We provide a breakthrough in transplant treatment

Our focus is on discovery and early clinical development of treatments for well-defined patient populations suggesting relevant commercial opportunities. We aim to retain ownership of product candidates through to proof of concept after which we expect to partner with established pharma companies for late-stage development and commercialisation.

US28 is a novel CMV-specific target


Leveraging the active function of US28 to gain access to CMV infected cells

  • Membrane protein encoded by the virus
  • Exclusively expressed on virus infected cells
  • Expressed during both lytic and latent phase
  • Continuously internalizing
  • Acts as a chemokine scavenger

Our patented SYN002 drug candidate


SELECTIVELY kills infected cells, without impacting organ function

SYN002 effectively kills CMV infected cells, eliminating infection

Uniquely Targets BOTH Latent and Lytic Infected Cells

Strong foundational
and translational science

Risk factors for CMV infection in transplantation

Latent viral load is key driver of CMV reactivation

The latent CMV reservoir facilitates CMV disease

Reduction of the latent CMV load significantly reduces risk of CMV disease

The latent virus load is the key parameter that determines risks of CMV Disease during immuno-suppression1

High latent virus load →

CMV reactivation
Reddehase JEM. 1994

Low latent virus load →

CMV reactivation

Lowering the latent virus in mice strongly affects the incidence of CMV recurrence2

5-fold reduction
lowers recurrence by


Steffens, JV1998

Clear correlation between latent viral load and reactivation & active productive infection (1) Reddehase JEM. 1994 and 2) Steffens, JV1998).