locate clinical trials
Nektar is actively investigating novel compounds in immuno-oncology across multiple tumor types—both alone and in combination with other therapies. You can search for Nektar clinical trials near you using the filters below.
Nektar is actively investigating novel compounds in immuno-oncology across multiple tumor types—both alone and in combination with other therapies. You can search for Nektar clinical trials near you using the filters below.
Purpose:
Detailed Description:
Contact:
Nektar Recruitment
855-482-8676
StudyInquiry@nektar.com
Locations:
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
United States, Arkansas | Recruiting
Investigator Site
Rogers, Arkansas, United States, 72758
Data obtained from ClinicalTrials.gov, a service of the U.S. National Institutes of Health.
Learn more at ClinicalTrials.gov
TLR 7/8 AS AN IMMUNOTHERAPY TARGET
Antigen-presenting cells (APCs) play a critical role in initiating the cancer-immunity cycle1
The toll-like receptor (TLR) 7/8 pathway activates APCs that prime T cells and recruit immune cells within the tumor microenvironment2,4
Activation of the TLR 7/8 signaling pathway [1] promotes the maturation of APCs, [2] which both:
TLR 7/8 agonists could improve antitumor immune response when combined with other immunotherapies2,4
Nektar is exploring sustained and targeted TLR 7/8 signaling in combination with other immunotherapies5
References: 1. Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39(1):1-10. 2. Adams S. Toll-like receptor agonists in cancer therapy. Immunotherapy. 2009;1(6):949-964. 3. Rabeony H, Pohin M, Vasseur P, et al. IMQ-induced skin inflammation in mice is dependent on IL-1R1 and MyD88 signaling but independent of the NLRP3 inflammasome. Eur J Immunol. 2015;45:2847-2857. doi:10.1002/eji.201445215. 4. Singh M, Khong H, Dai Z, et al. Effective innate and adaptive antimelanoma immunity through localized TLR7/8 activation. J Immunol. 2014;193:1-10. doi:10.4049/jimmunol.1401160. 5. Kivimäe S, Pena R, Hennessy M, et al. Systemic anti-tumor immunity and immune memory formation by a novel TLR7/8 targeting agent NKTR-262 combined with CD122-biased immunostimulatory cytokine NKTR-214. Presented at: Society for Immunotherapy of Cancer annual meeting. November 7-11, 2018; Washington, D.C., USA.
ENGAGING IMMUNE RESPONSE THROUGH THE IL-15 PATHWAY
Both innate and adaptive immunity are needed for sustained immune response
Activation of the IL-15 pathway engages both adaptive and innate antitumor immunity
IL-15 signaling [1] induces both the proliferation and activation [2] of both NK cells and of cytotoxic T cells to1,3,4
IL-15 agonists show potential in combination with other oncology therapeutics1
Nektar is investigating sustained and controlled engagement of the IL-15 pathway6
References: 1. Robinson TO, Schluns KS. The potential and promise of IL-15 in immuno-oncogenic therapies. Immunol Lett. 2017;190:159-168. 2. Messaoudene M, Frazao A, Gavlovsky PJ, Toubert A, Dulphy N, Caignard A. Patient's natural killer cells in the era of targeted therapies: role for tumor killers. Front Immunol. 2017;8:683. doi:10.3389/fimmu.2017.00683. 3. Osborne LC, Abraham N. Regulation of memory T cells by yc cytokines. Cytokine. 2010;50(2):105-113. 4. Kennedy MK, Glaccum M, Brown SN, et al. Reversible defects in natural killer and memory CD8 T cell lineages in interleukin 15-deficient mice. J Exp Med. 2000;191(5):771-780. 5. Stonier SW and Schluns KS. Trans-presentation: a novel mechanism regulating IL-15 delivery and responses. Immunol Lett. 2010;127(2):85-92. doi:10.1016/j.imlet.2009.09.009. 6. Data on File. Nektar Therapeutics.
THE ROLE OF THE IL-2 PATHWAY IN IMMUNE RESPONSE
Higher levels of cytotoxic T cells and natural killer (NK) cells raise tumor cell killing potential in the tumor microenvironment1,2
The IL-2 pathway can both stimulate and regulate immune responses
TAKE A CLOSER LOOK - CLICK BELOW TO WATCH THE IL-2 PATHWAY VIDEO
IMMUNE SYSTEM REGULATION:
IL-2 cytokine binding of the trimeric complex [alpha (CD25) + beta (CD122) + gamma (CD132)] on Tregs [2] causes their activation and proliferation, and thereby immune regulation [4]7-10
IMMUNE SYSTEM STIMULATION:
IL-2 cytokine binding of the dimeric complex [beta (CD122) + gamma (CD132)] on cytotoxic T cells and NK cells [2] induces their proliferation and activation leading to immune activation [3]7
Preferential dimeric activation of the IL-2 receptor is a target for further research7
References: 1. Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39(1):1-10. 2. Messaoudene M, Frazao A, Gavlovsky PJ, et al. Patient's natural killer cells in the era of targeted therapies: role for tumor killers. Front Immunol. 2017;8:683. doi:10.3389/fimmu.2017.00683. 3. Tumeh PC, Harview CL, Yearley JH, et al. PD-1 blockade induces responses by inhibiting adaptive immune resistance. Nature. 2014;515:568-583. 4. Halle S, Keyser KA, Stahl FR, et al. In vivo killing capacity of cytotoxic t cells is limited and involves dynamic interactions and t cell cooperativity. Immunity. 2016;44(2):233-245. 5. Cursons J, Souza-Fonseca-Guimaraes F, Foroutan M. et al. A gene signature predicting natural killer cell infiltration and improved survival in melanoma patients. Cancer Immunology Research. 2019;7(7):1162-1174. 6. Boyman O, Sprent J. The role of interleukin-2 during homeostasis and activation of the immune system. Nature Rev Immunol. 2012;12(3):180-190. 7. Charych D, Khalili S, Dixit V, et al. Modeling the receptor pharmacology, pharmacokinetics, and pharmacodynamics of NKTR-214, a kinetically-controlled interleukin-2 (IL2) receptor agonist for cancer immunotherapy. PLoS One. 2017;12(7):e0179431. doi:10.1371/journal.pone.0179431. eCollection 2017. 8. Ye C, Brand D, Zheng SG. Targeting IL-2: an unexpected effect in treating immunological diseases. Signal Transduct Target Ther. 2018;3:1-10. 9. Johnson K, Choi Y, Wu Z, et al. Soluble IL-2 receptor beta and gamma subunits: ligand binding and cooperativity. Eur Cytokine Netw. 1994;5:23-34. 10. Liparoto SF, Myszka DG, Wu Z, et al. Analysis of the role of the interleukin-2 receptor gamma chain in ligand binding. Biochemistry. 2002;41:2543-2551.