Ivermectin Suppresses Gastric Cancer in Patient-Derived Organoids (2026 Study)
A June 2026 South Korean study found ivermectin suppressed gastric cancer growth in patient-derived 3D organoids, achieving 82.48% cell death when combined with cisplatin — a more realistic tumor model than standard cell lines.
By Sanare Lab · July 25, 2026 · 6 min read
Key Takeaway
A June 2026 South Korean study tested ivermectin against gastric cancer using both standard cell lines and patient-derived 3D organoids — a more realistic tumor model. Ivermectin suppressed tumor growth and enhanced the effect of cisplatin in organoids, with cell death reaching 82.48% in combination treatment. The findings are preclinical and require further validation before any clinical conclusions can be drawn.
A June 2026 study from Kyungpook National University in South Korea tested ivermectin, an antiparasitic drug, against gastric cancer (stomach cancer). The researchers used standard cancer cell lines and patient-derived three-dimensional organoids, which are lab-grown mini tumor models that better mimic tumors in the body. Ivermectin suppressed tumor growth and made cisplatin work better in the organoids, with cell death reaching 82.48% when both were used together. This was preclinical research, not a proven or available cancer treatment, and needs more validation.
Gastric cancer (stomach cancer) remains one of the leading causes of cancer-related death worldwide, with limited treatment options for advanced or cisplatin-resistant disease. Drug repurposing — finding new uses for existing, approved medications — has emerged as a cost-effective strategy to expand the therapeutic arsenal against difficult-to-treat cancers.
Ivermectin, a Nobel Prize-winning antiparasitic drug widely used in humans and animals, has been the subject of growing preclinical cancer research. Previous studies have shown anticancer activity in breast, lung, and colorectal cancer models. A new 2026 study from Kyungpook National University in South Korea now extends this research to gastric cancer, using both conventional 2D cell lines and patient-derived 3D organoids — a more physiologically relevant model that better mimics how tumors behave in the body.
The study, published in the Journal of Gastrointestinal Oncology (June 30, 2026), was conducted by researchers at Kyungpook National University Chilgok Hospital and School of Medicine in Daegu, Republic of Korea. It investigated ivermectin's anticancer mechanisms and its potential to enhance cisplatin — the standard chemotherapy backbone for gastric cancer.
Table of Contents
- Study Design and Methods
- Key Findings: Cell Lines
- Key Findings: Patient-Derived Organoids
- Mechanism of Action
- Evidence Level and Limitations
- FAQ
- Shop Sanare Lab
- References
Study Design and Methods
The researchers used a two-pronged approach. First, they tested ivermectin in two established gastric cancer cell lines: SNU719 and SNU620. These are standard 2D (flat culture) models. Second — and more innovatively — they tested ivermectin in patient-derived gastric cancer organoids (GC7 and GC15). Organoids are 3D mini-tumor structures grown from actual patient tumor tissue, which preserve the genetic and structural characteristics of the original tumor far better than standard cell lines.
| Parameter | Detail |
|---|---|
| Study type | Preclinical — in vitro (2D cell lines + 3D patient-derived organoids) |
| Cancer type | Gastric cancer (stomach cancer) |
| Models used | SNU719, SNU620 cell lines; GC7, GC15 patient-derived organoids |
| Comparator drug | Cisplatin (standard gastric cancer chemotherapy) |
| Institution | Kyungpook National University Chilgok Hospital, Daegu, South Korea |
| Published | Journal of Gastrointestinal Oncology, June 30, 2026 |
| DOI | 10.21037/jgo-2025-710 |
Key Findings: Cell Lines (2D Models)
In the SNU719 cell line, ivermectin suppressed cell viability in a dose-dependent manner — meaning higher doses produced greater cell death. Ivermectin also enhanced the anticancer effect of cisplatin in this cell line. However, in the SNU620 cell line, ivermectin showed no significant effect on cell viability, highlighting that ivermectin's activity is not universal across all gastric cancer subtypes.
Western blot analysis revealed that ivermectin reduced the protein expression of YAP1 (Yes-associated protein 1) and CTGF (connective tissue growth factor) — two proteins involved in cancer cell survival and proliferation — after 24 hours of treatment. Interestingly, this suppression was attenuated at 48 hours and showed a rebound tendency at 72 hours, suggesting that cancer cells may develop adaptive resistance mechanisms over time.
Flow cytometry confirmed that ivermectin increased the proportion of apoptotic (dying) cells in a dose-dependent manner at 24 hours, though this effect also decreased at 48 hours.
