B220
目录号 : GC33986
B220是一种能抑制HSV-1，HSV-2和人巨细胞病毒(CMV)生长的抗病毒剂。
Cas No.:112228-65-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | Cells preincubated with or without B220 are stimulated with N-formylmethionyl-leucyl-phenylalanine (fMLP) for 5 min and then fixed in paraformaldehyde [4% w/v in phosphate-buffered saline (PBS); 30 min on melting ice]. For detection of CR3, 10 µL of conjugated mAb is added to a cell pellet (approximately 100 µL) of 106 cells. The mixture is incubated for 30 min on ice and then washed twice with PBS. The amount of antibody bound is examined by flow cytometry. The release of vitamin B12-binding protein is assayed after activation of the cells with fMLP for 5 min using the cyanocobalamin technique[2]. |
References: [1]. Mohammed Homman, et al. Pharmaceutical formulation of B220 for topical treatment of herpes. EP 2489354 A1. | |
B220 is an antiviral agent which can inhibit the growth of HSV-1, HSV-2 and human cytomegalovirus (CMV).
B220 is an antiviral agent which can inhibit the growth of HSV-1, HSV-2 and human cytomegalovirus (CMV)[1]. B220 inhibits neutrophil release of reactive oxygen species, as well as intracellular generation of reactive oxygen species. The inhibition is not achieved through direct oxygen radical scavenger activity of B220, and B220 has no immediate effects on the activity of the assembled oxidase. The neutrophil capability to phagocytose fluorescein-labeled opsonized yeast cells is reduced by B220. Cells preincubated with B220 (10 µg/mL) and then stimulated with the formylated peptide fMLP mobilize fewer C3 receptors on their surface than the control cells[2].
[1]. Mohammed Homman, et al. Pharmaceutical formulation of B220 for topical treatment of herpes. EP 2489354 A1. [2]. Harbecke O, et al. The synthetic non-toxic drug 2,3-dimethyl-6(2-dimethylaminoethyl)-6H-indolo-(2,3-b)quinoxaline inhibits neutrophil production of reactive oxygen species. J Leukoc Biol. 1999 Jun;65(6):771-7.
| Cas No. | 112228-65-6 | SDF | |
| Canonical SMILES | CC1=C(C)C=C2N=C3C(N(CCN(C)C)C4=C3C=CC=C4)=NC2=C1 | ||
| 分子式 | C20H22N4 | 分子量 | 318.42 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.1405 mL | 15.7025 mL | 31.4051 mL |
| 5 mM | 0.6281 mL | 3.1405 mL | 6.281 mL |
| 10 mM | 0.3141 mL | 1.5703 mL | 3.1405 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Identification and characterization of B220+/B220- subpopulations in murine Gr1+CD11b+ cells during tumorigenesis
Oncoimmunology 2021 Apr 14;10(1):1912472.PMID:33948392DOI:10.1080/2162402X.2021.1912472.
Although all murine MDSCs are defined as Gr1+CD11b+, their true immunophenotype remains elusive. In this study, we found murine Gr1+CD11b+ cells can be divided into two subsets: Gr1+CD11b+B220- and Gr1+CD11b+B220+, especially in the spleen tissues. Unlike the dominant B220- subset, the B220+ subpopulation was not induced by tumor in vivo. Moreover, Gr1+CD11b+B220+ cells from tumor-bearing mice spleens were unable to induce arginase 1 and inducible nitric oxide synthase expression, inhibit T cell proliferation, or promote tumor growth in primary tumor site. Nevertheless, these cells suppressed tumor metastasis in vivo and reduced cancer cell motility in vitro, while Gr1+CD11b+B220- cells from tumor-bearing mice spleens promoted tumor metastasis and enhanced cancer cell motility. Furthermore, both the polymorphonuclear (PMN-MDSCs) and monocytic MDSCs (Mo-MDSCs) could be further divided into B220- and B220+ subsets; interestingly, tumor only induced the expansion of B220- PMN-MDSCs and B220- Mo-MDSCs, but not the B220+ counterparts. Compared with B220- PMN-MDSCs and B220- Mo-MDSCs, the Ly6G+Ly6C-CD11b+B220+ and Ly6G-Ly6C+CD11b+B220+ cells from tumor-bearing mice spleens exhibited a more mature phenotype without immunosuppressive activity. Additionally, IL-6 deficiency attenuated the tumor-induced accumulation of MDSCs, B220- MDSCs and B220- PMN-MDSCs but increased the percentages of Gr1+CD11b+B220+, Ly6G+Ly6C-CD11b+B220+, and Ly6G-Ly6C+CD11b+B220+ cells, indicating the opposing roles of the IL-6 signaling pathway in the expansion of B220- MDSCs and their B220+ counterparts. Taken together, our findings indicate that the B220+ subset is a distinct subset of Gr1+CD11b+ cells functionally different from the B220- subpopulation during tumorigenesis and induction of MDSCs to B220+ cells may be helpful for cancer therapy.
[Analysis of CD11c+ B220+NK cells in peripheral lymphoid tissues and the liver of C57BL/6 mice]
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2022 Feb;38(2):116-121.PMID:35356879doi
Objective To investigate the distribution of CD11c+B220+NK cells in peripheral lymphoid tissues and liver and the surface expression of plasmacytoid dendritic cell antigen-1 (PDCA-1) on CD11c+ B220+ NK cells. Methods The spleen, lymph nodes and liver tissues of C57BL/6 mice were collected to prepare single-cell suspensions, and the proportion of CD11c+B220+NK cells in the tissues and their surface expression of PDCA-1 were detected by multi-color flow cytometry. Results CD11c+B220+NK cells were distributed widely in the spleen, lymph nodes and liver, with the highest proportion in the spleen (2.82±0.45)%. PDCA-1s were expressed in some of CD11c+B220+NK cells in the tissues, particularly in the spleen tissues. Conclusion CD11c+B220+NK cells are important subpopulation of NK cells in murine peripheral lymphoid tissues and liver. The expression of PDCA-1 on CD11c+B220+NK cells is different in different tissues.
