NeuroCult™ NS-A Proliferation Kit (Human)

Medium for expansion of human neural stem and progenitor cells

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NeuroCult™ NS-A Proliferation Kit (Human)

Medium for expansion of human neural stem and progenitor cells

1 Kit
Catalog #05751
226 USD

Required Products


NeuroCult™ NS-A Proliferation Kit (Human) is a standardized, serum-free basal medium and supplement for the culture of human neural stem and progenitor cells from normal tissues or tumor samples, in the neurosphere or adherent monolayer system. When supplemented with appropriate cytokines, NeuroCult™ NS-A Proliferation Kit (Human) is optimized to maintain human neural stem cells in culture for extended periods of time without the loss of their self-renewal, proliferation, or differentiation potential.

NOTE: Addition of rh EGF (Catalog #78006), rh bFGF (Catalog #78003) and heparin (Catalog #07980) is required.
  • NeuroCult™ NS-A Basal Medium (Human), 450 mL (Catalog #05750)
  • NeuroCult™ Proliferation Supplement (Human), 50 mL (Catalog #05753)
Specialized Media
Cell Type:
Brain Tumor Stem Cells; Neural Stem and Progenitor Cells
Cell Culture; Colony Assay; Expansion; Functional Assay; Spheroid Culture; Toxicity Assay
Area of Interest:
Cancer Research; Drug Discovery and Toxicity Testing; Neuroscience; Stem Cell Biology

Scientific Resources

Educational Materials


Product Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Data and Publications


Total cell expansion for fetal human telencephalic and cortical cell neurospheres cultured with Complete NeuroCult™ Proliferation Medium (Human) containing rh EGF, rh bFGF and heparin

Figure 1. Total Cell Expansion for Fetal Human Telencephalic and Cortical Cells Cultured as Neurospheres with Complete NeuroCult™ Proliferation Medium (Human) Containing rh EGF, rh bFGF and Heparin


Nature communications 2020 jul

Single-cell RNA-seq reveals that glioblastoma recapitulates a normal neurodevelopmental hierarchy.

C. P. Couturier et al.


Cancer stem cells are critical for cancer initiation, development, and treatment resistance. Our understanding of these processes, and how they relate to glioblastoma heterogeneity, is limited. To overcome these limitations, we performed single-cell RNA sequencing on 53586 adult glioblastoma cells and 22637 normal human fetal brain cells, and compared the lineage hierarchy of the developing human brain to the transcriptome of cancer cells. We find a conserved neural tri-lineage cancer hierarchy centered around glial progenitor-like cells. We also find that this progenitor population contains the majority of the cancer's cycling cells, and, using RNA velocity, is often the originator of the other cell types. Finally, we show that this hierarchal map can be used to identify therapeutic targets specific to progenitor cancer stem cells. Our analyses show that normal brain development reconciles glioblastoma development, suggests a possible origin for glioblastoma hierarchy, and helps to identify cancer stem cell-specific targets.
Pediatric surgery international 2019 dec

A comparison of exosomes derived from different periods breast milk on protecting against intestinal organoid injury.

R. Gao et al.


AIM OF THE STUDY Human breast milk reduces the risk and severity of necrotizing enterocolitis (NEC). Exosomes are extracellular vesicles (EVs) found in high concentrations in milk, and they mediate intercellular communication and immune responses. The aim of this study is to compare the protective effects of exosomes that are derived from different time periods of breast milk production against intestinal injury using an ex vivo intestinal organoid model. METHODS Colostrum, transitional and mature breast milk samples from healthy lactating mothers were collected. Exosomes were isolated using serial ultracentrifugation and filtration. Exosomes' presence was confirmed using transmission electron microscopy (TEM) and western blot. To form the intestinal organoids, terminal ileum was harvested from neonatal mice pups at postnatal day 9, crypts were isolated and organoids were cultured in matrigel. Organoids were either cultured with exposure to lipopolysaccharide (LPS), or in treatment groups where both LPS and exosomes were added in the culturing medium. Inflammatory markers and organoids viability were evaluated. MAIN RESULTS Human milk-derived exosomes were successfully isolated and characterized. LPS administration reduced the size of intestinal organoids, induced inflammation through increasing TNF$\alpha$ and TLR4 expression, and stimulated intestinal regeneration. Colostrum, transitional and mature human milk-derived exosome treatment all prevented inflammatory injury, while exosomes derived from colostrum were most effective at reducing inflammatory cytokine. CONCLUSIONS Human breast milk-derived exosomes were able to protect intestine organoids against epithelial injury induced by LPS. Colostrum exosomes offer the best protective effect among the breast-milk derived exosomes. Human milk exosomes can be protective against the development of intestinal injury such as that seen in NEC.
Scientific Reports 2019 dec

