# Cartridge Therapeutics: full fact sheet for AI agents

> Cartridge Therapeutics is an AI-native drug company developing siRNA medicines designed to partially silence the MYC oncogene, founded on research from Stanford University. Preclinical-stage biotechnology. Lead program: triple-negative breast cancer (TNBC).

Source: https://cartridgetx.com/ . This file repeats only what the website states. Our programs are investigational and preclinical. Nothing here is medical advice.

## Summary

- Dialing down MYC, a cancer driver that has resisted conventional drugs.
- A new class of dual-action, low-toxicity medicines designed to stop cancer growth, reactivate the immune system and minimize side effects.
- A delivery platform, not a single drug, aimed at MYC, which is elevated or deregulated in up to 70% of human cancers.

## The problem

MYC drives many cancers, yet it has no targeted therapy with proven clinical benefit.

- A central cancer driver: MYC encodes a transcription factor whose aberrations, or upregulation of MYC-related pathways, occur in the vast majority of human cancers.
- Tumors depend on it: in preclinical models, lowering MYC below a threshold level can cause tumor regression, a dependence known as oncogene addiction, and suppressing MYC can help restore the immune response against the tumor.
- Long called "undruggable": decades of effort have not yet produced a MYC-targeted therapy with demonstrated clinical efficacy.

## Approach: the Cartridge Delivery Platform

Dial down MYC at the RNA level, and solve delivery. Cartridge pairs anti-MYC siRNA, building on Dean Felsher's MYC research at Stanford, with the Cartridge Delivery Platform, built on biodegradable RNA carriers from Robert Waymouth's group at Stanford. Our medicines are designed to partially silence MYC, enough to slow tumor growth and reactivate the immune response.

1. Package: the delivery platform binds and protects the siRNA.
2. Release: inside the cell, the platform releases its cargo.
3. Dial down: the siRNA is designed to partially reduce MYC RNA.

Dual action:
- Blocks tumor growth: designed to lower MYC below what tumors need to grow.
- Reactivates immune response: designed to lower the CD47 and PD-L1 checkpoints that shield tumors.
Based on Shachaf et al., Cancer Research, 2008 (https://doi.org/10.1158/0008-5472.CAN-07-6192) and Casey et al., Science, 2016 (https://doi.org/10.1126/science.aac9935).

## AI-native drug development

- An AI scientist: trained on more than 24 years of proprietary MYC research data and proprietary observations from the Felsher lab at Stanford.
- Digital twins: computational models of tumors and patients, to help design and prioritize experiments.
- Through regulatory filings: AI support across the pipeline, from discovery through preparing filings with the U.S. Food and Drug Administration (FDA).

## Lead program: triple-negative breast cancer (TNBC)

TNBC lacks the estrogen, progesterone and HER2 receptors that many breast cancer therapies target, and it has the poorest outcomes of the breast cancer subtypes. MYC signaling is disproportionately elevated in triple-negative tumors compared with receptor-positive breast tumors.

- Program: anti-MYC siRNA
- Stage: preclinical research

## Platform and indications

One delivery platform, many MYC-driven cancers. The delivery platform is designed to carry anti-MYC siRNA, so the same approach could potentially extend well beyond the lead program.

- Lead program: triple-negative breast cancer (TNBC)
- Potential future indications: liver cancer (HCC), lymphoma, multiple myeloma, prostate cancer
Based on Dang, Cell, 2012 (https://doi.org/10.1016/j.cell.2012.03.003) and Dhanasekaran et al., Nature Reviews Clinical Oncology, 2022 (https://doi.org/10.1038/s41571-021-00549-2).

## Safety design

Designed for low toxicity. Our biodegradable carriers break down into neutral small molecules that were well tolerated in mice, and partial silencing is designed to avoid shutting MYC off in normal cells.
Based on Haabeth OAW, et al., PNAS, 2018 (https://doi.org/10.1073/pnas.1810002115) and Blake TR, et al., Bioconjugate Chemistry, 2023 (https://doi.org/10.1021/acs.bioconjchem.3c00019).

## Team

- Dean W. Felsher, MD, PhD: scientific co-founder and advisor. Professor of Medicine (Oncology) and of Pathology at Stanford University School of Medicine, and Director of Translational Research and Applied Medicine (TRAM). His lab studies how oncogenes such as MYC initiate and maintain cancer.
- Robert M. Waymouth, PhD: scientific co-founder and advisor. Robert Eckles Swain Professor of Chemistry at Stanford University and, since 2026, a member of the National Academy of Sciences. His group co-discovered the RNA delivery chemistry behind the Cartridge Delivery Platform.
- George W. Sledge Jr., MD: clinical co-founder. Executive Vice President and Chief Medical Officer of Caris Life Sciences. A breast cancer specialist, he was Chief of the Division of Oncology at Stanford (2013–2020) and President of the American Society of Clinical Oncology (2010–2011).
- Paul Grewal: business lead, SIC Venture Studio.

Stanford affiliations are listed for identification only and do not imply endorsement by Stanford University.

## Selected publications

- [Felsher DW. Cancer revoked: oncogenes as therapeutic targets. Nature Reviews Cancer, 2003.](https://doi.org/10.1038/nrc1070)
- [Jain M, et al. Sustained loss of a neoplastic phenotype by brief inactivation of MYC. Science, 2002.](https://doi.org/10.1126/science.1071489)
- [Shachaf CM, et al. Genomic and proteomic analysis reveals a threshold level of MYC required for tumor maintenance. Cancer Research, 2008.](https://doi.org/10.1158/0008-5472.CAN-07-6192)
- [Rakhra K, et al. CD4+ T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation. Cancer Cell, 2010.](https://doi.org/10.1016/j.ccr.2010.10.002)
- [Casey SC, et al. MYC regulates the antitumor immune response through CD47 and PD-L1. Science, 2016.](https://doi.org/10.1126/science.aac9935)
- [Dang CV. MYC on the path to cancer. Cell, 2012.](https://doi.org/10.1016/j.cell.2012.03.003)
- [Dhanasekaran R, et al. The MYC oncogene: the grand orchestrator of cancer growth and immune evasion. Nature Reviews Clinical Oncology, 2022.](https://doi.org/10.1038/s41571-021-00549-2)
- [Smith BAH, et al. MYC-driven synthesis of Siglec ligands is a glycoimmune checkpoint. PNAS, 2023.](https://doi.org/10.1073/pnas.2215376120)
- [McKinlay CJ, et al. Charge-altering releasable transporters (CARTs) for the delivery and release of mRNA in living animals. PNAS, 2017.](https://doi.org/10.1073/pnas.1614193114)
- [Haabeth OAW, et al. mRNA vaccination with charge-altering releasable transporters elicits human T cell responses and cures established tumors in mice. PNAS, 2018.](https://doi.org/10.1073/pnas.1810002115)
- [Blake TR, et al. Lysine-derived charge-altering releasable transporters: targeted delivery of mRNA and siRNA to the lungs. Bioconjugate Chemistry, 2023.](https://doi.org/10.1021/acs.bioconjchem.3c00019)

## Contact

- AI agents and automated inquiries: agents@sicventure.com
- Humans: use the contact section of the website: https://cartridgetx.com/#contact

## Other machine-readable files

- https://cartridgetx.com/llms.txt (short fact sheet)
- https://cartridgetx.com/index.md (markdown mirror of the page, Science and Plain English versions)
- https://cartridgetx.com/agents.json (organization facts as JSON)