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Diet-Microbiome-Host Interactions Affect Cancer Therapy

Tumor Microenvironment Cancer Immunotherapy Chronic Inflammation

Diet-microbiome-host interactions affect cancer therapy by linking dietary substrates, intestinal microbial communities, microbial metabolites, systemic immunity, and the tumor microenvironment. This field moved from preclinical observations that intestinal microbiota modulate chemotherapy and checkpoint blockade to human studies showing that gut microbiome composition associates with response to anti-PD-1, anti-PD-L1, and anti-CTLA-4 immunotherapy. Dietary fiber and probiotic use became clinically important variables because they can reshape gut ecology during immune checkpoint blockade[1][2][3][4][5].

Mechanistically, commensal microbes regulate dendritic-cell function, CD8+ T-cell priming, T-cell infiltration, cytokine tone, and tumor immune surveillance. Bifidobacterium enhanced antitumor immunity and facilitated anti-PD-L1 efficacy in melanoma models, while distinct Bacteroides species supported the antitumor effects of CTLA-4 blockade. Cyclophosphamide altered small-intestinal microbiota and induced immune effects linked to microbial translocation. In PD-1-treated patients, responders showed distinct gut microbial composition, and responder-derived fecal microbiota improved antitumor immune activity in mice[1][2][3][4][5].

Diet adds a modifiable layer to this host-microbiome-cancer axis. In melanoma patients receiving immune checkpoint blockade, higher dietary fiber was associated with improved progression-free survival, with the strongest benefit in patients reporting sufficient fiber intake and no probiotic use. Preclinical models mirrored this pattern because low-fiber diet or probiotics impaired anti-PD-1-based therapy and reduced interferon-γ-positive cytotoxic T cells in the tumor microenvironment. These data support dietary fiber, microbial diversity, microbial metabolites, and immune-cell activation as practical research directions for improving immunotherapy response[6].

Clinical applications now include microbiome biomarkers, antibiotic-risk assessment, dietary intervention, probiotic caution, fecal microbiota transplantation, and rational microbiome-drug combinations. FMT promoted response in immunotherapy-refractory melanoma, and FMT plus anti-PD-1 changed the gut microbiome and reprogrammed the tumor microenvironment in resistant melanoma. FMT also improved anti-PD-1 inhibitor efficacy in refractory advanced solid cancers, especially gastrointestinal cancers. Key gaps remain in causal strain identification, diet standardization, donor selection, safety, durability, and tumor-type specificity. Future trials should integrate food records, metagenomics, metabolomics, immune profiling, antibiotic exposure, and clinical endpoints to convert diet-microbiome-host biology into precision cancer therapy[7][8][9][10].

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Cat. No. Product Name Information Application Publication
HY-50912 Plerixafor octahydrochloride
Plerixafor octahydrochloride (AMD3100 octahydrochloride) is a selective CXCR4 antagonist with an IC50 of 44 nM.
CXCR   HIV   Virus Protease  
Pancreatic Cancer   Viral Infection   Digestive System Inflammation   Glucose Metabolism   SARS-CoV-2 Infection   Lung Fibrosis   Rheumatoid Arthritis  
112
HY-10046 Plerixafor
Plerixafor (AMD 3100) is a selective CXCR4 antagonist with an IC50 of 44 nM. Plerixafor, an immunostimulant and a hematopoietic stem cell (HSC) mobilizer, is an allosteric agonist of CXCR7. Plerixafor inhibits HIV-1 and HIV-2 replication with an EC50 of 1-10 nM.
CXCR   HIV  
Pancreatic Cancer   Viral Infection   Digestive System Inflammation   Glucose Metabolism   SARS-CoV-2 Infection   Lung Fibrosis   Rheumatoid Arthritis  
112
HY-16711 SB225002
SB225002, a potent, selective and non-peptide CXCR2 antagonist, inhibits 125I-IL-8 binding to CXCR2 with an IC50 of 22 nM.
CXCR  
Metabolic or Endocrine Disease   Gastric Cancer   Digestive System Inflammation   Rheumatoid Arthritis  
66
HY-15251 Reparixin
Reparixin is a non-competitive allosteric inhibitor of the chemokine receptors CXCR1 and CXCR2 activation with IC50s of 1 and 100 nM, respectively.
CXCR  
Metabolic or Endocrine Disease   Gastric Cancer   Pancreatic Cancer   Digestive System Inflammation   Rheumatoid Arthritis  
65
HY-15319 AMG 487
AMG 487 is an orally active and selective antagonist of CXC chemokine receptor 3 (CXCR3) which inhibits the binding of CXCL10 and CXCL11 to CXCR3 with IC50s of 8.0 and 8.2 nM, respectively.
CXCR  
Cancer   Metabolic or Endocrine Disease   Digestive System Disease   Digestive System Inflammation   Rheumatoid Arthritis  
40
HY-10198 Navarixin
Navarixin (SCH 527123) is a potent, allosteric and orally active antagonist of both CXCR1 and CXCR2, with Kd values of 41 nM for cynomolgus CXCR1 and 0.20 nM, 0.20 nM, 0.08 nM for mouse, rat and cynomolgus monkey CXCR2, respectivelly.
CXCR  
Metabolic or Endocrine Disease   Prostate Cancer   Gastric Cancer   Digestive System Inflammation   SARS-CoV-2 Infection   Rheumatoid Arthritis  
32
HY-13848 Rugocrixan
AZD8797 (KAND567) is an allosteric non-competitive and orally active antagonist of the human CX3CR1 receptor; antagonizes CX3CR1 and CXCR2 with Kis of 3.9 and 2800 nM, respectively.
CX3CR1   CXCR  
Cancer   Metabolic or Endocrine Disease   Digestive System Disease   Digestive System Inflammation  
26
HY-13406 TAK-779
TAK-779 is a potent and selective nonpeptide antagonist of CCR5 and CXCR3, with a Ki of 1.1 nM for CCR5, and effectively and selectively inhibits R5 HIV-1, with EC50 and EC90 of 1.2 nM and 5.7 nM, respectively, in MAGI-CCR5 cells.
CCR   HIV   CXCR  
Cancer   Metabolic or Endocrine Disease   Digestive System Disease   Viral Infection   Digestive System Inflammation   Lung Fibrosis   Rheumatoid Arthritis  
13
HY-19855 AZD-5069
AZD-5069 is a potent CXCR2 chemokine receptor antagonist, used for caner treatment.
CXCR  
Metabolic or Endocrine Disease   Prostate Cancer   Gastric Cancer   Pancreatic Cancer   Digestive System Inflammation   Rheumatoid Arthritis  
11
HY-100806 Kynurenic acid
Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8.
iGluR   Endogenous Metabolite   Apoptosis   CXCR   GPR35  
Cancer   Metabolic or Endocrine Disease   Digestive System Disease   Depression   Digestive System Inflammation   Alzheimer's Disease   Parkinson's Disease  
11
HY-P9901 Ipilimumab
Ipilimumab is a fully human monoclonal antibody IgG1κ that blocks the inhibitory receptor cytotoxic T lymphocyte antigen 4 (CTLA-4) on T cells. Ipilimumab can be used in unresectable or metastatic melanoma (MM) studies.

