Improving lives by advancing immuno-oncology treatments

At NewLink Genetics, our commitment is simple and passionate: we’re focused on discovering, developing and commercializing novel immuno-oncology products because we believe they are the future of cancer treatment.

Through science, clinical trials and future opportunities, immuno-oncology treatments will help improve the lives of cancer patients. Much of the focus in our research and development is on indoleamine 2,3-dioxygenase (IDO). IDO is an increasingly important and validated immuno-oncology target. Our lead programs consist of two differentiated product candidates that target the IDO pathway. Indoximod is most advanced with multiple phase 2 trials across various cancer indications. NLG802, which is a prodrug of indoximod will enter the clinic in 2017. These product candidates have independent clinical development paths with the potential to enhance the outcomes for patients when used in combination with anti-PD-1 agents, cancer vaccines, chemotherapy or other anticancer therapies.

Since IDO is a central pathway in tumor immuno-oncology, it is potentially applicable across a wide range of malignancies. Indoximod and NLG802 share a differentiated mechanism of action distinct from other drugs in this class, which focus exclusively on enzymatic inhibition, and reverse immunosuppression within the IDO pathway. By acting as a tryptophan mimetic, indoximod overcomes the immunosuppressive signal triggered by IDO or TDO activity.

Germane to discovering new immuno-oncology treatments, our scientific vision includes “over-the-horizon” programs, such as PTEN, that can help modulate the function of regulatory T cells (Tregs). Considering that an important goal of tumor immunotherapy is to identify and modulate tumor microenvironment conditions and pathways that control Tregs, several studies are revealing that PTEN is one of the critical molecules that regulate the function of Tregs. Similar to IDO and PD-1, the PTEN pathway in Tregs could be a critical target to disrupt tumor driven immunosuppression.

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