美国进口，现货，BI 2536，目录号S1109 ，CAS号:755038-02-9, 876126-71-5 (H2O)，细胞周期(Cell Cycle / Checkpoint) ， PLK YZ剂，美国Selleck_详细资料

产品信息

保质期：两年英文名： BI 2536 CAS号： 755038-02-9, 876126-71-5 (H2O) 数量：大量供应商：美国Selleck南京办事处保存条件：零下二十摄氏度保存规格： 5mg

信号转导通路:  细胞周期(Cell Cycle / Checkpoint) >> PLK >> PLK YZ剂 >> BI 2536
http://www.selleck.cn/bi-2536-S1109.html
技术数据:

分子量(MW): 521.66

化学式:
C₂₈H₃₉N₇O₃

溶解度: DMSO ≥104mg/mL   Water <1mg/mL   Ethanol ≥104mg/mL

纯度: >99%

稳定性: at -20℃ 2 years

CAS号: 755038-02-9, 876126-71-5 (H2O)

生物活性

YZPLK，作用于Plk1 ,Plk2,Plk3 时IC50分别为0.83 nM , 3.5 nM ,9.0 nM。^[1] BI 2536YZ多种细胞系的增殖，作用于K562细胞系时IC50为5–10nM，作用于抗Imatinib的K562细胞系时IC50为5–10 nM，作用于野生型Ba/F3p210细胞系时IC50为10–50 nM，作用于T315I 突变型Ba/F3p210 细胞系时IC50为10–50 nM。^[2]BI 2536阻止着丝点和ZX体中Plk1的富集。用BI 2536处理的细胞有丝分裂前期延长。在有丝分裂时BI 2536作用于心脏成纤维细胞时，IC50大约为43nM。BI 2536作用于人类原代静脉血管内皮细胞时也可以观察到类似的结果，IC50为30nM。但是BI 2536作用于HeLa癌细胞系时效果更强，IC50为9nM。BI 2536诱导HCT 116， BxPC-3 及A549标记的肿瘤衰退。^[1] 非小细胞肺癌是一种肺上皮癌，使用化学疗法效果不大。BI 2536用于ZL非小细胞肺癌已经处于二期阶段。^[3] BI 2536Z初是由Boehringer Ingelheim制药公司研究的。

参考文献

[1] Martin Steegmaier et al. Current Biology.2007 February 20;17(4):316-322
[2] Karoline V. Gleixner,et al. Cancer Res; 70(4) February 15, 2010
[3] http://clinicaltrials.gov/ct2/results?term=BI+2536
[4] Péter Lénárt,et al. Current Biology, Volume 17, Issue 4, 304-315, 20 February 2007

客户反馈数据

Comparison between Genetic Ablation of Cdc20 and Current Mitotic Drugs (C) Transformed Cdc20(lox/lox); RERT(+/Cre) MEFs were subcutaneously injected into the two flanks of SCID mice, and tumors were scored every 2–3 days.These mice were injected i.p. (three injections per week) with 4-OHT or mitotic drugs (taxol, vincristine, and BI2536) when tumors reached about 200 mm3 of volume (day 11; arrow) (n = 8 mice per group). (D) Representative images of these fibrosarcomas 3 days after injection with 4-OHT (to generate Cdc20(D/D) cells), BI2536, or taxol. These mice were injected with 10 mM BrdU to score DNA replication. CA3, immunodetection of active caspase 3. Scale bars, 50 or 10 mM (insets).

Treatment with BI 2536 induces cell-cycle arrest in NB TICs and aberrant accumulation of cyclin B1 and p21. C, expression of cyclin B1 and p21 was assessed in NB88R2 following 16 and 24-hour treatment with different doses of BI 2536 (10, 30, and 100 nmol/L). ERK1 (extracellular signal regulated kinase 1) was used as the loading control. D, inhibition of PLK1 was assessed by in vitro kinase assay following treatment of NB88R2 for 3 hours with BI 2536.

Treatment with BI 2536 induces cell death via apoptosis. A,treatment with BI 2536 (10, 30, and 100 nmol/L) reduces viable cell numbers as assessed by trypan blue exclusion. B, representative Western blot demonstrating accumulation of cleaved PARP following treatment with 10 nmol/L BI 2536 .

BI 2536 inhibits NB tumor growth in vivo. A and B, NOD/SCID mice bearing 50- to100-mm3 tumors were injected intravenously with either vehicle (0.1N HCl per saline) or 12.5 to 25mg/kg BI 2536 for 2 consecutive days a week, for a total of 3 cycles.Two independent experiments were performed in each case with 5 animals per group. Representative tumor growth data are shown.

animals with 50- to 100-mm3 tumors were randomized into 4 groups: group 1 injected intravenously with vehicle (0.1N HCl per saline), group 2 injected intravenously with 12.5 mg/kg of BI 2536 (2 consecutive days, 3 cycles), group 3 injected i.p. with 10 mg/kg of irinotecan (3 doses total, 3 days apart), and group 4 injected with BI 2536 and irinotecan. Both representative tumor growth data and a Kaplan–Meyer survival plot are shown.

