HS-27
目录号 : GC61784
HS-27，一种荧光Hsp90抑制剂，检测完整组织标本表面Hsp90的表达。HS-27由SNX-5422的核心元素组成，SNX-5422是一种Hsp90抑制剂，通过PEG连接物与荧光素衍生物(异硫氰酸荧光素或FITC)连接，后者与外周表达的Hsp90结合。HS-27在乳腺癌的观察与研究中有潜在的应用。
Cas No.:1562024-11-6
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
HS-27, a fluorescently-tethered Hsp90 inhibitor, assays surface Hsp90 expression on intact tissue specimens. HS-27 is made up of the core elements of SNX-5422, an Hsp90 inhibitor, tethered via a PEG linker to a fluorescein derivative (fluorescein isothiocyanate or FITC), that binds to ectopically expressed Hsp90. HS-27 has potential use in a see-and-treat paradigm in breast cancer[1].
HS-27 labels all receptor subtypes of breast cancer, but not normal cells, and specifically binds to Hsp90 expressed on the surface of breast cancer cells before being internalized. HS-27 fluorescence is greater in tumor than non-tumor tissue[1].
[1]. Crouch BT, et al. Exploiting heat shock protein expression to develop a non-invasive diagnostic tool for breast cancer. Sci Rep. 2019 Mar 5;9(1):3461.
| Cas No. | 1562024-11-6 | SDF | |
| Canonical SMILES | O=C(N)C1=CC=C(N2N=C(C)C3=C2CC(C)(C)CC3=O)C=C1NCCCOCCOCCOCCOCCOCCCNC(NC4=CC5=C(C6(C7=C(OC8=C6C=CC(O)=C8)C=C(O)C=C7)OC5=O)C=C4)=S | ||
| 分子式 | C52H60N6O12S | 分子量 | 993.13 |
| 溶解度 | DMSO: 125 mg/mL (125.86 mM) | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.0069 mL | 5.0346 mL | 10.0692 mL |
| 5 mM | 0.2014 mL | 1.0069 mL | 2.0138 mL |
| 10 mM | 0.1007 mL | 0.5035 mL | 1.0069 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。
Functionally distinct human marrow stromal cell lines immortalized by transduction with the human papilloma virus E6/E7 genes
Blood 1995 Feb 15;85(4):997-1005.PMID:7849321doi
A replication-defective recombinant retrovirus containing the human papilloma virus E6/E7 genes (LXSN-16 E6E7) was used to immortalize stromal cells from human marrow. The E6/E7 gene products interfere with the function of tumor-suppressor proteins p53 and Rb, respectively, thereby preventing cell cycle arrest without causing significant transformation. Twenty-seven immortalized clones designated HS-1 to HS-27 were isolated, four of which are characterized in this report. Two cell lines, HS-5 and HS-21, appear to be fibroblastoid and secrete significant levels of granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage-CSF (GM-CSF), macrophage-CSF (M-CSF), Kit ligand (KL), macrophage-inhibitory protein-1 alpha, interleukin-6 (IL-6), IL-8, and IL-11. However, only HS-5 supports proliferation of hematopoietic progenitor cells when cocultured in serum-deprived media with no exogenous factors. Conditioned media (CM) from HS-5 promotes growth of myeloid colonies to significantly greater extent than a cocktail of recombinant factors containing 10 ng/mL of IL-1, IL-3, IL-6, G-CSF, GM-CSF, and KL and 3 U of erythropoietin (Epo). Two additional clones, HS-23 and HS-27, resemble "blanket" cells, with an epithelioid morphology, and are much larger, broader, and flatter when compared with HS-5 and HS-21. These lines secrete low levels of growth factors and do not support proliferation of isolated progenitor cells in cocultures. CM from HS-23 and HS-27 also fail to support growth of myeloid colonies. Both HS-23 and HS-27 express relatively high levels of VCAM-1, yet HS-27 is the only line that supports the formation of "cobblestone" areas by isolated CD34+38lo cells. We hypothesize that HS-5, HS-21, HS-23, and HS-27 represent functionally distinct components of the marrow microenvironment.
Regulating the uptake of poly(N-(2-hydroxypropyl) methacrylamide)-based micelles in cells cultured on micropatterned surfaces
Biointerphases 2021 Jul 13;16(4):041002.PMID:34261325DOI:10.1116/6.0001012.
