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STEMdiff™ Neural Progenitor Medium

Medium for maintenance and expansion of neural progenitor cells derived from human ES and iPS cells

STEMdiff™ Neural Progenitor Medium

Medium for maintenance and expansion of neural progenitor cells derived from human ES and iPS cells

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Medium for maintenance and expansion of neural progenitor cells derived from human ES and iPS cells
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Product Advantages


  • Defined and serum-free

  • Supports expansion of NPCs generated using STEMdiff™ Neural Induction Medium

  • Optimized for efficient expansion of NPCs over multiple passages

  • Preserves NPC multipotency while minimizing spontaneous neuronal differentiation

  • Convenient, user-friendly format and protocol

What's Included

  • STEMdiff™ Neural Progenitor Basal Medium, 500 mL
  • STEMdiff™ Neural Progenitor Supplement A (50X), 10 mL
  • STEMdiff™ Neural Progenitor Supplement B (1000X), 500 µL

Overview

STEMdiff™ Neural Progenitor Medium is a defined and serum-free medium for the expansion of neural progenitor cells (NPCs) derived from human embryonic stem (ES) cells and induced pluripotent stem (iPS) cells using STEMdiff™ Neural Induction Medium (Catalog #05835). NPCs cultured in this medium can be expanded 3-5 fold per passage, and cultured for at least 10 passages, with minimal spontaneous neuronal differentiation.
Subtype
Specialized Media
Cell Type
Neural Cells, PSC-Derived, Neural Stem and Progenitor Cells, Pluripotent Stem Cells
Species
Human
Application
Cell Culture, Expansion
Brand
STEMdiff
Area of Interest
Disease Modeling, Drug Discovery and Toxicity Testing, Neuroscience, Stem Cell Biology
Formulation Category
Serum-Free

More Information

More Information
Safety Statement

CA WARNING: This product can expose you to chemicals including Nickel Compounds which are known to the State of California to cause cancer and birth defects or other reproductive harm. For more information go to

Data Figures

Morphology and Marker Expression of Neural Progenitor Cells Cultured in STEMdiff™ Neural Progenitor Medium

Figure 1. Morphology and Marker Expression of Neural Progenitor Cells Cultured in STEMdiff™ Neural Progenitor Medium

(A) Typical NPC morphology is observed in cultures (shown at day 6 of passage 1). (B-D) NPCs maintained in STEMdiff™ Neural Progenitor Medium express the CNS-type NPC markers PAX6 (B, D, red), SOX1 (C, red) and NESTIN (C, green), but not the neural crest marker SOX10 (D, green, single channel shown in inset). B-D were taken at the same magnification.

Expansion of Neural Progenitor Cells in STEMdiff™ Neural Progenitor Medium

Figure 2. Expansion of Neural Progenitor Cells in STEMdiff™ Neural Progenitor Medium

NPCs cultured in STEMdiff™ Neural Progenitor Medium can be expanded to generate a large number of cells. Three- to five-fold expansion can be achieved upon each passage. NPCs were derived using STEMdiff™ Neural Induction Medium and passaged once a week on average. n = 6.

Neural Progenitor Cells Cultured in STEMdiff™ Neural Progenitor Medium Show Minimal Spontaneous Neuronal Differentiation

Figure 3. Neural Progenitor Cells Cultured in STEMdiff™ Neural Progenitor Medium Show Minimal Spontaneous Neuronal Differentiation

Passages 1 (A) and 3 (B) of a representative NPC culture maintained in STEMdiff™ Neural Progenitor Medium. Cells were immunolabeled with SOX1 (red) to identify NPCs, and class III β-tubulin (green) to identify neurons. Spontaneous neuronal differentiation is low in NPC cultures maintained in STEMdiff™ Neural Progenitor Medium. A and B were taken at the same magnification.

Neural Progenitor Cells Maintained in STEMdiff™ Neural Progenitor Medium can Differentiate into Neurons and Astrocytes

Figure 4. Neural Progenitor Cells Maintained in STEMdiff™ Neural Progenitor Medium can Differentiate into Neurons and Astrocytes

When directed according to published protocols, NPCs can differentiate into neurons (A, class III β-tubulin shown in red) and astrocytes (B, GFAP shown in red). Nuclei are counterstained with DAPI (blue).

