# Our Science

#### Modulating Immune Function

Our bodies respond to inﬂammatory stimuli (like a pathogenic infection) with a protective inﬂammatory cascade. This inflammatory response is tightly regulated by molecular mechanisms involving circulating antibodies, which can re-establish homeostasis after an infection clears. Antibodies can be either pro-inflammatory or anti-inflammatory depending on a switch located on a specific part (Fc domain) of immunoglobulin G (IgG) antibodies. When antibodies are coated with a sugar group (sialylation), they can bind to Type II Fcγ receptors, which returns the immune environment to an anti-inflammatory (tolerant or vigilant) state.

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#### Limitations of IVIg Immune Modulation

IVIg immune modulation is effective in treating autoimmune diseases, but is limited by supply & preparation as a blood product therapy with inherent safety risks and narrow therapeutic window.

#### Limitations of Immunosuppression

Most autoimmune therapies suppress immune function, which can poke holes in the immune system's defense shield, presenting significant infection risks to patients.

#### NVG-2089

NVG-2089 triggers our bodies’ endogenous regulatory mechanisms to reduce autoimmune dysregulation without immunosuppression. NVG-2089 is designed to mimic the binding of sialylated IgG to immunomodulatory Type II Fcγ receptors. A Phase 1 clinical study demonstrated the safety and tolerability of NVG-2089 in healthy volunteers. NVG-2089 is currently in a Phase 2 clinical trial in [Europe](https://euclinicaltrials.eu/search-for-clinical-trials/?lang=en&EUCT=2024-515386-34-00) and the [U.S](https://clinicaltrials.gov/study/NCT07027111). (INVGOR) to evaluate the safety, tolerability, and potential clinical benefit in individuals with chronic inflammatory demyelinating polyneuropathy (CIDP) and is also in a Phase 2 clinical trial in [Europe](https://euclinicaltrials.eu/search-for-clinical-trials/?lang=en&EUCT=2024-520359-26-00) and the [U.S.](https://clinicaltrials.gov/study/NCT07095127) (INVOKE) to evaluate the safety, tolerability, and potential clinical benefit in individuals for immune thrombocytopenia (ITP). For more information, contact [clinicaltrials@nuvigtx.com](mailto:clinicaltrials@nuvigtx.com?subject=Request%20for%20more%20information%20about%20NVG-2089%20Clinical%20Trial).

#### Our Platform

At Nuvig, we incorporate our engineered Fc into full-length antibodies to create bi- and tri-functional antibodies. We call this BESTech™ (Biologic Enhancement of Self Tolerance).

In preclinical experiments we observed substantially enhanced efficacy with the combination of our BESTech Fc and an anti-cytokine variable region (e.g. together, a BESTech mAb) vs. the wild-type antibody. We believe BESTech can be applied to multiple anti-inflammatory targets.

### Publications & Presentations

### Publication

Chakraborty S, et al. (2024) Sialylated IgG induces the transcription factor REST in alveolar macrophages to protect against lung inflammation and severe influenza disease. Published in [Immunity](https://www.cell.com/immunity/fulltext/S1074-7613(24)00482-5). Featured in a Research Highlight in [Nature Reviews Immunology](https://www.nature.com/articles/s41577-024-01120-7).

Sneed SL, et al. (2024) An engineered immunomodulatory IgG1 Fc suppresses autoimmune inflammation through pathways shared with i.v. immunoglobulin. Published in [Journal of Clinical Investigation](https://www.jci.org/articles/view/172980).

### Presentation

Sneed SL, et al (2024) An engineered immunomodulatory IgG1 Fc suppresses autoimmune inflammation through pathways shared with IVIG. Presented at Keystone Symposia’s Antibodies as Drugs: The Art in Antibody Engineering. [View Abstract.](https://nuvigtx.com/wp-content/uploads/2024/08/Nuvig-Keystone-Abstract-May-2024.pdf)

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Our Pipeline

See our therapeutic areas.

[Pipeline](https://nuvigtx.com/pipeline/)