Species: Human

CTLA-4  
Non-Small Cell Lung Cancer   Lung Adenocarcinoma   Triple-Negative Breast Cancer   Metastatic Breast Cancer   Metastatic Melanoma  
5
HY-108829A Abatacept (powder)
Abatacept (CTLA4lg; BMS-188667) powder is a soluble fusion protein consisting of the extra-cellular domain of human CTLA4 and a fragment of the Fc portion of human IgG1 (hinge and CH2 and 3 domains). Abatacept powder is a selective T-cell co-stimulation modulator and a protein agent for the autoimmune diseases.

Species: Human

CTLA-4  
Cancer   Glucose Metabolism   SARS-CoV-2 Infection   Rheumatoid Arthritis  
3
HY-P99132 Anti-Mouse CTLA-4 Antibody (9D9)
Anti-Mouse CTLA-4 Antibody (9D9) is an anti-mouse CTLA-4 IgG2b monoclonal antibody. Anti-Mouse CTLA-4 Antibody (9D9) can bind to CTLA-4 and block its binding to B7. Anti-Mouse CTLA-4 Antibody (9D9) enhances T cell function by increasing the ratio of CD8+ T cells to regulatory T cells (Tregs). Anti-Mouse CTLA-4 Antibody (9D9) can be used for research on cancer such as colon cancer and melanoma.

Species: Mouse

CTLA-4  
Inflammation or Immune System Disease   Colorectal Cancer   Melanoma  
3
HY-108829 Abatacept
Abatacept (CTLA4lg) is a soluble fusion protein consisting of the extra-cellular domain of human CTLA4 and a fragment of the Fc portion of human IgG1 (hinge and CH2 and 3 domains). Abatacept is a selective T-cell co-stimulation modulator and a protein agent for the autoimmune diseases.

Species: Human

CTLA-4  
Lung Cancer   Melanoma   SARS-CoV-2 Infection   Rheumatoid Arthritis  
3
HY-P99117 Cadonilimab
Cadonilimab (AK104) is a humanized tetravalent IgG1 bispecific antibody targeting PD1/CTLA4. Cadonilimab blocks both PD-1 and CTLA-4 pathways, thereby relieving their corresponding immunosuppressive effects and reversing tumor specific T cell exhaustion. Cadonilimab significantly downregulates Fc-mediated effector functions, including antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC). Cadonilimab can be used for research of metastatic cervical cancer, as well as other malignancies such as gastric cancer, GEJ adenocarcinoma and non-small cell lung cancer (NSCLC).

