John Garner

mPEG-PLGA from PolySciTech used in research on immune checkpoint inhibitors for cancer therapy

Blog Post created by John Garner on Oct 19, 2018


One of the insidious features of cancer is that it has the ability to prevent the immune system from recognizing the diseased cells as ‘non-self.’ Immune checkpoint inhibitors, as chemotherapeutics, act to eliminate this feature of cancer and enable the immune system to attack it. Recently, researchers from Harvard Medical School, Hamad Bin Khalifa University (Qatar),  and University of California, Los Angeles, used mPEG-PLGA (PolyVivo AK102) from PolySciTech ( to develop anti-PD-1 loaded nanoparticles and investigated the effect of these nanoparticles on cancer therapy. This research holds promise for better understanding of immunotherapy cancer treatment options. read more: Farideh Ordikhani, Mayuko Uehara, Vivek Kasinath, Li Dai, Siawosh K. Eskandari, Baharak Bahmani, Merve Yonar, Jamil R. Azzi, Yousef Haik, Peter T. Sage, George F. Murphy, Nasim Annabi, Tobias Schatton, Indira Guleria, and Reza Abdi  “Targeting antigen-presenting cells by anti–PD-1 nanoparticles augments antitumor immunity” JCI Insight. 2018;3(20):e122700

  “Recent studies in cancer research have focused intensely on the antineoplastic effects of immune checkpoint inhibitors. While the development of these inhibitors has progressed successfully, strategies to further improve their efficacy and reduce their toxicity are still needed. We hypothesized that the delivery of anti–PD-1 antibody encapsulated in PLGA nanoparticles (anti–PD-1 NPs) to the spleen would improve the antitumor effect of this agent. Unexpectedly, we found that mice treated with a high dose of anti–PD-1 NPs exhibited significantly higher mortality compared with those treated with free anti–PD-1 antibody, due to the overactivation of T cells. Administration of anti–PD-1 NPs to splenectomized LT-α–/– mice, which lack both lymph nodes and spleen, resulted in a complete reversal of this increased mortality and revealed the importance of secondary lymphoid tissues in mediating anti–PD-1–associated toxicity. Attenuation of the anti–PD-1 NPs dosage prevented toxicity and significantly improved its antitumor effect in the B16-F10 murine melanoma model. Furthermore, we found that anti–PD-1 NPs undergo internalization by DCs in the spleen, leading to their maturation and the subsequent activation of T cells. Our findings provide important clues that can lead to the development of strategies to enhance the efficacy of immune checkpoint inhibitors.”