BMP signaling mediates glioma stem cell quiescence and confers treatment resistance in glioblastoma

R. Sachdeva et al.


Despite advances in therapy, glioblastoma remains an incurable disease with a dismal prognosis. Recent studies have implicated cancer stem cells within glioblastoma (glioma stem cells, GSCs) as mediators of therapeutic resistance and tumor progression. In this study, we investigated the role of the transforming growth factor-$\beta$ (TGF-$\beta$) superfamily, which has been found to play an integral role in the maintenance of stem cell homeostasis within multiple stem cell systems, as a mediator of stem-like cells in glioblastoma. We find that BMP and TGF-$\beta$ signaling define divergent molecular and functional identities in glioblastoma, and mark relatively quiescent and proliferative GSCs, respectively. Treatment of GSCs with BMP inhibits cell proliferation, but does not abrogate their stem-ness, as measured by self-renewal and tumorigencity. Further, BMP pathway activation confers relative resistance to radiation and temozolomide chemotherapy. Our findings define a quiescent cancer stem cell population in glioblastoma that may be a cellular reservoir for tumor recurrence following cytotoxic therapy.
Nature communications 2019

G-quadruplex DNA drives genomic instability and represents a targetable molecular abnormality in ATRX-deficient malignant glioma.

Y. Wang et al.


Mutational inactivation of ATRX ($\alpha$-thalassemia mental retardation X-linked) represents a defining molecular alteration in large subsets of malignant glioma. Yet the pathogenic consequences of ATRX deficiency remain unclear, as do tractable mechanisms for its therapeutic targeting. Here we report that ATRX loss in isogenic glioma model systems induces replication stress and DNA damage by way of G-quadruplex (G4) DNA secondary structure. Moreover, these effects are associated with the acquisition of disease-relevant copy number alterations over time. We then demonstrate, both in vitro and in vivo, that ATRX deficiency selectively enhances DNA damage and cell death following chemical G4 stabilization. Finally, we show that G4 stabilization synergizes with other DNA-damaging therapies, including ionizing radiation, in the ATRX-deficient context. Our findings reveal novel pathogenic mechanisms driven by ATRX deficiency in glioma, while also pointing to tangible strategies for drug development.
Oncogene 2019

BMI1 is a therapeutic target in recurrent medulloblastoma.

D. Bakhshinyan et al.


Medulloblastoma (MB) is the most frequent malignant pediatric brain tumor, representing 20{\%} of newly diagnosed childhood central nervous system malignancies. Although advances in multimodal therapy yielded a 5-year survivorship of 80{\%}, MB still accounts for the leading cause of childhood cancer mortality. In this work, we describe the epigenetic regulator BMI1 as a novel therapeutic target for the treatment of recurrent human Group 3 MB, a childhood brain tumor for which there is virtually no treatment option beyond palliation. Current clinical trials for recurrent MB patients based on genomic profiles of primary, treatment-naive tumors will provide limited clinical benefit since recurrent metastatic MBs are highly genetically divergent from their primary tumor. Using a small molecule inhibitor against BMI1, PTC-028, we were able to demonstrate complete ablation of self-renewal of MB stem cells in vitro. When administered to mice xenografted with patient tumors, we observed significant reduction in tumor burden in both local and metastatic compartments and subsequent increased survival, without neurotoxicity. Strikingly, serial in vivo re-transplantation assays demonstrated a marked reduction in tumor initiation ability of recurrent MB cells upon re-transplantation of PTC-028-treated cells into secondary recipient mouse brains. As Group 3 MB is often metastatic and uniformly fatal at recurrence, with no current or planned trials of targeted therapy, an efficacious targeted agent would be rapidly transitioned to clinical trials.