Next-IO™ Macrophages related Therapeutics

This program focuses on broad-spectrum modulation of the tumor microenvironment, specifically targeting tumor-associated macrophages to reverse immunosuppression and enhance overall anti-tumor responses in research.

We provide specialized antibodies designed to block CD11b, effectively inhibiting the recruitment and migration of myeloid-derived suppressor cells into the tumor stroma in research models.

This fusion protein program targets the IL-4 receptor to prevent M2 macrophage polarization, promoting a more inflammatory M1 phenotype within the investigated tumor microenvironment.

Our COX2-specific antibodies help modulate prostaglandin production, thereby reducing the pro-tumorigenic activity of macrophages and improving the inflammatory profile of the microenvironment in research.

This dual-targeting program simultaneously inhibits angiogenesis and macrophage-mediated immunosuppression, providing a comprehensive approach to destabilizing the vascular and immune niches of tumor models.

By blocking the "don't eat me" signaling axis, this program enhances the phagocytic capacity of macrophages, enabling them to actively engulf and destroy tumor cells.

Targeting inducible nitric oxide synthase allows researchers to modulate macrophage-derived oxidative stress and signaling pathways, impacting the overall metabolic balance within the tumor microenvironment.

This program explores the regulation of cytokine signaling pathways in macrophages, aiming to enhance their responsiveness to activating stimuli and improve anti-tumor effector functions.

Targeting CD163 enables the selective depletion or reprogramming of pro-tumoral M2-like macrophages, which are often associated with poor prognosis and immune exclusion in various models.

This antibody program targets scavenger receptors involved in lipid metabolism, investigating how lipid uptake influences macrophage polarization and their subsequent immunosuppressive functions in the stroma.

By inhibiting transglutaminase 2, this program aims to disrupt the structural remodeling of the extracellular matrix and the associated pro-fibrotic behavior of tumor-associated macrophages.

This bispecific approach targets both vascular growth and Notch signaling, aiming to normalize tumor vasculature while simultaneously modulating macrophage differentiation and recruitment in research.

This program focuses on the Notch ligand DLL4 to investigate its role in vascular development and its influence on myeloid cell fate within tumors.

Targeting DLL3 allows for the investigation of Notch-mediated pathways in specific tumor types and their impact on the surrounding innate immune cell populations.

This fusion protein acts as a high-affinity decoy for CD47, effectively triggering macrophage-mediated tumor cell phagocytosis while offering optimized pharmacokinetic properties for research applications.

Targeting Siglec-10 disrupts the interaction with CD24, a key immune checkpoint, thereby releasing the "molecular brakes" on macrophage-mediated anti-tumor activity in various research models.