibition after 48 hrs by MTT assay, IC50=2.3 μM	25960323
human SKHEP1 cells	Proliferation assay	48 h	Antiproliferative activity against human SKHEP1 cells assessed as cell growth inhibition after 48 hrs by MTT assay, IC50=4 μM	25960323
human K562 cells	Proliferation assay	48 h	Antiproliferative activity against human K562 cells assessed as cell growth inhibition after 48 hrs by MTT assay, IC50=10 μM	25960323
human HCT116 cells	Cytotoxicity assay	72 h	Cytotoxicity against human HCT116 cells after 72 hrs by SRB assay, IC50=0.3 μM	25462277
human T47D cells	Cytotoxicity assay	72 h	Cytotoxicity against human T47D cells after 72 hrs by SRB assay, IC50=0.7 μM	25462277
human HuH7 cells	Cytotoxicity assay	72 h	Cytotoxicity against human HuH7 cells after 72 hrs by SRB assay, IC50=1.8 μM	25462277
human Raji cells	Cytotoxicity assay	72 h	Cytotoxicity against human Raji cells after 72 hrs by MTT assay, IC50=0.009 μM	21840722
CCRF-CEM cells	Cytotoxicity assay	72 h	Cytotoxicity against human CCRF-CEM cells after 72 hrs by MTT assay, IC50=0.0005 μM	21840722
MES-SA	Cytotoxicity assay	3 days	Cytotoxicity against human MES-SA cells after 3 days by MTT assay, IC50=0.165μM	21711054
K562	Cytotoxicity assay	3 days	Cytotoxicity against human paclitaxel resistant K562 cells after 3 days by MTT assay, IC50=0.17μM	21711054
P388D1	Cytotoxicity assay	3 days	Cytotoxicity against mouse P388D1 cells after 3 days by MTT assay, IC50=0.285μM	21711054
CEM-DNR-bulk	Cytotoxicity assay	3 days	Cytotoxicity against human CEM-DNR-bulk cells after 3 days by MTT assay, IC50=0.352μM	21711054
L1210	Cytotoxicity assay	3 days	Cytotoxicity against mouse L1210 cells after 3 days by MTT assay, IC50=0.393μM	21711054
EL4	Cytotoxicity assay	3 days	Cytotoxicity against mouse EL4 cells after 3 days by MTT assay, IC50=0.848μM	21711054
MCF7	Cytotoxicity assay	3 days	Cytotoxicity against human MCF7 cells after 3 days by MTT assay, IC50=2.35μM	21711054
K562	Cytotoxicity assay	3 days	Cytotoxicity against human K562 cells after 3 days by MTT assay, IC50=7.69μM	21711054
PC3	Cytotoxicity assay	3 days	Cytotoxicity against human PC3 cells after 3 days by MTT assay, IC50=8.28μM	21711054
C6	Cytotoxicity assay	3 days	Cytotoxicity against rat C6 cells after 3 days by MTT assay, IC50=9.07μM	21711054
HPAC	Cytotoxicity assay	3 days	Cytotoxicity against human HPAC cells after 3 days by MTT assay, IC50=9.32μM	21711054
HCT116	Cytotoxicity assay	3 days	Cytotoxicity against human HCT116 cells after 3 days by MTT assay, IC50=9.43μM	21711054
HT-29	Cytotoxicity assay	3 days	Cytotoxicity against human HT-29 cells after 3 days by MTT assay, IC50=9.44μM	21711054
HCT116	Cytotoxicity assay	72 hrs	Cytotoxicity against human HCT116 cells assessed as growth inhibition after 72 hrs by SRB assay, IC50=0.3μM	28219046
HuH7	Cytotoxicity assay	72 hrs	Cytotoxicity against human HuH7 cells assessed as growth inhibition after 72 hrs by SRB assay, IC50=1.8μM	28219046
MCF7	Cytotoxicity assay	72 hrs	Cytotoxicity against human MCF7 cells assessed as growth inhibition after 72 hrs by SRB assay, IC50=2μM	28219046
P388 leukemic cell lines	Function assay		In vitro inhibitory effect was tested for cytostatic activity on the growth of lymphoid neoplasm P388 leukemic cell lines, ID50=0.03 μM	2995666
L1210 cell lines	Function assay		In vitro inhibitory effect was tested for cytostatic activity on the growth of murine leukemic L1210 cell lines, ID50=0.03 μM	2995666
L1210 cell lines	Cytotoxicity assay		Compound was tested for cytotoxicity against L1210 cell lines, IC50=0.07 Μm	1732556
HEp-2 cell lines	Cytotoxicity assay		Compound was tested for cytotoxicity against HEp-2 cell lines, IC50=0.03 μM	1732556
CCRF-CEM cell lines	Cytotoxicity assay		Compound was tested for cytotoxicity against CCRF-CEM cell lines, IC50=0.003 μM	1732556
TC32	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	29435139
SJ-GBM2	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	29435139
A673	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	29435139
SK-N-MC	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	29435139
BT-37	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	29435139
NB1643	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	29435139
LAN-5	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	29435139
OHS-50	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	29435139
MG 63 (6-TG R)	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	29435139
NB1643	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells	29435139
A673	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)	29435139
SK-N-MC	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells	29435139
BT-37	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells	29435139
TC32	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells	29435139
MG 63 (6-TG R)	qHTS assay		qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells	29435139
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生物活性

產(chǎn)品描述

Cladribine是一種腺苷脫氨酶抑制劑，作用于U266， RPMI8226，和MM1.S細胞，IC50分別約為2.43 μM， 0.75 μM，和0.18 μM。

