STEMdiff™ Cerebral Organoid Kit

Culture medium kit for establishment and maturation of human cerebral organoids

STEMdiff™ Cerebral Organoid Kit

Culture medium kit for establishment and maturation of human cerebral organoids

1 Kit
Catalog #08570
312 USD

STEMdiff™ Cerebral Organoid Maturation Kit

Culture medium kit for extended maturation of human cerebral organoids

1 Kit
Catalog #08571
107 USD

Required Products


STEMdiff™ Cerebral Organoid Kit (Catalog #08570) is a defined, serum-free cell culture medium that enables the robust generation of human pluripotent stem cell (hPSC)-derived cerebral organoids in a simple four-stage protocol. Cerebral organoids are three-dimensional in vitro models with a cellular composition and structural organization that is representative of the developing human brain. STEMdiff™ Cerebral Organoid Kit has been optimized to increase efficiency and reproducibility of organoid formation based on the formulation published by Lancaster et al. (Lancaster MA et al. Nature USA, 2013 and Lancaster MA et al. Science USA, 2014). Cerebral organoid formation is initiated through an intermediate embryoid body (EB) formation step followed by expansion of neuroepithelia. After a period of maturation, organoids generated using this kit feature cortical-like regions such as the ventricular zone (PAX6+/SOX2+/Ki-67+), outer subventricular zone (Ki-67+/p-Vimentin+), intermediate zone (TBR2+), and cortical plate (CTIP2+/MAP2+/TBR1+), which layer in similar orientations as observed in vivo. For extended periods of organoid culture (> 40 days), the components required for organoid maturation can be purchased as the STEMdiff™ Cerebral Organoid Maturation Kit (Catalog #08571).
  • STEMdiff™ Cerebral Organoid Kit (Catalog #08570)
    • STEMdiff™ Cerebral Organoid Basal Medium 1,100 mL
    • STEMdiff™ Cerebral Organoid Basal Medium 2, 250 mL
    • STEMdiff™ Cerebral Organoid Supplement A, 10 mL
    • STEMdiff™ Cerebral Organoid Supplement B, 0.5 mL
    • STEMdiff™ Cerebral Organoid Supplement C, 0.25 mL
    • STEMdiff™ Cerebral Organoid Supplement D, 0.5 mL
    • STEMdiff™ Cerebral Organoid Supplement E, 4.5 mL
  • STEMdiff™ Cerebral Organoid Maturation Kit (Catalog #08571)
    • STEMdiff™ Cerebral Organoid Basal Medium 2, 250 mL
    • STEMdiff™ Cerebral Organoid Supplement E, 4.5 mL
Specialized Media
Cell Type:
Neural Cells, PSC-Derived; Neural Stem and Progenitor Cells; Pluripotent Stem Cells
Cell Culture; Differentiation; Organoid Culture
Area of Interest:
Disease Modeling; Neuroscience; Stem Cell Biology

Scientific Resources

Educational Materials

Brochure Organoids
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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


(A) A representative phase-contrast image of a whole cerebral organoid at day 40 generated using the STEMdiff™ Cerebral Organoid Kit. Cerebral organoids at this stage are made up of phase-dark structures that may be surrounded by regions of thinner, more translucent structures that display layering (arrowheads). (B) Immunohistological analysis on cryosections of cerebral organoids reveals cortical regions within the organoid labelled by the apical progenitor marker PAX6 (red) and neuronal marker β-tubulin III (green). (C-F) Inset of boxed region from (B). (C) PAX6+ apical progenitors (red, enclosed by dotted line) are localized to a ventricular zone-like region. β-tubulin III+ neurons (green) are adjacent to the ventricular zone. (D) CTIP2, a marker of the developing cortical plate, co-localizes with β-tubulin III+ neurons in a cortical plate-like region. Organization of the layers recapitulates early corticogenesis observed during human brain development. (E) Proliferating progenitor cells labeled by Ki-67 (green) localize along the ventricle, nuclei are counterstained with DAPI (blue). (F) An additional population of Ki-67+ cells is found in an outer subventricular zone-like region (arrowheads). Scale Bar = (A) 1 mm, (B) 500 µm and (C-F) 200 µm.

Principal component analysis of hPSC and cerebral organoid transcriptomes. Cerebral organoids generated using the STEMdiff™ Cerebral Organoid Kit (filled blue circles) cluster together, and cluster with previously published (C Luo et al. Cell Rep, 2016) cerebral organoids (open blue circles). The first principal component accounts for the majority of variance seen (PC1; 80%) and distinguishes the cerebral organoid samples from the hPSCs (green circles). The second principal component accounts for only 9% of the variation, and highlights the modest expression differences between cultured organoids and primary embryonic fetal brain samples (19 post-conceptional weeks, brown circles).

Heatmap of expression levels for genes associated with synaptic transmission function and neurogenesis in Day 40 organoids. These data show that gene expression of cerebral organoids generated from the STEMdiff™ Cerebral Organoid Kit are similar to published results (C Luo et al. Cell Rep, 2016).


