Reprogramming Tumor-associated Macrophages (TAMs) with Nanomedicines

Tumor-associated macrophages (TAMs) are responsible for tumor promotion and malignant tumor development, which is usually associated with a poor prognosis. Because TAMs are highly plastic, reprogramming these cells toward a tumoricidal M1 phenotype has been a popular therapeutic strategy. Creative Biolabs has organized a staff of outstanding scientists who have engaged in macrophage reprogramming for many years. Our research scientists are experts in reprogramming TAMs to M1 phenotypes with nanomedicines. We are glad to serve our global clients with professionalism and expertise in TAM reprogramming.

TAM Repolarization and Nanomedicines

TAMs promote tumor development through the secretion of immunosuppressive agents. Therefore, TAMs are potential targets for cancer therapy by nano drugs that can reprogram TAMs into antitumorigenic macrophages. Reprogramming of TAMs, is currently the most attractive strategy for cancer treatment and can reverse the protumor phenotype into the antitumor phenotype. This method can slow or stop cancer growth by activating the antitumor functions of M1 macrophages and stimulating the activity of Th1-type cytotoxic T cells and other effector cells.

Nanomedicine represents a versatile platform that exploits nanoparticles, which are fine-tuned nanoscale materials for drug delivery and diagnosis. The physicochemical properties of nanoparticles, such as size, shape, and surface charge, can be tailored to perform controlled release of payloads, passively accumulate at tumors by the enhanced permeability and retention effects, or specifically target tumors. Nanomedicines incorporated with physical and biological technologies have already been utilized in the delivery of vaccine adjuvants, cytokines, and immune checkpoint blockades to modulate the tumor microenvironment (TME). In recent years, more researchers have focused on nanomedicines formulations for macrophage repolarization.

Schematic presentation of components of the TME and nanoparticle therapies. Fig.1 Schematic presentation of components of the TME and nanoparticle therapies. (Siegler, 2016)

Reprogramming TAMs with Nanomedicines at Creative Biolabs

TAMs can produce diverse proangiogenic molecules, anti-angiogenic molecules, versatile enzymes (such as cathepsins, matrix metalloproteinases, plasmin, urokinase type plasminogen activator and legumains), mannose receptors, and galactose receptors. Through these factors, TAM promotes tumor progression, damages the integrity of these blood vessels, remodels the tumor stroma and creates highly invasive tumor microenvironments. The abundant and leaky tumor vascular networks, aberrantly upregulated enzymes, and highly expressed receptors can be rationally considered to design intelligent nanomedicine, providing an opportunity to reprogram TAMs into antitumoral M1 phenotype.

Many agents have been approved for diverse clinical treatments, which could be the most feasible strategy to design nanomedicines for macrophage reprogramming to enhance the therapeutic efficacy. With an experienced team of in-house TAM reprogramming, Creative Biolabs has developed several efficient strategies to reprogram TAMs to M1 phenotype with nanomedicines. Our powerful strategies for TAM reprogramming include 1) Affecting TAM surface receptors by Targeted Delivery of microRNAs to TAM. 2) regulating TME by regulating acidic TME, inducing ROS in TME, relieving hypoxia in TME. The TAMs in the tumor can be effectively reprogrammed by diverse nanomedicines from protumoral M2-like to antitumoral M1 phenotypes to elicit the antitumoral immunity.

Based on our innovative Macrophage Therapeutics Development Platform, Creative Biolabs has built a team of experienced scientists for TAM reprogramming with nanomedicines. For more information, please feel free to contact us and further discuss with our scientists.


  1. Siegler, E.; et al. Nanomedicine targeting the tumor microenvironment: Therapeutic strategies to inhibit angiogenesis, remodel matrix, and modulate immune responses. Journal of Cellular Immunotherapy. 2016, 2(2):69-78.
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