OrganoPro™乳腺癌类器官培养基套装

产品购买咨询
KBR-100 包含以下产品
  • OrganoPro™乳腺癌培养基 100mL
  • OrganoPro™乳腺癌添加剂成分A 2mL
  • OrganoPro™乳腺癌添加剂成分B 1mL
KBR-1000 包含以下产品
  • OrganoPro™乳腺癌培养基 1000mL
  • OrganoPro™乳腺癌添加剂成分A 10mL x 2
  • OrganoPro™乳腺癌添加剂成分B 10mL
科途医学 科学家
名字
PhD

我们的科学家向您推荐

我们的产品简化了实验流程，集成多种因子，无需单独优化，扩增潜力高，14天内细胞数量可达到1×10^6。适用于多种培养形式，包括基质胶、低吸附孔板和生物反应器悬浮培养。GMP级别生产条件下制备，批次质量稳定，试剂含量是常规市售干细胞培养基的2倍，实现极佳的成本效益比。让复杂的培养变得简单快速，让科研变得更高效。

概览
产品使用说明及支持信息
资源及文献引用
COA查询

概览

此产品基于 Simumatrix 技术平台，通过工业化高通量筛选，针对中国高发的肿瘤类型进行培养基优化筛选而开发出的类器官培养基产品，可用于乳腺癌的类器官培养。

产品优势/特点：
  • 简单易用，节省验证时间：提供详细操作方案，产品使用简便，节省研究者大量类器官培养摸索验证时间；
  • 肿瘤组织覆盖类型广：覆盖多达15个组织瘤种，>900种肿瘤驱动基因突变模型；
  • 扩增潜力高：自研高活力高稳定性WNT与RSPOs，支持肿瘤类器官多代次连续稳定培养；
  • 肿瘤类器官验证数据齐备：多维类器官验证数据的整合，类器官驱动基因突变及表达谱，类器官组织病理学验证及类器官药敏数据等。
  • 多篇高分文献应用：多篇高分文献应用，口碑卓越；
  • 自主研发，产能充足，性价比高：全自研生产，源头品控，产品性价比高。
产品组成:
产品名称货号规格储存温度保质期
OrganoPro™Breast Cancer Organoid Culture Medium 乳腺癌类器官培养基KBR-100/1000-M100mL / 1000mL2-8°C12个月
OrganoPro™ Breast Cancer Organoid Culture Supplement A(50X) 乳腺癌类器官培养基添加剂A(50X)KBR-100/1000-A2mL / 20mL-20°C12个月
OrganoPro™ Breast Cancer Organoid Culture Supplement B(100X) 乳腺癌类器官培养基添加剂B(100X)KBR-100/1000-B1mL / 10mL-20°C12个月
等等再来看吧，暂时还没有呢

类型

类器官培养基

适用细胞

乳腺癌类器官

物种

人类

应用

培养人源乳腺癌类器官

商标

OrganoPro™

产品使用说明及支持信息

在产品文档中查找支持信息和使用说明，或在下方探索更多

文档类型产品名称Catalog #
User manualOrganoPro™乳腺癌类器官培养基套装KBR-100 KBR-1000

资源及文献引用

相关资源及文献引用

A Highly Potent Small-Molecule Antagonist of Exportin-1 Selectively Eliminates CD44+CD24- Enriched Breast Cancer Stem-like Cells
Liu, Caigang, et al. | Drug Resistance Updates (2023)

Abstract:
Breast cancer stem-like cells (BCSCs) have been suggested as the underlying cause of tumor recurrence, metastasis and drug resistance in triple-negative breast cancer (TNBC). Here, we report the discovery and biological evaluation of a highly potent small-molecule antagonist of exportin-1, LFS-1107. We ascertained that exportin-1 (also named as CRM1) is a main cellular target of LFS-1107 by nuclear export functional assay, bio-layer interferometry binding assay and C528S mutant cell line. We found that LFS-1107 significantly inhibited TNBC tumor cells at low-range nanomolar concentration and LFS-1107 can selectively eliminate CD44+CD24- enriched BCSCs. We demonstrated that LFS-1107 can induce the nuclear retention of Survivin and consequent strong suppression of STAT3 transactivation abilities and the expression of downstream stemness regulators. Administration of LFS-1107 can strongly inhibit tumor growth in mouse xenograft model and eradicate BCSCs in residual tumor tissues. Moreover, LFS-1107 can significantly ablate the patient-derived tumor organoids (PDTOs) of TNBC as compared to a few approved cancer drugs. Lastly, we revealed that LFS-1107 can enhance the killing effects of chemotherapy drugs and downregulate multidrug resistance related protein targets. These new findings provide preclinical evidence of defining LFS-1107 as a promising therapeutic agent to deplete BCSCs for the treatment of TNBC.