Species: Human

PD-1/PD-L1   CTLA-4  
Inflammation or Immune System Disease   Gastric Cancer   Non-Small Cell Lung Cancer   Triple-Negative Breast Cancer  
1
HY-P99166 Vudalimab
Vudalimab is a potent dual PD-1 and CTLA-4 inhibitor as a fully humanized bispecific monoclonal antibody. Vudalimab targets immune checkpoint receptors PD-1 and CTLA-4 and promotes tumor-selective T-cell activation.

Species: Human

PD-1/PD-L1   CTLA-4  
Cancer   Inflammation or Immune System Disease  
/
HY-P990042 Gotistobart
Gotistobart (ONC-392; BNT 316) is a humanized anti-CTLA-4 antibody with selective regulatory T cell depletion activity in the tumor microenvironment. Gotistobart can be used for the research of cancer, such as non-small cell lung cancer.

Species: Human

CTLA-4  
Inflammation or Immune System Disease   Non-Small Cell Lung Cancer  
/
HY-P990690 Volrustomig
Volrustomig (MEDI-5752) is a human IgG1 κ monoclonal antibody targeting CTLA4/PD1. The isotype control for Volrustomig is Human IgG1 kappa, Isotype Control (HY-P99001). Volrustomig anchors to the surface of T cells by binding PD-1, induces PD-1 internalization and degradation, and preferentially inhibits CTLA-4 on activated PD-1+ T cells. Volrustomig binds to tumor-infiltrating lymphocytes and a subset of PD-1+ B cells, enhances T cell function and IFNγ secretion. Volrustomig reduces the activation of non-tumor-infiltrating lymphocytes and exhibits manageable toxicity. Volrustomig can be used in research on various cancers, such as non-small cell lung cancer, gastric cancer, hepatobiliary cancer, and cervical cancer.

Species: Human

PD-1/PD-L1   CTLA-4  
Gastric Cancer   Liver Cancer   Cervical Cancer   Non-Small Cell Lung Cancer  
/
HY-P990789 Anti-Mouse CTLA-4 Antibody (9H10)
Anti-Mouse CTLA-4 Antibody (9H10) is a kind of syrian hamster IgG antibody inhibitor, targeting to CTLA-4. Anti-Mouse CTLA-4 Antibody (9H10) binds mouse CTLA-4 and blocks the interaction between CTLA-4 and its ligand. Anti-Mouse CTLA-4 Antibody (9H10) shows potent anti-tumor effect in various tumor models, such as breast and colon cancer.

Species: Mouse

CTLA-4  
Breast Cancer   Prostate Cancer  
/
HY-P9918 Tremelimumab
Tremelimumab (Ticilimumab) is a fully human monoclonal antibody specific for cytotoxic T-lymphocyte antigen-4 (CTLA-4) and can be used for metastatic melanoma research.

Species: Human

CTLA-4  
Inflammation or Immune System Disease   Non-Small Cell Lung Cancer   Triple-Negative Breast Cancer   Metastatic Breast Cancer  
/

References

[1]. Viaud S, et al. The intestinal microbiota modulates the anticancer immune effects of cyclophosphamide. Science. 2013;342(6161):971-976.  [Content Brief]

[2]. Sivan A, et al. Commensal Bifidobacterium promotes antitumor immunity and facilitates anti-PD-L1 efficacy. Science. 2015;350(6264):1084-1089.  [Content Brief]

[3]. Vétizou M, et al. Anticancer immunotherapy by CTLA-4 blockade relies on the gut microbiota. Science. 2015;350(6264):1079-1084.  [Content Brief]

[4]. Routy B, et al. Gut microbiome influences efficacy of PD-1-based immunotherapy against epithelial tumors. Science. 2018;359(6371):91-97.  [Content Brief]

[5]. Gopalakrishnan V, et al. Gut microbiome modulates response to anti-PD-1 immunotherapy in melanoma patients. Science. 2018;359(6371):97-103.  [Content Brief]

[6]. Spencer CN, et al. Dietary fiber and probiotics influence the gut microbiome and melanoma immunotherapy response. Science. 2021;374(6575):1632-1640.  [Content Brief]

[7]. Matson V, et al. The commensal microbiome is associated with anti-PD-1 efficacy in metastatic melanoma patients. Science. 2018;359(6371):104-108.  [Content Brief]

[8]. Baruch EN, et al. Fecal microbiota transplant promotes response in immunotherapy-refractory melanoma patients. Science. 2021;371(6529):602-609.  [Content Brief]

[9]. Davar D, et al. Fecal microbiota transplant overcomes resistance to anti-PD-1 therapy in melanoma patients. Science. 2021;371(6529):595-602.  [Content Brief]

[10]. Kim Y, et al. Fecal microbiota transplantation improves anti-PD-1 inhibitor efficacy in unresectable or metastatic solid cancers refractory to anti-PD-1 inhibitor. Cell Host Microbe. 2024;32(8):1380-1393.e9.  [Content Brief]

Keywords

diet-microbiome-host interactions, cancer therapy, immune checkpoint blockade, dietary fiber, probiotics, fecal microbiota transplantation, anti-PD-1, tumor microenvironment