CD4(+)B220(+)TCRγδ(+) T cells produce IL-17 in lupus-prone MRL/lpr mice
Int Immunopharmacol 2016 Sep;38:31-9.PMID:27235595DOI:10.1016/j.intimp.2016.05.004.
Systemic lupus erythematosus is an autoimmune disease with comprehensive immune cell disorders. Recent studies suggested that pro-inflammatory cytokine IL-17 plays important role in lupus, leaving the cellular sources and their pathogenic and physiologic characters largely unknown. In the current study, by using lupus-prone MRL/lpr mice, we demonstrated that Th17 response prevails in lupus disease regarding significantly accumulated serum IL-17, increased IL-17-producing splenocytes, and elevated phospho-STAT3 in CD4(+) T cells. Intracellular staining revealed that unusual CD4(+)B220(+) T cells are major IL-17-producing cells, whereas conventional CD4(+)B220(-) T cells are major IFN-γ-producing cells. Subsequent studies showed that CD4(+)B220(+) cells contains both αβ and γδ T cells in the spleen and thymus of MRL/lpr mice. Further study showed that around 60% of γδ T cells in MRL/lpr mice co-express both B220 and CD4 on their surface, and are the major RORγt(+) cells in MRL/lpr mice. Finally, CD4(+)B220(+) T cells alone do not proliferate, but could enhance the proliferation and IFN-γ-production of conventional CD4(+)B220(-) T cells. Our findings suggest the pathogenic role of unusual CD4(+)B220(+) T cells in lupus disease in MRL/lpr mice according to their IL-17-producing ability and stimulatory function for conventional CD4(+)B220(-) T cells.
Hepato-entrained B220+CD11c+NK1.1+ cells regulate pre-metastatic niche formation in the lung
EMBO Mol Med 2018 Jul;10(7):e8643.PMID:29930175DOI:10.15252/emmm.201708643.
Primary tumours establish metastases by interfering with distinct organs. In pre-metastatic organs, a tumour-friendly microenvironment supports metastatic cells and is prepared by many factors including tissue resident cells, bone marrow-derived cells and abundant fibrinogen depositions. However, other components are unclear. Here, we show that a third organ, originally regarded as a bystander, plays an important role in metastasis by directly affecting the pre-metastatic soil. In our model system, the liver participated in lung metastasis as a leucocyte supplier. These liver-derived leucocytes displayed liver-like characteristics and, thus, were designated hepato-entrained leucocytes (HepELs). HepELs had high expression levels of coagulation factor X (FX) and vitronectin (Vtn) and relocated to fibrinogen-rich hyperpermeable regions in pre-metastatic lungs; the cells then switched their expression from Vtn to thrombospondin, both of which were fibrinogen-binding proteins. Cell surface marker analysis revealed that HepELs contained B220+CD11c+NK1.1+ cells. In addition, an injection of B220+CD11c+NK1.1+ cells successfully eliminated fibrinogen depositions in pre-metastatic lungs via FX Moreover, B220+CD11c+NK1.1+ cells demonstrated anti-metastatic tumour ability with IFNγ induction. These findings indicate that liver-primed B220+CD11c+NK1.1+ cells suppress lung metastasis.
Systemic blockade of proBDNF inhibited the expansion and altered the transcriptomic expression in CD3+B220+ cells in MRL/lpr lupus mice
Lupus Sci Med 2022 Dec;9(1):e000836.PMID:36581381DOI:10.1136/lupus-2022-000836.
Objectives: The overexpansion of CD3+B220+ cells is the hallmark and main pathological mechanism of clinical manifestations of spontaneously developed MRL/lpr mice, which are primarily used as a mouse model of SLE. Our recent report demonstrated that blocking brain-derived neurotrophic factor precursor (proBDNF) suppressed the antibody-secreting cell differentiation and proliferation and inhibited the progression of SLE; however, the effect of proBDNF blockade on these CD3+B220+ cells in MRL/lpr mice is unclear. Methods: To explore the effect of proBDNF on CD3+B220+ cells, MRL/lpr mice at 12 weeks old were intraperitoneally injected with monoclonal anti-proBDNF antibody (McAb-proB) or control IgG continuously for 8 weeks. The manifestations in mice were observed, and peripheral blood and splenocytes were collected and analysed via flow cytometry at 20 weeks old. In addition, splenic CD3+B220+ cells were subjected to RNA sequencing (RNA-seq) analysis to identify transcriptomic alterations. Results: CD3+B220+ cells in peripheral blood (p=0.0101) and spleen (p<0.0001) were expanded in MRL/lpr mice. Meanwhile, inhibition of proBDNF signalling reduced the percentage of CD3+B220+ cells in peripheral blood (p=0.0036) and spleen (p=0.0280), alleviated lymphadenopathy, reduced urine protein level (p<0.0001) and increased the body weight (p=0.0493). RNA-seq revealed 501 upregulated and 206 downregulated genes in splenic CD3+B220+ cells in McAb-proB-treated MRL/lpr mice compared with IgG-treated mice. The differentially expressed genes were found to be involved in apoptosis, tumour necrosis factor signalling, and T cell differentiation and proliferation. Conclusion: Systemic blockade of proBDNF inhibited the overexpansion of CD3+B220+ cells and altered their signals related to cell cycle, cell apoptosis and the immune response, which may contribute to the attenuation of disease symptoms in murine lupus.