Pioneering
immune science

Rezpegaldesleukin is an innovative biologic acting as an agonist to target Interleukin-2 receptors located on regulatory T cells (Tregs). This biologic investigational therapy is being developed to address a number of immunology disorders.

By targeting receptors on regulatory T cells, rezpegaldesleukin stimulates the proliferation of these cells, including FOX-P3+ Tregs. Regulatory T cells act as a master immune-modulator upstream of the pro-inflammatory cytokine pathways, which drive Th1, Th2, Th17-mediated inflammatory disorders, such as atopic dermatitis or eczema. By increasing the number and functionality of regulatory T cells, this investigational therapy aims to reduce inflammation more effectively than specific antagonist mechanisms that may target only one pathway.

Rezpegaldesleukin is an innovative biologic acting as an agonist to target Interleukin-2 receptors located on regulatory T cells (Tregs). This biologic investigational therapy is being developed to address a number of immunology disorders.

By targeting receptors on regulatory T cells, rezpegaldesleukin stimulates the proliferation of regulatory T cells, including FOX-P3+ Tregs. In alopecia, a pro-inflammatory environment causes the collapse of immune privilege around the anagen hair bulb. This leads to hair follicle focal inflammation driven by NKG2D+ T cells, NK cells, as well as auto-reactive CD8+ T cells. Regulatory T cells act upstream of these inflammatory cytokines to reduce their activity. By increasing the number and functionality of regulatory T cells, this investigational therapy aims to reduce the hair follicle local inflammation and restore immune privilege.

Rezpegaldesleukin is an innovative biologic acting as an agonist to target interleukin-2 receptors located on regulatory T cells (Tregs). This biologic investigational therapy is being developed to address a number of immunology disorders.

By targeting receptors on regulatory T cells, rezpegaldesleukin stimulates the proliferation of regulatory T cells, including FOX-P3+ Tregs. In Type 1 diabetes, the destruction of insulin-producing pancreatic beta cells is caused by T cells of the immune system. Regulatory T cells act upstream of these T cell and pro-inflammatory cytokines to reduce their activity. By increasing the number and functionality of regulatory T cells, this investigational therapy aims to slow the progression of new onset Type 1 diabetes.

NKTR-0165 is a unique bivalent antibody agonist of the tumor necrosis factor receptor 2 receptor targeting tissue-specific regulatory T cells (Tregs). This investigational therapy is being developed to address a number of autoimmune disorders, such as multiple sclerosis, vitiligo and ulcerative colitis. The first clinical study in humans is planned for 2026.

By targeting TNFR2, a co-stimulatory receptor preferentially expressed on the surface of highly suppressive tissue-specific regulatory T cells, B-regulatory cells, neuronal cells and endothelial cells, NKTR-0165 has been shown to promote the activation, function, proliferation and phenotypic stability of these cells. TNFR2 signaling is an important gatekeeper of inflammation and its absence or deficit is associated with a broad range of autoimmune diseases. As a monomeric bivalent antibody with a unique epitope, NKTR-0165 selectively stimulates TNFR2 receptor activity, without modulation of TNFR1 signaling. This novel first-in-class compound has the potential to modulate acute exacerbations and chronic trajectory of a number of autoimmune diseases.

NKTR-0166 is a unique bivalent antibody incorporating a TNFR2 agonist epitope and an antagonist epitope validated in the treatment of rheumatology diseases. As a dual agonist:antagonist of known pathways associated with key pathways linked to disease pathogenesis, this investigational antibody is being developed to address a number of rheumatic disorders.

NKTR-422 is an innovative biologic agonist of Colony Stimulating Factor 1 Receptor (CSF1R) designed to selectively activate the physiological processes of inflammation resolution. This program has applications in a number of therapeutic indications including acute and chronic inflammation.

Colony Stimulating Factor 1 (CSF1), also known as macrophage colony-stimulating factor (M-CSF), is a cytokine that plays a crucial role in the development, survival and function of mononuclear phagocytes, including macrophages and monocytes. In tissues, CSF1 signaling regulates the biology of anti-inflammatory tissue-resident macrophages and NKTR-422 is designed to specifically target and drive the biology of this key anti-inflammatory cell population.

NKTR-255 is a novel, engineered interleukin-15 (IL-15) receptor agonist designed to enhance cancer immunotherapy, including in combination with checkpoint inhibitors like PD-L1 inhibitors and cellular therapies like tumor-infiltrating lymphocyte (TIL) therapy and chimeric antigen receptor T-cell therapy (CAR-T).

NKTR-255 mimics endogenous IL-15 activity, optimally activating the IL-15 pathway to increase proliferation and survival of a variety of cells including cancer-fighting natural killer (NK) cells, CD8+ T cells, TILs and CAR-T cells. By engaging the entire IL-15 receptor complex (IL-15R⍺/IL-2Rβ𝛾), NKTR-255 is designed to enhance long-term immunological memory, a crucial factor in sustained anti-tumor responses. By producing consistent, dose-dependent expansion of immune cells, NKTR-255 could potentially amplify the effects of cancer fighting therapies. NKTR-255 is currently being evaluated in combination with Bavencio^® (NCT05327530), Imfinzi^® (NCT05632809), C-TIL051 (NCT05676749), and Breyanzi^® (NCT05359211). By enhancing proliferation and survival of these cell types, NKTR-255 may prolong its anti-tumor activity to improve outcomes in both hematological malignancies and solid tumors.