Plk-1 knockdown and inhibition by BI 2536 and viability of human melanoma cell lines M14 and WM-115 as demonstrated by MTT assay. Experiments were performed in triplicate. One representative experiment is shown. *Po0.001, ANOVA test with Tukey’s post-test. ANOVA, analysis of variance; MTT, 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Plk-1, polo-like kinase 1; siRNA, small-interfering RNA; WB, western blot.

(a,b) RPE1 cells transfected with control or either of two B56-PP2A siRNA pools (1, 2) were incubated in MG132 (10 M, 15 min), followed by the addition of BI2536 (40 nM) or DMSO for 45 min. (a) The frequency of mitotic cells with few or absent cold-stable K-bres . (b) Maximum-intensity projection of tubulin (green) and an overlay with kinetochores (CREST, red) in B56-PP2A-siRNA (pool 2) cells treated with DMSO or BI2536 (40 nM). Insets are 3 enlargement of the optical sections spanning the outlined centromeres.

如果需要长期保存，请于零下二十度低温保存。

禁止用于人体及ZL！

特定的存储和包装每个产品的信息在产品说明书上都有注明。大多数Selleck产品，在推荐的条件下存储可稳定保存两年。产品有时建议的储存温度不同，大多数建议储存在-20 ° C ，抗体及蛋白等产品建议-60℃。YZ剂属于化学试剂，可在常温下运输储存两周左右。即使如此，我们保证产品的出货量将保持产品质量的条件下，一般都会放入冰袋。望阁下收到产品后，请按照产品数据表建议适当存储。

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温馨提示：不可用于临床ZL。

分子量(MW):	521.66
化学式:	C₂₈H₃₉N₇O₃
溶解度:	DMSO ≥104mg/mL Water <1mg/mL Ethanol ≥104mg/mL
纯度:	>99%
稳定性:	at -20℃ 2 years
CAS号:	755038-02-9, 876126-71-5 (H2O)

	Comparison between Genetic Ablation of Cdc20 and Current Mitotic Drugs (C) Transformed Cdc20(lox/lox); RERT(+/Cre) MEFs were subcutaneously injected into the two flanks of SCID mice, and tumors were scored every 2–3 days.These mice were injected i.p. (three injections per week) with 4-OHT or mitotic drugs (taxol, vincristine, and BI2536) when tumors reached about 200 mm3 of volume (day 11; arrow) (n = 8 mice per group). (D) Representative images of these fibrosarcomas 3 days after injection with 4-OHT (to generate Cdc20(D/D) cells), BI2536, or taxol. These mice were injected with 10 mM BrdU to score DNA replication. CA3, immunodetection of active caspase 3. Scale bars, 50 or 10 mM (insets).
	Treatment with BI 2536 induces cell-cycle arrest in NB TICs and aberrant accumulation of cyclin B1 and p21. C, expression of cyclin B1 and p21 was assessed in NB88R2 following 16 and 24-hour treatment with different doses of BI 2536 (10, 30, and 100 nmol/L). ERK1 (extracellular signal regulated kinase 1) was used as the loading control. D, inhibition of PLK1 was assessed by in vitro kinase assay following treatment of NB88R2 for 3 hours with BI 2536.
	Treatment with BI 2536 induces cell death via apoptosis. A,treatment with BI 2536 (10, 30, and 100 nmol/L) reduces viable cell numbers as assessed by trypan blue exclusion. B, representative Western blot demonstrating accumulation of cleaved PARP following treatment with 10 nmol/L BI 2536 .
	BI 2536 inhibits NB tumor growth in vivo. A and B, NOD/SCID mice bearing 50- to100-mm3 tumors were injected intravenously with either vehicle (0.1N HCl per saline) or 12.5 to 25mg/kg BI 2536 for 2 consecutive days a week, for a total of 3 cycles.Two independent experiments were performed in each case with 5 animals per group. Representative tumor growth data are shown.
	animals with 50- to 100-mm3 tumors were randomized into 4 groups: group 1 injected intravenously with vehicle (0.1N HCl per saline), group 2 injected intravenously with 12.5 mg/kg of BI 2536 (2 consecutive days, 3 cycles), group 3 injected i.p. with 10 mg/kg of irinotecan (3 doses total, 3 days apart), and group 4 injected with BI 2536 and irinotecan. Both representative tumor growth data and a Kaplan–Meyer survival plot are shown.
	Plk-1 knockdown and inhibition by BI 2536 and viability of human melanoma cell lines M14 and WM-115 as demonstrated by MTT assay. Experiments were performed in triplicate. One representative experiment is shown. *Po0.001, ANOVA test with Tukey’s post-test. ANOVA, analysis of variance; MTT, 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Plk-1, polo-like kinase 1; siRNA, small-interfering RNA; WB, western blot.
	(a,b) RPE1 cells transfected with control or either of two B56-PP2A siRNA pools (1, 2) were incubated in MG132 (10 M, 15 min), followed by the addition of BI2536 (40 nM) or DMSO for 45 min. (a) The frequency of mitotic cells with few or absent cold-stable K-bres . (b) Maximum-intensity projection of tubulin (green) and an overlay with kinetochores (CREST, red) in B56-PP2A-siRNA (pool 2) cells treated with DMSO or BI2536 (40 nM). Insets are 3 enlargement of the optical sections spanning the outlined centromeres.

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