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Document Type
Product Name
Catalog #
05833
Lot #
All
Language
English
Document Type
Product Name
Catalog #
05833
Lot #
All
Language
English
Document Type
Product Name
Catalog #
05833
Lot #
All
Language
English
Document Type
Product Name
Catalog #
05833
Lot #
All
Language
English
Document Type
Product Name
Catalog #
05833
Lot #
All
Language
English

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.

Resources and Publications

Publications (26)

Endolysosomal processing of neuron-derived signaling lipids regulates autophagy and lipid droplet degradation in astrocytes J. N. Bhupana et al. Nature Communications 2025 May

Abstract

Dynamic regulation of metabolic activities in astrocytes is critical to meeting the demands of other brain cells. During neuronal stress, lipids are transferred from neurons to astrocytes, where they are stored in lipid droplets (LDs). However, it is not clear whether and how neuron-derived lipids trigger metabolic adaptation in astrocytes. Here, we uncover an endolysosomal function that mediates neuron-astrocyte transcellular lipid signaling. We identify Tweety homolog 1 (TTYH1) as an astrocyte-enriched endolysosomal protein that facilitates autophagic flux and LD degradation. Astrocyte-specific deletion of mouse Ttyh1 and loss of its Drosophila ortholog lead to brain accumulation of neutral lipids. Computational and experimental evidence suggests that TTYH1 mediates endolysosomal clearance of ceramide 1-phosphate (C1P), a sphingolipid that dampens autophagic flux and LD breakdown in mouse and human astrocytes. Furthermore, neuronal C1P secretion induced by inflammatory cytokine interleukin-1β causes TTYH1-dependent autophagic flux and LD adaptations in astrocytes. These findings reveal a neuron-initiated signaling paradigm that culminates in the regulation of catabolic activities in astrocytes. Subject terms: Organelles, Glial biology, Lipid signalling
CACNA1A loss-of-function affects neurogenesis in human iPSC-derived neural models I. Musante et al. Cellular and Molecular Life Sciences: CMLS 2025 Jun

Abstract

CACNA1A encodes the pore-forming α 1A subunit of the Ca V 2.1 calcium channel, whose altered function is associated with various neurological disorders, including forms of ataxia, epilepsy, and migraine. In this study, we generated isogenic iPSC-derived neural cultures carrying CACNA1A loss-of-function mutations differently affecting Ca V 2.1 splice isoforms. Morphological, molecular, and functional analyses revealed an essential role of CACNA1A in neurodevelopmental processes. We found that different CACNA1A loss-of-function mutations produce distinct neurodevelopmental deficits. The F1491S mutation, which is located in a constitutive domain of the channel and therefore causes a complete loss-of-function, impaired neural induction at very early stages, as demonstrated by changes in single-cell transcriptomic signatures of neural progenitors, and by defective polarization of neurons. By contrast, cells carrying the Y1854X mutation, which selectively impacts the synaptically-expressed Ca V 2.1[EFa] isoform, behaved normally in terms of neural induction but showed altered neuronal network composition and lack of synchronized activity. Our findings reveal previously unrecognized roles of CACNA1A in the mechanisms underlying neural induction and neural network dynamics and highlight the differential contribution of the divergent variants Ca V 2.1[EFa] and Ca V 2.1[EFb] in the development of human neuronal cells. The online version contains supplementary material available at 10.1007/s00018-025-05740-7.
Protein Kinase C promotes peroxisome biogenesis and peroxisome–endoplasmic reticulum interaction A. Borisyuk et al. The Journal of Cell Biology 2025 Jul

Abstract

Borisyuk et al. identify a signaling regulatory network of peroxisome proliferation, uncovering PKC as a positive regulator of peroxisome–ER interaction. During neuronal differentiation, activation of PKC contributes to an increase in peroxisome formation.