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Human iPSC-Derived Intestinal Organoid Differentiation Kit

For research use only.

组分(Materials Provided)

Box A(2-8°C)
IDComponentsSize
RIPO-IWM005K-C01Intestinal organoid Basal Medium B14.5ml
RIPO-IWM005K-C02Intestinal organoid Basal Meidium C14.5ml
RIPO-IWM005K-C03Intestinal organoid Basal Medium D90ml

 

Box B(-20°C)
IDComponentsSize
RIPO-IWM005K-1-C01Intestinal organoid Medium A10ml
RIPO-IWM005K-1-C02Intestinal organoid Supplement B1.5ml
RIPO-IWM005K-1-C03Intestinal organoid Supplement C1.5ml
RIPO-IWM005K-1-C04Intestinal organoid Supplement D10ml

产品描述(Product Details)

Human iPSC-Derived Intestine Organoid Differentiation Kit (Ca. No. RIPO-IWM005K) allows hESC or hiPSC to differentiate into intestine organoids. Intestine organoids are three-dimensional in vitro models with a cellular composition and structural organization that is representative to the human intestine regions. This kit can produce 48 intestinal organoids in four steps. Organoids generated using Human iPSC-Derived intestine Organoid Differentiation Kit (Ca. No. RIPO-IWM005K) feature various types of cells, including intestine epithelium cells, mesenchyme cells, enterocytes, Paneth cells, goblet cells, etc. These intestine organoids show intestine crypt like structure, Villi and Microvilli like structure. These intestine organoids show normal intestinal function validated by the absorption of fatty acid and glucose.

产品特征(Product Specification)

The basic medium of this differentiation kit is a serum-free, well-defined medium with minimal batch variation to which differentiation factors are added. This medium does not contain antibiotics, the addition of which may affect organoid differentiation.

存储(Storage)

The unopened Box A is stable for 12 months from the date of manufacture if stored under 2-8°C.
The unopened Box B is stable for 12 months from the date of manufacture if stored under -20°C.
The opened kit should be stored according to components table.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
*请注意,为了支持完整的类器官培养和维持过程,本产品必须与Human iPSC-Derived Intestinal Organoid Maintenance Kit (Cat. No. RIPO-IWM006)一起使用。您可以点击此链接获取产品信息。
 

产品示意(Product Diagram)

Organoids PRODUCT DIAGRAM

Protocol Diagram of intestine organoid differentiation.

验证数据(Validation Data)

Organoid Histology and State

Organoids Organoid Histology And State

The intestine organoids differentiated using the Human iPSC-Derived intestine Organoid Differentiation Kit (Ca. No. RIPO-IWM005K) show regular peristalsis.

Orgnaoid Histology

Organoids ORGNAOID HISTOLOGY

Observation of granulocyte like cells, adipocyte like cells, smooth muscle like cells and intestinal crypt like structure by morphology on day 120 intestine organoids.

Marker Expression

Organoids MARKER EXPRESSION

The intestine organoids differentiated using the Human iPSC-Derived intestine Organoid Differentiation Kit (Ca. No. RIPO-IWM005K) show expression of enterochromaffin cells (CHGA) and endothelial cells (CD31).

Organoids MARKER EXPRESSION

The intestine organoids differentiated using the Human iPSC-Derived intestine Organoid Differentiation Kit (Ca. No. RIPO-IWM005K) show expression of goblet cells (mucus-producing, MUC2) and endothelial cells (CD31).

Organoids MARKER EXPRESSION

The intestine organoids differentiated using the Human iPSC-Derived intestine Organoid Differentiation Kit (Ca. No. RIPO-IWM005K) show expression of smooth muscle cell (α-SMA); epithelial cell (EPCAM); macrophage (CD68); goblet cell (MUC2); Ki67 (intestinal stem cell) and enteroendocrine cells (CHGA).

Organoid Activity

Organoids ORGANOID ACTIVITY

Intestine organoids differentiated using the Human iPSC-Derived intestine Organoid Differentiation Kit (Ca. No. RIPO-IWM005K) show normal intestinal function validated by the absorption of fatty acid and glucose.

 
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Wu, Zeng, Wu et al
Clin Transl Med (2025) 15 (3), e70244
Abstract: Chemoresistance remains a major hurdle in ovarian cancer (OC) treatment, as many patients eventually develop resistance to platinum-based chemotherapy and/or PARP inhibitors (PARPi).We performed transcriptome-wide analysis by RNA sequencing (RNA-seq) data of platinum-resistant and -sensitive OC tissues. We demonstrated the role of LINC02776 in platinum resistance in OC cells, mice models and patient-derived organoid (PDO) models.We identify the long noncoding RNA LINC02776 as a critical factor of platinum resistance. Elevated expression of LINC02776 is observed in platinum-resistant OC and serves as an independent prognostic factor for OC patients. Functionally, silencing LINC02776 reduces proliferation and DNA damage repair in OC cells, thereby enhancing sensitivity to platinum and PARPi in both xenograft mouse models and patient-derived organoid (PDO) models with acquired chemoresistance. Mechanistically, LINC02776 binds to the catalytic domain of poly (ADP-ribose) polymerase 1 (PARP1), promoting PARP1-dependent polyADP-ribosylation (PARylation) and facilitating homologous recombination (HR) restoration. Additionally, high HIF-1α expression in platinum-resistant tissues further stimulates LINC02776 transcription.Our findings suggest that targeting LINC02776 represents a promising therapeutic strategy for OC patients who have developed resistance to platinum or PARPi.LINC02776 promotes OC cell proliferation by regulating DNA damage and apoptosis signaling pathways. LINC02776 binds PARP1 to promote DNA damage-triggered PARylation in OC cells. LINC02776 mediates cisplatin and olaparib resistance in OC cells by enhancing PARP1-mediated PARylation activity and regulating the PARP1-mediated HR pathway. The high expression of LINC02776 is induced by HIF-1α in platinum-resistant OC cells and tissues.© 2025 The Author(s). Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.
Organoid-based single cell sequencing revealed the lineage evolution during docetaxel treatment in gastric cancer
Yang, Zhang, Hu et al
Cancer Lett (2025)
Abstract: Docetaxel resistance in gastric cancer poses a major therapeutic challenge. In this study, we established docetaxel-sensitive and -resistant gastric cancer organoids and performed single-cell RNA sequencing to identify cellular and molecular alterations. We observed significant shifts in cell populations, with increased secretory, immune-chemotactic, and transitional gastric cancer cells in the resistant group. Key resistance-related genes, including FOS, IFI27, and PTTG1IP, were upregulated in resistant organoids and gastric cancer patients. A pseudo-time trajectory analysis revealed that resistant cells predominantly occupied terminal differentiation stages. Knocking down FOS, IFI27, and PTTG1IP enhanced docetaxel sensitivity in both cell lines and organoids, regulating ROS production, autophagy, and apoptosis. In vivo, silencing these genes reduced tumor growth in response to docetaxel. These findings suggest that targeting FOS, IFI27, and PTTG1IP could overcome resistance and improve treatment outcomes for gastric cancer patients.Copyright © 2025. Published by Elsevier B.V.
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