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STING inhibitors target the cyclic dinucleotide binding pocket.

Ze Hong1, Jiahao Mei1, Chenhui Li1

  • 1State Key Laboratory of Natural Medicines, Department of Life Science and Technology, China Pharmaceutical University, 211198 Nanjing, China.

Proceedings of the National Academy of Sciences of the United States of America
|June 8, 2021
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A novel STING inhibitor, SN-011, effectively blocks the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. This discovery offers a promising therapeutic strategy for autoimmune diseases driven by excessive interferon production.

Keywords:
Aicardi–Goutières syndromeSAVISTINGantagonisttype I interferons

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • The cGAS-STING pathway is crucial for innate immunity against pathogens and cancer.
  • Dysregulation of cGAS-STING signaling, due to cytosolic self-DNA or STING mutations, causes autoimmune diseases like Aicardi-Goutière's syndrome and SAVI.
  • These conditions lead to harmful overproduction of type I interferons and inflammatory cytokines.

Purpose of the Study:

  • To identify and characterize a novel antagonist of the STING signaling pathway.
  • To evaluate the therapeutic potential of this antagonist in preclinical models of STING-driven autoimmune disease.

Main Methods:

  • In silico docking was employed to identify potential STING antagonists.
  • The identified compound, SN-011, was tested for its binding affinity to the STING cyclic dinucleotide (CDN)-binding pocket.
  • The inhibitory effects of SN-011 on STING activation were assessed in various cellular and in vivo models, including those mimicking Aicardi-Goutière's syndrome and SAVI.
  • Pharmacokinetic and safety profiles of SN-011 were evaluated in Trex1 deficient mice.

Main Results:

  • SN-011 was identified as a potent STING antagonist with higher binding affinity than endogenous 2'3'-cGAMP.
  • SN-011 stabilizes STING in an inactive conformation, inhibiting downstream interferon and inflammatory cytokine production.
  • Treatment with SN-011 ameliorated inflammation and autoimmune disease hallmarks in Trex1 deficient mice, preventing mortality.
  • SN-011 demonstrated good tolerability in the animal model.

Conclusions:

  • SN-011 is a specific STING inhibitor targeting the CDN-binding pocket.
  • This compound represents a promising therapeutic lead for treating STING-driven autoimmune and inflammatory conditions.
  • Targeting the STING pathway offers a viable strategy for managing diseases characterized by excessive type I interferon responses.