BioTools (VY-M / VY-OZ / VY-X)
Optimizing Gene Delivery, Cell Potency & Cell Expansion
Vycellix has developed a robust portfolio of proprietary small molecules and RNA modulators for the enhancement of cell and gene therapies:

→ VY-M: Enabling Accelerated Large-scale Cell Expansion with Significant Cost/Speed Efficiencies
VY-M confers significant cell manufacturing benefits as an ex vivo cell manufacturing reagent which optimizes proliferation of T cells, NK cells and other cells with conserved functional capacity (autologous or allogeneic).
VY-M is readily adaptable to multiple protocols and is highly differentiated from other expansion platforms in its ability to decrease non-dividing lag time, resulting in shorter ‘vein-to-vein’ delivery time to patients at lower production costs.
→ VY-OZ: Enabling Superior Cell Transduction & Increasing CRISPR-mediated Gene-editing Rates
VY-OZ is a small molecule which confers significant cell manufacturing benefits as an ex vivo reagent to enhance gene transduction into cytotoxic lymphocytes and hematopoietic stem cells using viral vectors with reproducible and consistent results.
VY-OZ is readily adaptable into multiple gene delivery protocols and is highly differentiated from other genetic modification platforms in its ability to transiently downregulate intracellular anti-viral defense mechanisms, thus enabling desired genes to be more readily integrated into target cells.
VY-OZ is also used to significantly improve gene editing rates for CRISPR-based systems.
→ VY-X: Amplifying Effector Cell Potency for Enhanced Serial Killing
VY-X is a novel small non-coding RNA which increases the efficacy of cytotoxic cell therapies.
VY-X increases the density/load of perforin and granzyme B in cytotoxic effector cells resulting in higher serial killing including faster “time-to-next-kill”.
Potential applications include: 1) ex vivo treatment of cells before adoptive transfer, and; 2) in vivo administration as an adjuvant with T cell and/or NK cell therapies/engagers, or as consolidation/maintenance monotherapy following complete response to boost endogenous effector cells to target minimal residual disease.