Cellular uptake of nanoparticles plays a crucial role in cell-targeted biomedical applications. Despite abundant studies trying to understand the interaction between nanoparticles and cells, the influence of cell geometry traits such as cell spreading area and cell shape on the uptake of nanoparticles remains unclear. In this study, poly(vinyl alcohol) is micropatterned on polystyrene cell culture plates using ultraviolet photolithography to control the spreading area and shape of individual cells. The effects of these factors on the cellular uptake of poly(N-(2-hydroxypropyl)methacrylamide)-based micelles were investigated at a single-cell level. Human carcinoma MCF-7 and A549 cells as well as normal HS-27 and MRC-5 fibroblasts were cultured on micropatterned surfaces. MCF-7 and A549 cells, both with larger sizes, had a higher total micelle uptake. However, the uptake of HS-27 and MRC-5 cells decreased with increasing spreading area. In terms of cell shapes, MCF-7 and A549 cells with round shapes showed a higher micelle uptake, while those with a square shape had a lower cellular uptake. On the other hand, HS-27 and MRC-5 cells showed opposite behaviors. The results indicate that the geometry of cells can influence the nanoparticle uptake and may shed light on the design of functional nanoparticles.
Exploiting heat shock protein expression to develop a non-invasive diagnostic tool for breast cancer
Sci Rep 2019 Mar 5;9(1):3461.PMID:30837677DOI:10.1038/s41598-019-40252-y.
Leveraging the unique surface expression of heat shock protein 90 (Hsp90) in breast cancer provides an exciting opportunity to develop rapid diagnostic tests at the point-of-care setting. Hsp90 has previously been shown to have elevated expression levels across all breast cancer receptor subtypes. We have developed a non-destructive strategy using HS-27, a fluorescently-tethered Hsp90 inhibitor, to assay surface Hsp90 expression on intact tissue specimens and validated our approach in clinical samples from breast cancer patients across estrogen receptor positive, Her2-overexpressing, and triple negative receptor subtypes. Utilizing a pre-clinical biopsy model, we optimized three imaging parameters that may affect the specificity of HS-27 based diagnostics - time between tissue excision and staining, agent incubation time, and agent dose, and translated our strategy to clinical breast cancer samples. Findings indicated that HS-27 florescence was highest in tumor tissue, followed by benign tissue, and finally followed by mammoplasty negative control samples. Interestingly, fluorescence in tumor samples was highest in Her2+ and triple negative subtypes, and inversely correlated with the presence of tumor infiltrating lymphocytes indicating that HS-27 fluorescence increases in aggressive breast cancer phenotypes. Development of a Gaussian support vector machine classifier based on HS-27 fluorescence features resulted in a sensitivity and specificity of 82% and 100% respectively when classifying tumor and benign conditions, setting the stage for rapid and automated tissue diagnosis at the point-of-care.
Understanding the sources of errors in ex vivo Hsp90 molecular imaging for rapid-on-site breast cancer diagnosis
Biomed Opt Express 2021 Mar 23;12(4):2299-2311.PMID:33996230DOI:10.1364/BOE.418818.
Overexpression of heat shock protein 90 (Hsp90) on the surface of breast cancer cells makes it an attractive molecular biomarker for breast cancer diagnosis. Before a ubiquitous diagnostic method can be established, an understanding of the systematic errors in Hsp90-based imaging is essential. In this study, we investigated three factors that may influence the sensitivity of ex vivo Hsp90 molecular imaging: time-dependent tissue viability, nonspecific diffusion of an Hsp90 specific probe (HS-27), and contact-based imaging. These three factors will be important considerations when designing any diagnostic imaging strategy based on fluorescence imaging of a molecular target on tissue samples.
Methionine dependence of tumours: a biochemical strategy for optimizing paclitaxel chemosensitivity in vitro
Biochem Pharmacol 2006 Mar 14;71(6):772-8.PMID:16414026DOI:10.1016/j.bcp.2005.12.014.
Methionine dependence is a unique feature of cancer cells characterized by growth and cell cycle arrest (typically in S and G2/M) under conditions of methionine depletion. Following replenishment of media with methionine, the cell cycle blockade is reversible and during this recovery period, cells may become more susceptible to the action of cell cycle specific drugs. The response of a panel of methionine dependent (HTC, Phi-1, PC3 and 3T3) cells to vinblastine and paclitaxel was compared to methionine independent HS-27 cells under conditions of methionine depletion (M-H+; methionine depleted media supplemented with homocysteine) and starvation (M-H-; media without methionine or homocysteine). All cell lines were significantly more resistant to both agents under M-H+ and M-H- conditions compared to controls under normal culture conditions [M+H-]; however, the magnitude of resistance was reduced in the methionine independent HS-27 cells. During recovery from methionine depletion and starvation, the response of the methionine dependent cells to vinblastine and paclitaxel was significantly enhanced compared to controls. Although the activity of vinblastine on the HS-27 cell line was comparable to controls, these methionine independent cells became significantly more resistant to paclitaxel during recovery studies (IC50 = 2.13 +/- 0.5 microM) compared to control cultures (IC50 = 0.13 +/- 0.15 microM). Whilst the mechanism responsible for this remains uncertain, the increased activity of paclitaxel against methionine dependent cells in conjunction with the decreased activity against HS-27 cells suggests that methionine depletion strategies may enhance the therapeutic index of paclitaxel.