Read More: https://doi.org/10.1016/j.drup.2022.100903

Discovery of AXL Degraders with Improved Potencies in Triple-Negative Breast Cancer (TNBC) Cells
He, Rui, et al. | Journal of Medicinal Chemistry (2023)

Abstract:
AXL kinase is heavily involved in tumorigenesis, metastasis, and drug resistance of many cancers, and several AXL inhibitors are in clinical investigations. Recent studies demonstrated that the N-terminal distal region of AXL plays more important roles in cell invasiveness than its C-terminal kinase domain. Therefore, degradation of AXL may present a novel superior therapeutic approach than the kinase inhibitor therapy. Herein, we report the discovery of a series of new AXL PROTAC degraders. One representative compound 6n potently depletes AXL with a DC50 value of 5 nM in MDA-MB-231 TNBC cells. It also demonstrates significantly improved potencies against the AXL signaling activation, cell proliferation, migration and invasion of TNBC cells comparing with the corresponding kinase inhibitor. Moreover, the compound exhibits promising therapeutic potential both in patient-derived organoids and a xenograft mouse model of MDA-MB-231 cells.
Read More: https://doi.org/10.1021/acs.jmedchem.2c01682

CDK12 inhibition enhances sensitivity of HER2+ breast cancers to HER2-tyrosine kinase inhibitor via suppressing PI3K/AKT
Li, Hui, et al. | European Journal of Cancer (2021)

Abstract:
Background
Alhtough anti-HER2 tyrosine kinase inhibitors (TKIs) have radically prolonged survival and improved prognosis in HER2-positive breast cancer patients, resistance to these therapies is a constant obstacle leading to TKIs treatment failure and tumour progression.
Methods
To develop new strategies to enhance TKIs efficiency by combining synergistic gene targets, we performed panel library screening using the CRISPR/Cas9 knockout technique based on data mining across TCGA data sets and verified the candidate target in preclinical models and breast cancer high-throughput sequencing data sets.
Results
We identified that CDK12, co-amplified with HER2 in a high frequency, is powerful to sensitise or resensitise HER2-positive breast cancer to anti-HER2 TKIs lapatinib, evidenced by patient-derived organoids in vitro and cell-derived xenograft or patient-derived xenograft in vivo. Exploring mechanisms, we found that inhibition of CDK12 attenuated PI3K/AKT signal, which usually serves as an oncogenic driver and is reactivated when HER2-positive breast cancers develop resistance to lapatinib. Combining CDK12 inhibition exerted additional suppression on p-AKT activation induced by anti-HER2 TKIs lapatinib treatment. Clinically, via DNA sequencing data for tumour tissue and peripheral blood ctDNA, we found that HER2-positive breast cancer patients with CDK12 amplification responded more insensitively to anti-HER2 treatment than those without accompanying CDK12 amplification by harbouring a markedly shortened progression-free survival (PFS) (median PFS: 4.3 months versus 6.9 months; hazards ratio [HR] = 2.26 [95% confidence interval [CI] = 1.32–3.86]; P = 0.0028).
Conclusions
Dual inhibition of HER2/CDK12 will prominently benefit the outcomes of patients with HER2-positive breast cancer by sensitising or resensitising the tumours to anti-HER2 TKIs treatment.
Read More: https://doi.org/10.1016/j.ejca.2020.11.045

Inhibition of cIAP1 as a strategy for targeting c-MYC–driven oncogenic activity
Li, Haoyan, et al. | Proceedings of the National Academy of Sciences (2018)

Abstract:

Protooncogene c-MYC, a master transcription factor, is a major driver of human tumorigenesis. Development of pharmacological agents for inhibiting c-MYC as an anticancer therapy has been a longstanding but elusive goal in the cancer field. E3 ubiquitin ligase cIAP1 has been shown to mediate the activation of c-MYC by destabilizing MAD1, a key antagonist of c-MYC. Here we developed a high-throughput assay for cIAP1 ubiquitination and identified D19, a small-molecule inhibitor of E3 ligase activity of cIAP1. We show that D19 binds to the RING domain of cIAP1 and inhibits the E3 ligase activity of cIAP1 by interfering with the dynamics of its interaction with E2. Blocking cIAP1 with D19 antagonizes c-MYC by stabilizing MAD1 protein in cells. Furthermore, we show that D19 and an improved analog (D19-14) promote c-MYC degradation and inhibit the oncogenic function of c-MYC in cells and xenograft animal models. In contrast, we show that activating E3 ubiquitin ligase activity of cIAP1 by Smac mimetics destabilizes MAD1, the antagonist of MYC, and increases the protein levels of c-MYC. Our study provides an interesting example using chemical biological approaches for determining distinct biological consequences from inhibiting vs. activating an E3 ubiquitin ligase and suggests a potential broad therapeutic strategy for targeting c-MYC in cancer treatment by pharmacologically modulating cIAP1 E3 ligase activity.

Read More: https://doi.org/10.1073/pnas.1807711115

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