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Poster session 13

477P - MTL-STING increases STING expression and potentiates efficacy of checkpoint inhibitor in murine preclinical model

Date

10 Sep 2022

Session

Poster session 13

Topics

Tumour Immunology;  Targeted Therapy;  Molecular Oncology;  Immunotherapy

Tumour Site

Presenters

Choon Ping Tan

Citation

Annals of Oncology (2022) 33 (suppl_7): S197-S224. 10.1016/annonc/annonc1049

Authors

C.P. Tan1, B.M. Ryan1, V. Gomez1, R. Hodgson1, L. Sinigaglia1, G. Pizza1, K.S. Stathaki1, S. Hegre2, R. Habib1, J. Rossi3, N. Habib4

Author affiliations

  • 1 Translation & Innovation Hub, MiNA Therapeutics, W12 0BZ - London/GB
  • 2 Bioinformatics And Gene Regulation, Norwegian University of Science and Technology, 7491 - Trondheim/NO
  • 3 Center For Rna Biology And Therapeutics, City of Hope Comprehensive Cancer Center, 91010 - Duarte/US
  • 4 Surgery & Cancer Department, Hammersmith Hospital, W12 0HS - London/GB

Resources

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Abstract 477P

Background

Activation of the cGAS-cGAMP-STING pathway is essential for sensing foreign DNA from pathogens or self-DNA from dying cancer cells. This pathway is critical for the innate immune response and directs the full efficacy of cancer therapeutics, including checkpoint and PARP inhibitors, radiotherapy, and CAR T-cells. Intense efforts have focused on triggering this pathway with cGAMP analogs, which are small-molecule activators of STING. However, recent reports show that STING is downregulated by promoter methylation in various cancers. Furthermore, T-cells activated by cGAMP undergo apoptosis, which limits the efficacy of T-cells based tumor eradication. Indeed, emerging studies suggest that STING activation in myeloid cells is most critical for maximal anti-cancer efficacy of therapeutics.

Methods

Oncogenic silencing of STING expression is generally considered as “undruggable”. At MiNA Therapeutics, we utilized our proprietary platform of RNA activation (RNAa) to design small activating RNA (saRNA) oligos that restore the transcription of the STING gene to levels that are necessary for eliciting anti-tumor effect either alone or in combination with other drugs, including cGAMP analogs.

Results

The clinical lead, saSTING increases in vitro STING expression in the range of 4 to 11-fold in multiple cell lines, and the upregulation is sustained for at least a week. The increase in STING expression is also confirmed at the protein level and an RNAseq experiment validated the functional increase of genes downstream of the STING pathway. The clinical development candidate, MTL-STING, encapsulates saSTING in NOV340 liposomes for intratumoral administration. NOV340 liposomes have previously been clinically validated to efficiently deliver saRNA to myeloid cells, which is the critical cellular subset to benefit from STING activation from an anti-tumor perspective. In the first preclinical proof of concept study, the murine surrogate of MTL-STING combined with PD-1 antibody resulted in early inhibition of tumor growth and was the only group to regress tumor below pre-treatment sizes.

Conclusions

MTL-STING is expected to enter phase I in 2023.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

MiNA Therapeutics.

Funding

MiNA Therapeutics.

Disclosure

C.P. Tan, B.M. Ryan, V. Gomez, R. Hodgson, L. Sinigaglia, G. Pizza, K.S. Stathaki, S. Hegre: Financial Interests, Institutional, Full or part-time Employment: MiNA Therapeutics. R. Habib, N. Habib: Financial Interests, Institutional, Leadership Role: MiNA Therapeutics. J. Rossi: Financial Interests, Institutional, Advisory Role: MiNA Therapeutics.

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