Glucose Metabolism Inhibitor Development Service for Cancer Immunotherapy

Targeting glucose metabolism for Cancer Immunotherapy

Tumor metabolism, particularly abnormal glucose metabolism, is crucial for tumor immune evasion and may be a promising target for combination therapies with immunotherapy. Tumor cells adjust their metabolism by taking up glucose, promoting uncontrolled proliferation, regulating immune checkpoint molecules, and utilizing glycolysis for energy production. This leads to nutrient depletion and the production of immunosuppressive compounds in the tumor microenvironment, hindering immune cell function. As a result, inhibiting glucose metabolism has become a viable cancer treatment strategy.

Fig. 1 Glycolysis-targeted strategies in cancer therapy. (Chelakkot, et al., 2023)Fig.1 Glycolysis-targeted strategies in cancer therapy.1

Our Glucose Metabolism Inhibitor Development Service for Cancer Immunotherapy: Customized! Short-turnaround! Reliable!

Leveraging our expertise and experience in inhibitor development, Creative Biolabs delivers a reliable and supportive glucose metabolism inhibitor development service for cancer immunotherapy to advance global customers' meaningful therapeutic development projects.

Our service covers all stages of pre-clinical trials, including target selection, molecular design and optimization, glucose metabolism inhibitor development, medicine chemistry assay, in vitro examination, in vivo examination, and prediction of clinical trials. We provide numerous advanced technologies (i.e. 3D cell culture, high-content imaging, etc.) to support these stages, allowing us to achieve your projects with great accuracy, superior efficacy, and excellent quality. In addition, to satisfy customers' different demands, we have the ability to achieve the development of multiple glucose metabolism inhibitor types. Noteworthy, if you have the desirable types, our experienced research team is willing to help you in designing the appropriate assay schemes.

Fig. 2 Workflow of our glucose metabolism inhibitor development service for cancer immunotherapy. (Creative Biolabs Original)Fig. 2 Workflow of our glucose metabolism inhibitor development service for cancer immunotherapy.

Types of Glucose Metabolism Inhibitors at Creative Biolabs

Strategies and Hot Targets Available at Creative Biolabs

Abnormal glucose metabolism in tumor microenvironments has drawn researchers' interest in developing anti-tumor therapeutics. Here we deliver several strategies and related targets for customers' convenience in designing and optimizing your glucose metabolism inhibitor development scheme.

STRATEGIES TARGETS
Inhibiting glycolytic activity HK; PFK; GLUT1; PK; GAPDH; PGAM1; PKM2.
Targeting lactate in the TME LDH-A; MCTs; Acidic pH; Proton pump.
Alleviating hypoxia in the TME Hypoxia; Mitochondrial respiratory complex I.
Targeting PI3K/AKT/mTOR signaling pathway mTOR; PI3K isoforms; AKT.

Frequently Asked Question

Q1: What is the focus of these four strategies for glucose metabolism?

A1: The altered glucose metabolism in tumors negatively impacts the function of immune cells and promotes immunosuppression. Increased glycolytic activity in cancer cells results in glucose deprivation and lactate accumulation, which suppresses antitumor immune cell effector function and encourages the growth and recruitment of immunosuppressive cell populations. Moreover, the fast multiplication of tumor cells causes significant oxygen consumption and hypoxia in the TME, interfering with the differentiation and activation of anti-tumor immune cells. PI3K/AKT/mTOR recognizes nutrition and promotes glycolysis in tumor and effector T cells. As a result, decreasing tumor glucose metabolism by blocking glucose metabolism-related enzymes or utilizing a competitive glucose mimic may assist in slowing tumor development.

For more details about our glucose metabolism inhibitor development service for cancer immunotherapy, please don't hesitate to reach out to us.

Reference

  1. Chelakkot, Chaithanya, et al. "Modulating glycolysis to improve cancer therapy." International Journal of Molecular Sciences 24.3 (2023): 2606.

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