Scientific reports 2019 nov

Extracellular Membrane Vesicles from Lactobacilli Dampen IFN-$\gamma$ Responses in a Monocyte-Dependent Manner.

M. Mata Forsberg et al.


Secreted factors derived from Lactobacillus are able to dampen pro-inflammatory cytokine responses. Still, the nature of these components and the underlying mechanisms remain elusive. Here, we aimed to identify the components and the mechanism involved in the Lactobacillus-mediated modulation of immune cell activation. PBMC were stimulated in the presence of the cell free supernatants (CFS) of cultured Lactobacillus rhamnosus GG and Lactobacillus reuteri DSM 17938, followed by evaluation of cytokine responses. We show that lactobacilli-CFS effectively dampen induced IFN-$\gamma$ and IL-17A responses from T- and NK cells in a monocyte dependent manner by a soluble factor. A proteomic array analysis highlighted Lactobacillus-induced IL-1 receptor antagonist (ra) as a potential candidate responsible for the IFN-$\gamma$ dampening activity. Indeed, addition of recombinant IL-1ra to stimulated PBMC resulted in reduced IFN-$\gamma$ production. Further characterization of the lactobacilli-CFS revealed the presence of extracellular membrane vesicles with a similar immune regulatory activity to that observed with the lactobacilli-CFS. In conclusion, we have shown that lactobacilli produce extracellular MVs, which are able to dampen pro-inflammatory cytokine responses in a monocyte-dependent manner.
Cell stem cell 2019 aug

Interconversion between Tumorigenic and Differentiated States in Acute Myeloid Leukemia.

M. D. McKenzie et al.


Tumors are composed of phenotypically heterogeneous cancer cells that often resemble various differentiation states of their lineage of origin. Within this hierarchy, it is thought that an immature subpopulation of tumor-propagating cancer stem cells (CSCs) differentiates into non-tumorigenic progeny, providing a rationale for therapeutic strategies that specifically eradicate CSCs or induce their differentiation. The clinical success of these approaches depends on CSC differentiation being unidirectional rather than reversible, yet this question remains unresolved even in prototypically hierarchical malignancies, such as acute myeloid leukemia (AML). Here, we show in murine and human models of AML that, upon perturbation of endogenous expression of the lineage-determining transcription factor PU.1 or withdrawal of established differentiation therapies, some mature leukemia cells can de-differentiate and reacquire clonogenic and leukemogenic properties. Our results reveal plasticity of CSC maturation in AML, highlighting the need to therapeutically eradicate cancer cells across a range of differentiation states.
American journal of physiology. Gastrointestinal and liver physiology 2018

Linaclotide improves gastrointestinal transit in cystic fibrosis mice by inhibiting sodium/hydrogen exchanger 3.

D. R. McHugh et al.


Gastrointestinal dysfunction in cystic fibrosis (CF) is a prominent source of pain among patients with CF. Linaclotide, a guanylate cyclase C (GCC) receptor agonist, is a US Food and Drug Administration-approved drug prescribed for chronic constipation but has not been widely used in CF, as the cystic fibrosis transmembrane conductance regulator (CFTR) is the main mechanism of action. However, anecdotal clinical evidence suggests that linaclotide may be effective for treating some gastrointestinal symptoms in CF. The goal of this study was to determine the effectiveness and mechanism of linaclotide in treating CF gastrointestinal disorders using CF mouse models. Intestinal transit, chloride secretion, and intestinal lumen fluidity were assessed in wild-type and CF mouse models in response to linaclotide. CFTR and sodium/hydrogen exchanger 3 (NHE3) response to linaclotide was also evaluated. Linaclotide treatment improved intestinal transit in mice carrying either F508del or null Cftr mutations but did not induce detectable Cl- secretion. Linaclotide increased fluid retention and fluidity of CF intestinal contents, suggesting inhibition of fluid absorption. Targeted inhibition of sodium absorption by the NHE3 inhibitor tenapanor produced improvements in gastrointestinal transit similar to those produced by linaclotide treatment, suggesting that inhibition of fluid absorption by linaclotide contributes to improved gastrointestinal transit in CF. Our results demonstrate that linaclotide improves gastrointestinal transit in CF mouse models by increasing luminal fluidity through inhibiting NHE3-mediated sodium absorption. Further studies are necessary to assess whether linaclotide could improve CF intestinal pathologies in patients. GCC signaling and NHE3 inhibition may be therapeutic targets for CF intestinal manifestations. NEW {\&} NOTEWORTHY Linaclotide's primary mechanism of action in alleviating chronic constipation is through cystic fibrosis transmembrane conductance regulator (CFTR), negating its use in patients with cystic fibrosis (CF). For the first time, our findings suggest that in the absence of CFTR, linaclotide can improve fluidity of the intestinal lumen through the inhibition of sodium/hydrogen exchanger 3. These findings suggest that linaclotide could improve CF intestinal pathologies in patients.