Irreversible DGKα inhibitors for enhanced T‑cell activation in cancer immunotherapy

Background

Cancer immunotherapy seeks to harness the immune system to target and eliminate malignant cells. However, immune suppression within the tumor microenvironment poses a major challenge, blunting T-cell activation and allowing cancer cells to evade immune detection. Diacylglycerol Kinase α (DGKα) is a key enzyme that suppresses T-cell receptor signaling, limiting effective anti-tumor responses. Although reversible DGK inhibitors have been explored, their short duration of action and poor isoform selectivity have constrained their clinical impact. These agents often require frequent dosing and may produce off-target effects, making it difficult to achieve sustained immune activation.

Technology overview

This technology introduces a novel class of naphthyridinone-based small molecules that irreversibly inhibit DGKα through covalent binding. Each molecule features a sulfonyl triazole electrophilic warhead designed to target lysine and tyrosine residues in the DGKα catalytic domain. By forming a covalent bond, these compounds achieve long-lasting inhibition of DGKα, restoring T-cell receptor signaling and enhancing immune activation. The inhibitors have been optimized using sulfur-triazole exchange (SuTEx) chemistry to achieve a balance between potency and selectivity while mini­mizing off-target reactivity. These compounds exhibit potential allosteric binding and isoform selectivity, and they are suitable for systemic administra­tion in cancer immunotherapy. In preclinical models, they have shown promise for treating solid tumors such as melanoma and glioblastoma, as well as boosting antiviral immune responses.

Benefits

  • Achieves irreversible, covalent inhibition of DGKα for sustained T-cell activation
  • Targets key lysine and tyrosine residues within the DGKα catalytic domain
  • Enhances selectivity and duration of action compared to reversible inhibitors
  • Demonstrates potential allosteric engagement and isoform specificity
  • Supports systemic administration for solid tumor and antiviral applications

Applications

  • Cancer immunotherapy
  • T-cell activation enhancement
  • Melanoma and glioblastoma treatment
  • Antiviral immune response support
  • Immune checkpoint combination therapy

Opportunity

  • Provides a novel mechanism to overcome immune suppression in cancer
  • Differentiated by covalent targeting and extended therapeutic effect
  • Compatible with systemic administration and existing immunotherapy regimens
  • Available for exclusive licensing

Intellectual Property

Provisional US patent application filed 04/09/2025

 

Patent Information: