mTeSR™ Plus
cGMP, stabilized feeder-free maintenance medium for human ES and iPS cells
Need a high-quality cell source? Choose from our hiPSC healthy control lines, manufactured with mTeSR™ Plus.
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What Our Scientist Says
Innovation is a core value at ƽ. The evolution to mTeSR™ Plus reflects that and our desire to serve the next generation of pluripotent stem cell researchers.
Matthew WongScientist
Overview
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Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
The Certificate of Analysis for this product has been updated for newly released materials. To access respective CoAs please use this tool.
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
Educational Materials (57)
Publications (257)
Development of potent, selective cPLA2 inhibitors for targeting neuroinflammation in Alzheimer’s disease and other neurodegenerative disorders
Npj Drug Discovery 2026 Jan
Abstract
Chronic neuroinflammation plays a key role in the progression of Alzheimer’s disease (AD), and the cytosolic calcium-dependent phospholipase A2 (cPLA2) enzyme is a critical mediator of inflammatory lipid signaling pathways. Here we investigate the therapeutic potential of novel cPLA2 inhibitors in modulating neuroinflammation in AD. By leveraging the giga-scale V-SYNTHES2 virtual screening in on-demand chemical space and conducting two rounds of optimization for potency and selectivity, we have identified BRI-50460, achieving an IC50 of 0.88 nM in cellular assays that measure cPLA2-mediated arachidonic acid release. In vivo studies revealed favorable brain-to-plasma ratios, highlighting the ability of BRI-50460 to penetrate the central nervous system, modulating neuroinflammatory pathways, and restoring lipid homeostasis. In astrocytes and neurons derived from human induced pluripotent stem cells, BRI-50460 mitigates the effects of amyloid beta 42 oligomers on cPLA2 activation, tau hyperphosphorylation, and synaptic loss. Our results support that small molecule inhibitors of cPLA2 can modulate the downstream inflammatory signaling, offering a promising therapeutic strategy for neurodegenerative diseases.
Engineered T cell therapy for the treatment of cardiac fibrosis during chronic phase of myocarditis
Theranostics 2026 Jan
Abstract
Background: Chronic myocarditis (CMYO) progresses to fibrosis and heart failure, yet no therapies effectively target fibrosis. Fibroblast activation protein (FAP) marks pathogenic myofibroblasts, but its therapeutic potential remains unexplored in inflammatory settings.Methods: Using bulk/scRNA-seq of human myocarditis samples, we identified FAP as a fibrosis-specific marker. We engineered FAP-targeted CAR-T (FAP.CAR-T) cells and tested their efficacy in autoimmune (EAM) and viral (CVB3) myocarditis models. Human cardiac organoids (hCOs) treated with IL-17A modeled inflammatory fibrosis.Results: FAP expression correlated with fibrosis severity in patients (r = 0.96, P = 0.0028). In EAM and CVB3 models, FAP.CAR-T cells reduced fibrosis by 65% and 55%, respectively (P < 0.001), restored ejection fraction to higher than 65%. hCOs treated with FAP.CAR-T cells showed 55% less fibrosis (P < 0.05). No toxicity was observed in healthy mice.Conclusions: FAP.CAR-T cells eliminate fibrosis-driving myofibroblasts, reversing cardiac dysfunction in chronic myocarditis. This strategy, validated in human organoids, offers translatable immunotherapy for fibrosis-driven heart disease.
CXCL9 and CXCL10 Induce Expression of Nociceptive Ion Channels in Primary Sensory Neurons in Models of HIV-Associated Distal Sensory Polyneuropathy
International Journal of Molecular Sciences 2026 Jan
Abstract
HIV-associated distal sensory polyneuropathy (HIV-DSP) remains prevalent even in the antiretroviral therapy (ART) era. Previously, we identified the upregulation of nociceptive ion channels transient receptor potential vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1) in the dorsal root ganglia (DRG) of simian immunodeficiency virus (SIV)-infected ART-treated macaques. To investigate upstream mechanisms, we performed bulk RNA-seq and pathway analysis on DRGs from uninfected, SIV-infected, and SIV-infected/ART macaques. SIV infection drove strong activation of upstream regulators of interferon γ (IFNγ) and lipopolysaccharide (LPS). Although ART reduced overall IFNγ and LPS pathway activity, the IFNγ-inducible chemokines C-X-C motif chemokine ligand (CXCL)9 and CXCL10 remained significantly upregulated. To determine whether these chemokines influence TRPV1/TRPA1 expression, we treated induced pluripotent stem cell-derived peripheral sensory neurons (iPSC-PSNs) with CXCL9 and CXCL10, which induced a significant increase in TRPV1 but not TRPA1 expression. In parallel experiments, IFNγ but not LPS stimulated monocyte-derived macrophages (MDMs) to release CXCL9 and CXCL10. Conditioned media from IFNγ-treated MDMs modestly increased TRPV1 expression in iPSC-PSNs, and pharmacological inhibition of CXCR3, the receptor of CXCL9/10, did not reduce this effect. Together, these data indicate that persistent IFNγ-driven CXCL9/10 signaling may be one contributor to nociceptor sensitization underlying HIV-DSP, even in the presence of ART.
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Legal Statement:
This product was developed under license to intellectual property owned by WiCell™ Research Institute. This product is sold for research use only (whether the buyer is an academic or for-profit entity) under a non-transferable, limited-use license. Purchase of this product does not include the right to sell, use or otherwise transfer this product for commercial purposes (i.e., any activity undertaken for consideration, such as use of this product for manufacturing, or resale of this product or any materials made using this product, or use of this product or any materials made using this product to provide services) or clinical use (i.e., administration of this product or any material using this product to humans) or the right to implant any material made using this product into an animal by, or in collaboration with, a for-profit entity, for purposes other than basic pre-clinical research applications (including without limitation teratoma assays) to validate the function of the cells. Purchasers who do not agree to the terms and conditions set forth above should return the product in acceptable conditions to the seller for a refund.
This product was developed under license to intellectual property owned by WiCell™ Research Institute. This product is sold for research use only (whether the buyer is an academic or for-profit entity) under a non-transferable, limited-use license. Purchase of this product does not include the right to sell, use or otherwise transfer this product for commercial purposes (i.e., any activity undertaken for consideration, such as use of this product for manufacturing, or resale of this product or any materials made using this product, or use of this product or any materials made using this product to provide services) or clinical use (i.e., administration of this product or any material using this product to humans) or the right to implant any material made using this product into an animal by, or in collaboration with, a for-profit entity, for purposes other than basic pre-clinical research applications (including without limitation teratoma assays) to validate the function of the cells. Purchasers who do not agree to the terms and conditions set forth above should return the product in acceptable conditions to the seller for a refund.
Quality Statement:
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT ƽ, REFER TO WWW.ƽ.COM/COMPLIANCE.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT ƽ, REFER TO WWW.ƽ.COM/COMPLIANCE.
