STEMdiff™ Intestinal Organoid Kit
Serum-free medium kit for establishment and maintenance of human intestinal organoids from hPSCs
Need a high-quality cell source? Choose from our hiPSC healthy control lines, manufactured with mTeSR™ Plus.
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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.
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 (48)
Publications (7)
Cross-tissue immune profiling of APOE ε4 reveals early dysregulation in Alzheimer's disease.
Alzheimer's & dementia : the journal of the Alzheimer's Association 2026 Sep
Abstract
INTRODUCTION: Apolipoprotein E (APOE) ε4 is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), but its contribution to disease pathogenesis remains incompletely understood. METHODS: Here, we integrate proteomic profiling of plasma (n = 9028), cerebrospinal fluid (n = 1099), dorsolateral prefrontal cortex (n = 720), and superior temporal gyrus (n = 105) to define the immune phenotype associated with APOE ε4. RESULTS: We identify a conserved, allele dose-dependent pro-inflammatory immune protein signature across peripheral and central tissues independent of AD diagnosis. This signature also emerges in patient-derived cortical organoids prior to amyloid beta and tau pathology, supporting a genotype-driven mechanism. Cross-tissue comparisons reveal shared innate and antiviral responses alongside tissue-specific immune signaling. Notably, a 12-week medical ketogenic diet partially reversed the APOE ε4 immune signature. DISCUSSION: These findings position immune dysregulation as an early and tractable driver of AD risk in APOE ε4 carriers with direct implications for targeted prevention strategies.
IL-22 increases proglucagon-expressing enteroendocrine cells via STAT3 in human iPSC-derived intestinal epithelium.
Endocrinology 2026 Sep
Abstract
Intestinal epithelial differentiation is tightly regulated to maintain tissue homeostasis and systemic metabolic function. Although the intrinsic transcriptional programs governing enteroendocrine cell (EEC) development have been characterized extensively, the role of extrinsic immune signals in directing lineage specification is not completely understood. In particular, how cytokine signaling influences differentiation of EEC subtypes remains unclear. Here, we investigated the role of interleukin-22 (IL-22) in EEC differentiation using human induced pluripotent stem cell-derived intestinal organoids and in vivo models. IL-22 selectively increased proglucagon (GCG) expression and the number of glucagon-like peptide-1 (GLP-1)-positive EECs without affecting other EEC markers. This effect was associated with enhanced expression of the lineage-related transcription factors neurogenin 3 and forkhead box A2. Pharmacological inhibition of signal transducer and activator of transcription 3 (STAT3) signaling attenuated the IL-22-induced increases in GCG expression and GLP-1-positive cell abundance, indicating a role of STAT3 in mediating these effects. Mechanistically, relatively high expression of IL-22 receptor subunit alpha 1 in undifferentiated epithelial cells was associated with STAT3 activation induced by IL-22. Consistent with these findings, in vivo IL-22 administration increased intestinal GCG expression and GLP-1 levels in the circulation and intestinal tissue. Importantly, our findings indicate that IL-22 does not globally promote EEC differentiation but rather selectively directs epithelial lineage commitment toward the GCG-positive EEC fate. These results suggest that IL-22/STAT3 signaling induces human intestinal epithelial differentiation into GCG-positive EECs and may represent a strategy for modulating epithelial cell fate to influence systemic metabolic homeostasis.
Organoid phenotypic screening identified glycyrrhizin that confers protection against tumor necrosis factor-induced cell death
Stem Cell Reports 2026 Apr
Abstract
Human organoids are considered physiological models that reflect human physiology; however, their applications in drug screening studies are limited. To develop a fundamental treatment for recurrent Crohn’s disease (CD), in which tumor necrosis factor (TNF) is a key pathogenic factor, we conducted phenotypic drug screening to prevent TNF-induced cell death in human intestinal epithelial organoids. Glycyrrhizin, a natural product of licorice root, dose-dependently blocked TNF-induced cell death in organoids but not in TNF-sensitive L929 cells; L929 cells exhibited necroptosis, whereas organoid-derived cells preferentially showed apoptosis upon TNF treatment, determining the specificity of glycyrrhizin. Glycyrrhizin inhibited downstream caspase-8 signaling, which is essential for TNF-dependent apoptosis, and ameliorated intestinal inflammation in vivo. These results demonstrate that glycyrrhizin may be a novel therapeutic compound for CD and highlight the importance of using organoids for phenotypic drug screening. Graphical abstract Highlights•Human intestinal organoids are sensitive to TNF-induced cytotoxicity•We developed an assay system to screen for compounds that resist TNF in organoids•Glycyrrhizin inhibited TNF-induced apoptosis but not necroptosis in organoids•Glycyrrhizin ameliorated intestinal inflammation in a murine model in vivo Takahashi et al. developed a high-throughput phenotypic screening platform using human intestinal organoids, which exhibited higher sensitivity to TNF than conventional intestinal epithelial cell lines, and identified glycyrrhizin that protected TNF-induced cell death both in organoids and in vivo. Phenotypic screening using organoids, as demonstrated in this study, paves the way for drug development and chemical biology.
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Need a high-quality cell source? Choose from our hiPSC healthy control lines, manufactured with mTeSR™ Plus.
Legal Statement:
STEMdiff™ Intestinal Organoid Kit was developed under license to intellectual property owned by the Cincinnati Children’s Hospital.
STEMdiff™ Intestinal Organoid Kit was developed under license to intellectual property owned by the Cincinnati Children’s Hospital.
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 STEMCELL, REFER TO WWW.STEMCELL.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 STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
Safety Statement:
CA WARNING: This product can expose you to Progesterone which is known to the State of California to cause cancer. For more information go to www.P65Warnings.ca.gov