特性

Cladribine主要在淋巴組織中具有活性。

靶點

Adenosine deaminase (MM1.S cells) ^[1]	Adenosine deaminase (RPMI8226 cells) ^[1]	Adenosine deaminase (U266 cells) ^[1]
0.18 μM	0.75 μM	2.43 μM

體外研究(In Vitro)
體外研究活性	Cladribine對毛細胞白血病(HCL)，一種慢性B淋巴細胞增生疾病發(fā)揮顯著的活性，延長完全緩解期。Cladribine誘導(dǎo)DNA鏈斷裂累積，隨后激活淋巴細胞中抑癌基因p53。Cladribine可能調(diào)節(jié)MM細胞中STAT3活性。Cladribine劑量依賴性抑制U266，RPMI8226和MM1.S細胞的增殖/存活。其中U266對cladribine敏感性最低，而對MM1.S敏感性最高。Cladribine治療逐漸增加細胞周期中G1期的細胞比例，并減少S期細胞。Cladribine處理24小時后似乎能夠增加U266細胞中G2-M期的比例。在RPMI8226和MM1.S細胞中都能觀察到cladribine誘導(dǎo)的細胞凋亡劑量依賴性增加。0.2 μM cladribine治療時間依賴性顯著誘導(dǎo)MM1.S 中caspase-3，-8，和-9激活和PARP裂解。Cladribine劑量依賴性顯著降低磷酸STAT3 (P-STAT3)水平，但是不影響總STAT3蛋白質(zhì)水平。^[1] Cladribine在HSB2細胞中具有濃度依賴性誘導(dǎo)細胞凋亡的潛能。^[2] Cladribine以劑量依賴的方式抑制原代肥大細胞(MC)和MC系HMC-1生長，含有KIT D816V的HMC-1.2細胞與KIT D816V缺失的HMC-1.1細胞相比，具有較低的IC50值。^[3] Cladribine降低CD14⁺單核細胞，以及CD4⁺和CD8⁺ T淋巴細胞的遷移能力。^[4]
細胞實驗	細胞系	U266，RPMI8226 和 MM1.S
	濃度	0 μM - 32 μM
	孵育時間	72小時
	方法	非放射性細胞增殖試劑盒用于測定細胞活性。簡而言之，人MM細胞系U266，RPMI8226和MM1.S接種到96孔板，0.1 mL完全培養(yǎng)基(5% FBS)為對照組，0.1 mL包含一系列劑量cladribine的相同培養(yǎng)基為試驗組，培養(yǎng)72小時。使用微板讀書器在490 nm下讀取所有孔中的細胞數(shù)量，每組相對于100%存活率對照組的存活細胞百分數(shù)，通過MTS的減少測定。

體內(nèi)研究(In Vivo)
體內(nèi)研究活性	Cladribine (0.7-3.5 mM)和/或diltiazem (2.4 mM)，腹腔注射到成年斑馬魚，通過HPLC分析心血管健康的潛在標(biāo)志物，紅血球(RBC)裂解物嘌呤核苷酸(例如ATP)的水平。Diltiazem增加RBC ATP濃度，該作用被共注射cladribine所抑制。^[5] Ia 和s.c.給藥后，伴隨雙相下降，Cladribine血漿濃度急速減少。單劑Cladribine 以1 mg/kg ia 和 2 mg/kg s.c. 注射后，AUC和t _1/2β分別為0.66: 1.2 μg ×h/mL和3.5: 4.5小時。^[6]
動物實驗	Animal Models	成年野生型(AB)斑馬魚
	Dosages	0.7 mM - 3.5?mM
	Administration	腹腔注射給藥

NCT Number	Recruitment	Conditions	Sponsor/Collaborators	Start Date	Phases
臨床試驗信息 (data from https://clinicaltrials.gov, updated on 2024-05-22)
NCT05797740	Recruiting	Multiple Sclerosis	Merck Healthcare KGaA Darmstadt Germany an affiliate of Merck KGaA Darmstadt Germany	August 3 2023	--
NCT04997148	Completed	Relapsing-Remitting Multiple Sclerosis	Merck Healthcare KGaA Darmstadt Germany an affiliate of Merck KGaA Darmstadt Germany\|Merck Serono Limited an affiliate of Merck KGaA Darmstadt Germany	August 11 2021	--

參考文獻
[1] Ma J, et al. BMC Cancer. 2011, 11, 255. [2] Guchelaar HJ, et al. Cancer Chemother Pharmacol. 1998, 42(1), 77-83. [3] B?hm A, et al. Exp Hematol. 2010, 38(9), 744-755. [4] Kopadze T, et al. Eur J Neurol. 2009, 16(3), 409-412. [5] Klein LC, et al. Biomarkers. 2009, 14(8), 554-559. [6] Yeung PK, et al. Drug Metabol Drug Interact. 2008, 23(3-4), 291-298. [7] Szmigielska-Kaplon A, et al. Ann Hematol. 2002, 81(9), 508-513. + 展開

參考文獻

[1] Ma J, et al. BMC Cancer. 2011, 11, 255.
[2] Guchelaar HJ, et al. Cancer Chemother Pharmacol. 1998, 42(1), 77-83.
[3] B?hm A, et al. Exp Hematol. 2010, 38(9), 744-755.

[4] Kopadze T, et al. Eur J Neurol. 2009, 16(3), 409-412.
[5] Klein LC, et al. Biomarkers. 2009, 14(8), 554-559.
[6] Yeung PK, et al. Drug Metabol Drug Interact. 2008, 23(3-4), 291-298.
[7] Szmigielska-Kaplon A, et al. Ann Hematol. 2002, 81(9), 508-513.

+ 展開