Key Findings: Patient-Derived Organoids (3D Models)
The organoid experiments produced particularly notable results. In the GC7 organoid (derived from a real patient's gastric tumor), ivermectin alone caused 48.25% cell death. When combined with cisplatin, cell death increased to 82.48% — a substantial enhancement. In the GC15 organoid, ivermectin alone produced 43.65% cell death, rising to 65.77% with combination treatment.
| Model | Ivermectin Alone | Ivermectin + Cisplatin |
|---|---|---|
| GC7 organoid | 48.25% cell death | 82.48% cell death |
| GC15 organoid | 43.65% cell death | 65.77% cell death |
These organoid results are particularly meaningful because patient-derived organoids preserve the tumor's original genetic makeup and 3D architecture, making them a more reliable predictor of clinical response than standard cell lines.
Mechanism of Action: YAP1, CTGF, and Lysosomal Pathways
The study identified several molecular targets through which ivermectin appears to act in gastric cancer. In 2D cell lines, ivermectin suppressed YAP1 and CTGF — proteins that promote cancer cell survival. In organoids, however, the picture was more complex: ivermectin elevated the expression of TFE3 (a transcription factor linked to lysosomal biogenesis), LAMP1 (a lysosomal membrane protein), and YAP1 in organoids, while CTGF remained unchanged in GC7.
This divergence between 2D and 3D models — where ivermectin suppressed anti-apoptotic genes in flat cultures but increased them in organoids — underscores why organoid models are important. The 3D tumor microenvironment activates different survival pathways, and understanding these differences is essential for predicting how a drug will behave in actual patients.
Evidence Level and Limitations
This study represents a meaningful step forward in ivermectin cancer research because it uses patient-derived organoids — a more clinically relevant model than standard cell lines. However, it remains a preclinical study with important limitations:
- No animal (in vivo) experiments were conducted
- Only two organoid lines were tested; gastric cancer is highly heterogeneous
- Optimal ivermectin dosing for human gastric cancer is unknown
- The rebound in anti-apoptotic gene expression at 48–72 hours suggests potential resistance mechanisms that need further study
- No clinical trial data exists for ivermectin in gastric cancer
For background, see our guide to how ivermectin works.
We cover this in more depth in our article on ivermectin cancer protocols and dosing.
Plan the numbers in our interactive dosing workspace.
Frequently Asked Questions
Frequently Asked Questions
What is a gastric cancer organoid and why does it matter?
A gastric cancer organoid is a 3D mini-tumor grown from a real patient's tumor tissue in the laboratory. Unlike standard flat (2D) cell cultures, organoids preserve the genetic characteristics and 3D structure of the original tumor, making them a more realistic model for predicting how a drug will behave in actual patients.
What cell death rates did ivermectin achieve in the organoid study?
In the GC7 patient-derived organoid, ivermectin alone caused 48.25% cell death. When combined with cisplatin, this increased to 82.48%. In the GC15 organoid, ivermectin alone produced 43.65% cell death, rising to 65.77% with combination treatment. These are preclinical results and cannot be directly applied to human patients.
Did ivermectin work in all gastric cancer cell lines tested?
No. Ivermectin suppressed cell viability in the SNU719 cell line but showed no significant effect in the SNU620 cell line. This suggests that ivermectin's activity varies depending on the specific molecular subtype of gastric cancer, which is an important consideration for future clinical research.
What molecular targets does ivermectin affect in gastric cancer?
The study found that ivermectin reduced YAP1 and CTGF protein expression in 2D cell lines — proteins involved in cancer cell survival. In organoids, it also elevated TFE3 and LAMP1, which are linked to lysosomal pathways. The molecular effects differed between 2D and 3D models, highlighting the complexity of ivermectin's mechanism.
Is ivermectin approved for gastric cancer treatment?
No. Ivermectin is approved only as an antiparasitic drug. Its use in cancer is entirely experimental and not approved by any regulatory agency. This study is preclinical research; clinical trials in gastric cancer patients would be needed before any conclusions about efficacy or safety in humans can be made.
Where was this ivermectin gastric cancer study conducted?
The study was conducted at Kyungpook National University Chilgok Hospital and School of Medicine in Daegu, Republic of Korea, and published in the Journal of Gastrointestinal Oncology in June 2026.
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References
- Lee S, Jung DK, Kim D, Lim HJ, Nam SY. Tumor growth suppression of ivermectin in gastric cancer cell lines and primary gastric cancer organoids. J Gastrointest Oncol. 2026 Jun 30;17(3):143. doi: 10.21037/jgo-2025-710. PMID: 42434256.
- Juarez M, Schcolnik-Cabrera A, Dueñas-Gonzalez A. The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug. Am J Cancer Res. 2018;8(2):317-331.
- Draganov D, Gopalakrishna-Pillai S, Chen YR, et al. Modulation of P2X4/P2X7/Pannexin-1 sensitivity to extracellular ATP via Ivermectin induces a non-apoptotic and inflammatory form of cancer cell death. Sci Rep. 2015;5:16222.
Medical Disclaimer
This article is for educational and informational purposes only. It is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
Sanare Lab
Science-based health education team reviewing published research on repurposed drugs, integrative oncology, and evidence-based protocols.