top of page


We are fascinated by the ability of tumors to evade immune elimination. Many of our current programs focus on restoring the power of the immune system to achieve clean tumor kills.

Tumors subvert immunity in a variety of ways. They can hide their very existence from innate cellular alarm systems and circulating surveillance immune cells, frustrate the buildup and amplification of immune responses and subvert established inflammatory responses by evoking potent immunosuppressive factors.

The recent approvals of inhibitors targeting checkpoint blockade are the first steps in the establishment of host directed immune therapies as durable methods for the treatment of a number of cancers. The coming decade will see the emergence of new generations of immune system targeted oncology drugs which can be used as monotherapy or in combination with other IO agents or existing anti-cancer drugs.



Greater than 90% of ingested tryptophan is metabolized to kynurenine by Tryptophan dioxygenase (TDO2) and Indoleamine 2,3 dioxygenase (IDO1) which are rate limiting oxidoreductase enzymes of the kynurenine pathway (KP).  The action of kynurenine and its metabolites and the depletion of local tryptophan levels have immunosuppressive consequences in the tumor microenvironment by subduing active immune responses by creating a tolerogenic tumor microenvironment characterized by increased numbers of circulating regulatory T cells and a decreased number of CD8+ T cells.  Elevated kynurenine to tryptophan (K/T) ratios are associated with resistance to checkpoint blockade drugs that target CTLA4 or PD-L1/PD1.  

Curadev has discovered potent small molecule enzyme inhibitors that fall into two classes – IDO specific inhibitors and first in class TDO/IDO dual inhibitors. The therapeutic goal is to combine these molecules with other immune check point inhibitors or specific cytotoxic therapies to potentiate immune response against various types of tumors.

Curadev’s lead small molecule drug candidate is a powerful dual inhibitor of TDO and IDO and reduces kynurenine levels in rodents, dogs and primates. 

STING agonist


The STING agonist program focuses on kick-starting an innate immune response in tumors which are devoid of a T cell infiltrate and are consequently immunologically silent. Generating a Type I Interferon response in these non-inflamed tumors leads to the activation of CD8α dendritic cells which recruit CD8 T-cells and initiate strong anti-tumor responses. We have designed and developed potent classical small molecule (non-nucleoside) human STING agonists that activate all isoforms of human STING leading to robust secretion of Type I interferons and related cytokines. In order to increase the therapeutic index of our portfolio we have created modular sets of linkers and spacers to enable conjugation of our compounds to peptides and biomolecules.



High expression of HPK1 (Hematopoietic Progenitor Kinase 1) correlates with reduced patient survival in several cancer types. The small molecule HPK1 inhibitor program attempts to block this kinase from inactivating several types of immune cells. HPK1 driven phosphorylation down regulates signaling by T and B cell receptors, prostaglandins and ligands of the TNF superfamily and plays a regulatory role in turning off nearly every step of an inflammatory immune response.  Within the cancer immunity cycle, HPK1 decreases neo-antigen release and presentation, T cell priming and activation, the trafficking and infiltration of T cells into tumors and helps create the immunosuppressive tumor microenvironment that blunts the action of T lymphocytes.

bottom of page