In animal models, taking creatine supplements increases the effectiveness of anti-PD-1 immunotherapy in reducing colorectal tumor growth.
See the scientific wording
Creatine supplementation enhances the sensitivity of colorectal tumors to anti-PD-1 immunotherapy in animal models.
Correlational — new studies may shift this
ObservationalOne low-scoring study links this claim to the outcome, but causation is not established.
What the research says
1 study reviewedSupporting (1)
Case-Control StudyAnimal2025
In mice with colon cancer, adding creatine to their diet helped their immune system fight the tumor better when given a special cancer drug (anti-PD-1), making the drug work more effectively.
Contradicting (0)
No contradicting studies found yet
That doesn't mean it's settled — it just means no study has tested the opposite.
Quality-weighted scoring: we follow the GRADE framework — each study is rated High, Moderate, Low, or Very Low based on study design, methodology rigor, and risk of bias. A single high-quality RCT can outweigh several weaker observational studies.
Scores reflect study quality, not just count.
Creatine enters cancer cells and blocks a protein that normally protects them from a type of cell death caused by fat damage. When this protection is removed, the cancer cells die from fat damage, releasing signals that attract immune cells. These immune cells then attack the tumor more effectively when a drug that removes immune system brakes is given.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting study
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In animal models, taking creatine supplements increases the effectiveness of anti-PD-1 immunotherapy in reducing colorectal tumor growth.
Mechanism
1 studyCreatine stops a protective protein in cancer cells from working, causing the cells to die from fat damage. This death releases signals that bring immune cells to the tumor. When a drug that releases the immune system's brakes is given, these immune cells destroy the tumor more effectively.
Creatine enters cancer cells and blocks a protein that normally protects them from a type of cell death caused by fat damage. When this protection is removed, the cancer cells die from fat damage, releasing signals that attract immune cells. These immune cells then attack the tumor more effectively when a drug that removes immune system brakes is given.
Creatine binds directly to extracellular signal-regulated kinase 2 (ERK2), preventing its activation by MEK1
Inactive ERK2 fails to phosphorylate ferroptosis suppressor protein 1 (FSP1) at Thr109
Unphosphorylated FSP1 is destabilized and degraded, losing its ability to suppress lipid peroxidation
Uninhibited lipid peroxidation triggers ferroptotic cell death in colorectal cancer cells
Ferroptotic cell death releases damage-associated molecular patterns that recruit and activate CD8+ T cells
Activated CD8+ T cells infiltrate the tumor and enhance tumor cell killing when PD-1-mediated immune inhibition is blocked
Evidence from Studies
Supporting (1)
Community contributions welcome
SLC6A8-mediated creatine uptake suppresses ERK2-FSP1 signaling and induces ferroptosis in colorectal cancer.
In mice with colon cancer, adding creatine to their diet helped their immune system fight the tumor better when given a special cancer drug (anti-PD-1), making the drug work more effectively.
Contradicting (0)
Community contributions welcome
Score Breakdown
No multi-axis breakdown available yet. The overall Pro / Against score above is the best signal.
- No clinical evidence is available; the score reflects mechanistic plausibility only.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
Systematic Review of Creatine Supplementation and Anti-PD-1 Response in Animal Models of Colorectal Cancer
Systematic review and meta-analysis of all published controlled animal studies comparing anti-PD-1 therapy with and without creatine supplementation in colorectal tumor models, measuring tumor volume, survival, and immune cell infiltration.
Randomized Controlled Trial of Creatine vs Placebo with Anti-PD-1 in Murine Colorectal Cancer Models
Randomized, blinded, placebo-controlled trial in mice with induced colorectal tumors, comparing anti-PD-1 therapy plus creatine versus anti-PD-1 therapy plus placebo, measuring tumor regression, survival, and T-cell activation over 4–8 weeks.
Cohort Study of Tumor Response to Anti-PD-1 in Animals Receiving Creatine vs No Supplement
Prospective cohort study in multiple strains of mice with colorectal tumors, tracking tumor progression and survival over time in groups with and without creatine supplementation during anti-PD-1 treatment.
In Vitro Analysis of Creatine’s Effect on Colorectal Cancer Cell Response to Anti-PD-1 Treated Immune Cells
Co-culture experiments using murine colorectal cancer cell lines and T cells treated with anti-PD-1, with and without creatine, measuring cytotoxicity, cytokine release, and PD-1/PD-L1 expression over 72 hours.
Pilot Animal Study Assessing Creatine and Anti-PD-1 Combination in Colorectal Tumor-Bearing Mice
Small pilot study in C57BL/6 mice with MC38 colorectal tumors, comparing tumor growth and immune markers in four groups: control, creatine only, anti-PD-1 only, and creatine + anti-PD-1, over 3 weeks.