
7BIOcaspase independent nonapoptotic cell death inducer |
Sample solution is provided at 25 µL, 10mM.
































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- Purity = 98.00%
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Chemical structure


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Cas No. | 916440-85-2 | SDF | Download SDF |
Synonyms | 7-Bromoindirubin-3’-oxime | ||
Chemical Name | 7-bromo-3-[1,3-dihydro-3-(hydroxyimino)-2H-indol-2-ylidene]-1,3-dihydro-2H-indol-2-one | ||
Canonical SMILES | O/N=C(C1=CC=CC=C1N2)/C2=C3C(NC4=C(Br)C=CC=C4/3)=O | ||
Formula | C16H10BrN3O2 | M.Wt | 356.2 |
Solubility | Soluble in ethanol;DMSO | Storage | Store at -20°C |
Physical Appearance | A solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
7-bromoindirubin-3"-oxime (7BIO), a derivative of indirubin, is a caspase independent nonapoptotic cell death inducer [1]. 7-bromoindirubin-3"-oxime is an inhibitor of FLT3, DYRK1A, DYRK2, Aurora B and Aurora C kinases.
FLT3 is a cytokine receptor expressed on the surface of many hematopoietic progenitor cells. Signalling of FLT3 is important for the normal development of haematopoietic stem cells and progenitor cells. DYRK1A and DYRK2 have been involved in catalyzing its autophosphorylation on serine/threonine and tyrosine residues and play a significant role in a signaling pathway regulating cell proliferation. Aurora kinases are serine/threonine kinases which are essential for cell proliferation and cellular division by controlling chromatid segregation.
7-bromoindirubin-3"-oxime (7BIO) showed a marginal inhibitory activity towards CDKs and GSK-3. 7BIO triggered a rapid cell death process distinct from apoptosis. 7BIO induced the appearance of large pycnotic nuclei, without classical features of apoptosis such as chromatin condensation and nuclear fragmentation. 7BIO-induced cell death was not accompanied by cytochrome c release neither by any measurable effector caspase activation. 7BIO triggered the activation of non-apoptotic cell death, possibly through necroptosis or autophagy. 7BIO inhibited FLT3, the dual-specificity tyrosine phosphorylation-regulated kinases, DYRK1A and DYRK2 with the IC50 values of 0.34 μM, 1.9 and 1.3 μM, respectively [2]. 7BIO also inhibited the activity of Aurora B and C kinases with IC50 values of 4.6 and 0.7 μM, respectively [3].
References:[1] Ribas J, Bettayeb K, Ferandin Y, et al. 7-Bromoindirubin-3′-oxime induces caspase-independent cell death[J]. Oncogene, 2006, 25(47): 6304-6318.[2] Myrianthopoulos V, Kritsanida M, Gaboriaud-Kolar N, et al. Novel inverse binding mode of indirubin derivatives yields improved selectivity for DYRK kinases[J]. ACS medicinal chemistry letters, 2012, 4(1): 22-26.[3] Myrianthopoulos V, Magiatis P, Ferandin Y, et al. An integrated computational approach to the phenomenon of potent and selective inhibition of aurora kinases B and C by a series of 7-substituted indirubins[J]. Journal of medicinal chemistry, 2007, 50(17): 4027-4037.
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转运体是介导分子或离子转运跨过生物膜的物质。通常是蛋白质或酶。说得简单一点就是“运输工具”
受体是能与细胞外专一信号分子(配体)结合引起细胞反应的蛋白质。受体与配体结合即发生分子构象变化,从而引起细胞反应,如介导细胞间信号转导、细胞间黏合、细胞胞吞等细胞过程。它起的是“传达员” 的作用
感觉这样的提问是没有意义的
还是自己找下资料吧
1、被动转运(顺梯度转运):药物依赖于膜两侧的浓度差,从高浓度的一侧向低浓度的一侧扩散转运的过程。大多数药物属于被动转运。
(1)特点:不需要载体,不消耗能量,无饱和现象和竞争性抑制。
(2)影扩散速度的因素:
①膜两侧的药物浓度差。
②药物的理化性质:分子量小、脂溶性大、极性小、非解离型的药物易通过生物膜转运,反之难跨膜转运。
2、主动转运:是一种逆浓度(或电位)差的转运。
特点:需要载体,消耗能量,有饱和现象和竞争性抑制。

