Rebalancing The
Immune System

How CTO1681 Works

The NF-kB and PGE2 pathways play a critical role in the body’s natural regulation, activation, and differentiation of inflammatory T-cells. Excessive NF-kB and PGE2 signaling results in pro-inflammatory cytokine amplification, as seen in the tumor microenvironment (TME). It contributes to toxicities such as CRS and ICANS as well as the pathogenic processes of various inflammatory diseases such as asthma, COPD and atopic dermatitis.

CytoAgents’s drug candidate CTO1681 reduces inflammation in the TME, prevents toxicity such as CRS and ICANS and potentially has benefit in treating other inflammatory indications such as asthma, COPD and atopic dermatitis by targeting the NF-kB and PGE2 signaling pathways reducing cytokine driven inflammation while still allowing for a functioning immune system.

Rebalancing the Immune System
Controlled Downregulation of Key Cytokines

CTO1681 has demonstrated in multiple In Vivo and Ex Vivo models reduction of a broad range of cytokines driving disease pathogenesis and complications across a pipeline of indications and other inflammation pathologies. It reduces cytokine production regardless of the initial stimulus. CTO1681 does not overly suppress the immune system leaving it functionally intact. It has demonstrated a superb safety profile even among vulnerable patient populations.

The Advantages of CTO1681

CTO1681 provides a number of advantages over other therapeutic options in treating and preventing inflammatory pathologies. By combining a broad mechanism of action to modulate cytokine production with a well-established safety record, it is positioned to become a new standard of care in the prevention and treatment of inflammatory indications.

Unlike other approaches, CTO1681 limits the potential damage caused by an overreaction of the immune system, but spares the patient from the potential of overly harsh immunosuppression associated with other potent therapies.