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°Õ±ð³§¸éâ„¢-·¡8â„¢

Feeder-free, animal component-free culture medium for maintenance of human ES and iPS cells

°Õ±ð³§¸éâ„¢-·¡8â„¢

Feeder-free, animal component-free culture medium for maintenance of human ES and iPS cells

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Feeder-free, animal component-free culture medium for maintenance of human ES and iPS cells
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Product Advantages


  • Simplified, low-protein formulation based on the popular ³¾°Õ±ð³§¸éâ„¢1 medium for maintaining human ES and iPS cells

What's Included

  • °Õ±ð³§¸éâ„¢-·¡8â„¢ Basal Medium, 480 mL
  • °Õ±ð³§¸éâ„¢-·¡8â„¢ 25X Supplement, 20 mL

Overview

°Õ±ð³§¸éâ„¢-·¡8â„¢ is a feeder-free, animal component-free culture medium for human embryonic stem (ES) cells and human induced pluripotent stem (iPS) cells. It is based on the E8 formulation developed by the laboratory of Dr. James Thomson (University of Wisconsin-Madison), the lead research group behind the design of ³¾°Õ±ð³§¸éâ„¢1, the most widely published feeder-free culture medium for pluripotent stem cells.

Like the whole TeSRâ„¢ family of products, °Õ±ð³§¸éâ„¢-·¡8â„¢ medium is made with the highest level of quality and care. Specifically developed to only contain the essential components required for maintenance of ES and iPS cells, providing the simplest medium for the culture of pluripotent stem cells. °Õ±ð³§¸éâ„¢-·¡8â„¢ may be used with either Corning® Matrigel® hESC-Qualified Matrix (Corning 354277), or for a completely defined xeno-free system, use Vitronectin XFâ„¢ (Catalog #07180) or Laminin-521 (Catalog #77003) as the culture matrix.
Subtype
Specialized Media
Cell Type
Pluripotent Stem Cells
Species
Human
Application
Cell Culture, Expansion, Maintenance
Brand
TeSR
Area of Interest
Stem Cell Biology
Formulation Category
Animal Component-Free

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 #
05990
Lot #
All
Language
English
Document Type
Product Name
Catalog #
05990
Lot #
All
Language
English
Document Type
Product Name
Catalog #
05990
Lot #
All
Language
English
Document Type
Product Name
Catalog #
05990
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 (50)

Autism Spectrum Disorder Induced Pluripotent Stem Cells Display Dysregulated Calcium Signaling During Neural Differentiation A. J. AlShawaf et al. Cells 2025 Sep

Abstract

Autism Spectrum Disorder (ASD) is a neurodevelopmental condition that affects communication, social interaction, and behavior. Calcium (Ca2+) signaling dysregulation has been frequently highlighted in genetic studies as a contributing factor to aberrant developmental processes in ASD. Herein, we used ASD and control induced pluripotent stem cells (iPSCs) to investigate transcriptomic and functional Ca2+ dynamics at various stages of differentiation to cortical neurons. Idiopathic ASD and control iPSC lines underwent the dual SMAD inhibition differentiation protocol to direct their fate toward cortical neurons. Samples from multiple time points along the course of differentiation were processed for bulk RNA sequencing, spanning the following sequential stages: the iPSC stage, neural induction (NI) stage, neurosphere (NSP) stage, and differentiated cortical neuron (Diff) stage. Our transcriptomic analyses suggested that the numbers of Ca2+ signaling-relevant differentially expressed genes between ASD and control samples were higher in the iPSC and Diff stages. Accordingly, samples from the iPSC and Diff stages were processed for Ca2+ imaging studies. Results revealed that iPSC-stage ASD samples displayed elevated maximum Ca2+ levels in response to ATP compared to controls. By contrast, in the Diff stage, ASD neurons showed reduced maximum Ca2+ levels in response to ATP but increased maximum Ca2+ levels in response to KCl and DHPG relative to controls. Considering the distinct functional signaling contexts of these stimuli, this differential profile of receptor- and ionophore-mediated Ca2+ response suggests that aberrant calcium homeostasis underlies the pathophysiology of ASD neurons. Our data provides functional evidence for Ca2+ signaling dysregulation during neurogenesis in idiopathic ASD.
Optimizing the in vitro neuronal microenvironment to mitigate phototoxicity in live-cell imaging C. R. Hoffmann et al. Stem Cell Research & Therapy 2025 Sep

Abstract

Long-term imaging formats are ideal for capturing dynamic neuronal network formation in vitro, yet fluorescent techniques are often constrained by the impact of phototoxicity on cell survival. Here we present a live-imaging protocol that was optimised via quantitative analysis of 3 target culturing conditions on neuromorphological health: extracellular matrix (human- versus murine-derived laminin), culture media (Neurobasal™ versus Brainphys™ Imaging media), and seeding density (1 × 105 versus 2 × 105 cells/cm2). A cortical neuron reporter line was differentiated from human embryonic stem cells by transduction of Neurogenin-2 and green fluorescent protein, then fluorescently imaged in 8 different microenvironments daily for 33 days. Alongside viability analysis by PrestoBlue assay and gene quantification by digital polymerase chain reaction, an automated image analysis pipeline was developed to characterise network morphology and organisation over time. Brainphys™ Imaging medium was observed to support neuron viability, outgrowth, and self-organisation to a greater extent than Neurobasal™ medium with either laminin type, while the combination of Neurobasal™ medium and human laminin reduced cell survival. Further, a higher seeding density fostered somata clustering, but did not significantly extend viability compared to low density. These findings suggest a synergistic relationship between species-specific laminin and culture media in phototoxic environments, which is positively mediated by light-protective compounds found in Brainphys™ Imaging medium.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13287-025-04591-0.
Functional characterization of the MED12 p.Arg1138Trp variant in females: implications for neural development and disease mechanism N. C. Shaw et al. Molecular Medicine 2025 Sep

Abstract

Seven female individuals with multiple congenital anomalies, developmental delay and/or intellectual disability have been found to have a genetic variant of uncertain significance in the mediator complex subunit 12 gene ( MED12 c.3412C>T, p.Arg1138Trp). The functional consequence of this genetic variant in disease is undetermined, and insight into disease mechanism is required. We identified a de novo MED12 p.Arg1138Trp variant in a female patient and compared disease phenotypes with six female individuals identified in the literature. To investigate affected biological pathways, we derived two induced pluripotent stem cell (iPSC) lines from the patient: one expressing wildtype MED12 and the other expressing the MED12 p.Arg1138Trp variant. We performed neural disease modelling, transcriptomics and protein analysis, comparing healthy and variant cells. When comparing the two cell lines, we identified altered gene expression in neural cells expressing the variant, including genes regulating RNA polymerase II activity, transcription, pre-mRNA processing, and neural development. We also noted a decrease in MED12L expression. Pathway analysis indicated temporal delays in axon development, forebrain differentiation, and neural cell specification with significant upregulation of pre-ribosome complex gene pathways. In a human neural model, expression of MED12 p.Arg1138Trp altered neural cell development and dysregulated the pre-ribosome complex providing functional evidence of disease aetiology and mechanism in MED12-related disorders. The online version contains supplementary material available at 10.1186/s10020-025-01365-5.