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Targeting cell states in cancer
Mechanism of Action

Targeting Cancer Cell States

to Block Cancer Growth & Proliferation

In normal, healthy development, cells divide rapidly and proliferate to form the tissues and organs of the human body. Once these cells terminally differentiate, they are committed to a particular cell state and lose the ability to proliferate.

Genetic alterations have the potential to promote tumorigenesis – the process by which normal cells transform into cancer cells. These alterations hijack normal development pathways, pushing cancer cells into an earlier, proliferative cell state – also known as a plastic state. They do this by blocking terminal differentiation, inducing dedifferentiation (reversing a cell’s state to a less specialized and earlier cell state) or inducing transdifferentiation (the conversion of one cell state to another cell state).

The plastic states of cancer cells are associated with the most aggressive, metastatic, and drug-resistant tumors. By targeting the drivers that lock cancer cells in an altered cell state, we can revert the tumor cells back to their normal cell state and inhibit their growth and proliferation.

Our Platform

AURIGIN™ Platform

for Rapid Drug Discovery & Development

We have built a proprietary platform called AURIGIN that we are leveraging for the rapid discovery and development of the next generation of targeted cancer therapies.

AURIGIN is a proprietary platform that integrates our developmental biology expertise with AI Machine Learning algorithms. It includes a database of single cell genomics data that allows it to compare normal cell states to cancer cell states. The power of AURIGIN is its ability to harnesses novel insights into tumor biology and generate validated targets, identify optimized model systems for early program de-risking, and identify biomarkers for effective patient selection.

Our Pipeline

Pipeline Development

for the Next Generation of Targeted Cancer Therapies

We are developing a portfolio that is the direct output of our AURIGIN platform. We have identified a set of priority targets and programs that represent first-in-class or best-in-class opportunities for both solid tumor cancers and hematological malignancies.

  • Includes Breast Cancer, Non-Small Cell Lung Cancer, and Colorectal Cancer
  • Includes Neuroendocrine Prostate Cancer, Small Cell Lung Cancer, Neuroendocrine Tumors, and Neuroblastoma
  • EMT = Epithelial-Mesenchymal Transition
Publications, Presentations, & Posters
December 9, 2024
Presentation
Presentation
POSTER

AUTX-703, a novel and potent KAT2A and KAT2B protein degrader, induces differentiation and offers survival advantage in a primary human AML xenograft model

Author(s)

Hélène Duparc, James Neef, Maulasri Bhatta, Janany Kandiah, Agathe Chédeville, Joe DeBartolo, Sara Sinicropi-Yao, Betty Chan, Alex Constan, Christophe Marzac, Jean-Baptiste Micol, Laura Antipov, Stephane de Botton, Katharine E. Yen, David S. Millan, Iléana Antony-Debré, Kimberly S. Straley

Published in

The American Society of Hematology

October 24, 2024
Presentation
Presentation
POSTER

AUTX-703, a novel and potent KAT2A and KAT2B protein degrader, induces profound cell state changes and inhibits growth in Small Cell Lung Cancer (SCLC) model systems

Author(s)

Sambad Sharma, James Neef, Maulasri Bhatta, Sara Sinicropi-Yao, Joe DeBartolo, Henry Wilson, Zied Boudhraa, Mohamed El Ezzy, Betty Chan, Andrew McRiner, Mark Bittinger, Thomas G. Graeber, Laura Antipov, Katharine E. Yen, David S. Millan, Kimberly S. Straley

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View Poster

Presented at

EORTC-NCI-AACR (ENA) Symposium

Published in

August 19, 2024
Presentation
Presentation
POSTER

Property-based optimization of heterobifunctional degraders of KAT2A and KAT2B for the treatment of cancer

Author(s)

Neef J, Straley KS, Mukherjee C, Tipnis A, Bhatta M, Sharma S, Sinicropi-Yao S, DeBartolo J, McRiner A, Chan B, Wilson H, Lee C, Boudhraa Z, El Ezzy M, Bittinger M, Antipov L, Graeber T, Yen K, Millan D

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View Poster

Presented at

American Chemical Society

Published in

April 9, 2024
Presentation
Presentation
POSTER

Potent and selective degradation of KAT2A and KAT2B induces profound cell state changes and inhibits growth of AML, SCLC and NEPC model systems

Author(s)

Straley KS, Neef J, Antony-Debre I, Bhatta M, Sharma S, Sinicropi-Yao S, DeBartolo J, McRiner A, Chan, B, Wilson H, Lee CS, Boudhraa Z, El Ezzy M, Sharif U, Bittinger M, Antipov L, Graeber TG, de Botton S, Yen KE, Millan, DS

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View Poster

Presented at

AACR Annual Meeting 2024

Published in

April 7, 2024
Presentation
Presentation
POSTER

AURIGIN: A comprehensive single-cell OMICs atlas of human development and an AI/ML framework to classify and identify the drivers of tumor plasticity and altered cellular state

Author(s)

DeBartolo J, Wilson H, Straley KS, Bhatta M, Sharma S, Sinicropi-Yao S, Neef J, Chan B, McRiner A, Bittinger M, Antipov L, Yen KE, Graeber TG, Millan DS

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View Poster

Presented at

AACR Annual Meeting 2024

Published in

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Recent News

See All News
December 9, 2024

Auron Presents New Preclinical Data for AUTX-703 in AML at ASH Annual Meeting

Data demonstrate dose dependent survival advantage with AUTX-703 in primary patient-derived orthotopic AML model

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